Journal of Inflammation Research

Dove Medical Press is pleased to invite you to submit your research to an upcoming Article Collection on "Anti-inflammatory Biologics – A Game Changer for Chronic Inflammation", in the Journal of Inflammation Research.

This Collection, edited by the Editor-In-Chief Prof. Ning Quan, is part of the new Game Changer series of Article Collections, focusing on breakthrough therapies, drugs, and technologies that have significantly altered the standard of care, leading to game-changing improvements in patient outcomes.

Chronic inflammation is the hallmark of many diseases. These conditions can be crippling to patients. Traditional anti-inflammatory drugs, such as non-steroidal anti-inflammatory drugs (NSAIDs) or corticosteroids, are non-specific, causing further systemic problems with continued use. By contrast, biologic therapies harness the specificity necessary to relieve inflammation while also reducing off-target and non-specific effects.

While this call is open to receive manuscripts highlighting all anti-inflammatory biologics, the Editors are particularly interested in manuscripts relating to the following areas:

• Tumor necrosis factor inhibitors
• Interleukin inhibitors
• Monoclonal antibody specificity studies
• Novel mechanisms of action of new candidate biologics
• The role of biosimilars in treating inflammatory disease
• Indications and contraindications
• Cell-based therapies to quell inflammation

Submitting authors are eligible for a 20% discount on the Article Publishing charge by applying the following code at the point of submission: OTIPZ. If you have any queries regarding the Article Collection or would like to discuss a submission, then please email the Commissioning Editor Ashley Ambros ([email protected]). Papers published within the Game Changer series will benefit from additional promotional activities across Taylor and Francis, increasing the discoverability and visibility of your research.

All manuscripts submitted to this Article Collection will undergo a full peer-review. Please review the journal’s aims and scope and author submission instructions prior to submitting a manuscript. Please submit your manuscript on our website. The deadline for submitting a manuscript is 1 April 2026.

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Dove Medical Press is pleased to invite you to submit your research to an upcoming Article Collection on "Targeting the IL-4/IL-13 Axis in the Treatment of Type 2 Inflammation", in the Journal of Inflammation Research.

This Collection, edited by the Editor-In-Chief Prof. Ning Quan, is part of the new Game Changer series of Article Collections, focusing on breakthrough therapies, drugs, and technologies that have significantly altered the standard of care, leading to game-changing improvements in patient outcomes.

Type 2 inflammation occurs when immune cells, including eosinophils and mast cells, are activated, producing the cytokine IL-4 and Il-13. These cytokines are responsible for signaling the production of eosinophils, mast cells, and IgE antibodies, that lead to the release of more pro-inflammatory cytokines. Type 2 inflammatory conditions affect 10-30% of the global population, and include common conditions such as allergy, asthma, eczema, and eosinophilic esophagitis. By targeting IL-4 and IL-13, overactive immune systems can be regulated, and many patients will see a better quality of life.

While this call is open to receive manuscripts highlighting all aspects of drugs targeting the IL-4/Il-13 axis, the Editors are particularly interested in manuscripts relating to the following areas:

• Clinical studies on the efficacy and safety of IL-4 and/or IL-13 inhibitors
• Novel drug mechanistic actions
• Biologics directed against cells or pathways involved in the IL-4/IL-13 axis
• New drug candidates directed against IL-4 and/or IL-13
• Tailoring treatment in individuals with multiple Type 2 inflammatory conditions
• Drugs to treat non-allergic type 2 inflammation, such as nasal polyps
• Treatment strategies and potential side effects

Submitting authors are eligible for a 20% discount on the Article Publishing charge by applying the following code at the point of submission: YXVCF. If you have any queries regarding the Article Collection or would like to discuss a submission, then please email the Commissioning Editor Ashley Ambros ([email protected]). Papers published within the Game Changer series will benefit from additional promotional activities across Taylor and Francis, increasing the discoverability and visibility of your research.

All manuscripts submitted to this Article Collection will undergo a full peer-review. Please review the journal’s aims and scope and author submission instructions prior to submitting a manuscript. 

Please submit your manuscript on our website. The deadline for submitting a manuscript is 1 April 2026.

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Dove Medical Press is pleased to invite you to submit your research to an upcoming Article Collection on "Integrating Artificial Intelligence into Inflammation and Cancer Immunology: From Biomarkers Discovery and Mechanistic Insights to Precision Therapeutics", in the Journal of Inflammation Research.

Inflammation exerts a complex and context-dependent influence on both oncogenesis and the efficacy of cancer therapies. Acute inflammatory responses may enhance anti-tumor immunity; however, chronic inflammation is more commonly implicated in tumor initiation, progression, and the facilitation of immune evasion. Persistent inflammatory signaling contributes to the development of an immunosuppressive tumor microenvironment (TME) by promoting the infiltration of immunoregulatory cell populations, including regulatory T cells, myeloid-derived suppressor cells, and M2-polarized macrophages. This immunosuppressive milieu hinders the therapeutic effectiveness of immune checkpoint inhibitors and adoptive cell therapies such as chimeric antigen receptor T cells. Inflammatory cytokines such as IL-6, IFN-, and TNF-α also play dual roles, with context-dependent capacities to either promote immune resistance or augment immune activation.

Consequently, the modulation of inflammatory pathways holds promise for the development of patient-specific therapeutic strategies aimed at enhancing responses to anti-cancer treatments. For example, the combination of anti-inflammatory agents with immune checkpoint inhibitors may be particularly beneficial in patients exhibiting elevated baseline levels of inflammation. Among the most promising anti-inflammatory approaches is the use of epigenetic inhibitors, including histone deacetylase (HDAC) inhibitors and DNA methyltransferase (DNMT) inhibitors, which have demonstrated synergistic potential when used in combination with immunotherapies to overcome resistance mechanisms. Importantly, the identification of inflammation-associated biomarkers is essential for effective patient stratification. Such biomarkers would enable the rational design of combinatorial treatment regimens and improve the predictive capacity for therapeutic responses in the context of cancer immunotherapy.

The complex regulatory networks that control inflammation within TME are pivotal to the rational design of combinatorial strategies. Recent advances in artificial intelligence (AI), multi-omics technologies, and computational biology now offer powerful tools for the identification and validation of inflammation-associated biomarkers, as well as for elucidating the epigenetic alterations that drive their activation. These insights can be leveraged to inform the development of targeted therapeutic approaches, thereby facilitating the identification of individuals most likely to benefit from specific immunoepigenetic interventions.

This Article Collection seeks interdisciplinary research that investigate the role and underlying mechanisms of epigenetic alterations in the regulation of inflammation and tumor immunity. We welcome original research articles, reviews, clinical trial studies, and case reports. Submissions are also encouraged that examine the application of AI in predicting therapeutic responses and guiding precision immuno-oncology strategies.

Keywords

1. Inflammation and Tumor Immunity
2. Epigenetic Modulation
3. Artificial Intelligence in Oncology
4. Tumor Microenvironment and Metabolism
5. Diagnostic and Prognostic Biomarkers

All manuscripts submitted to this Article Collection will undergo a full peer-review. Please review the journal’s aims and scope and author submission instructions prior to submitting a manuscript.

Please submit your manuscript on our website, using the promo code 34582 to indicate that the manuscript is intended for this Article Collection. The deadline for submitting a manuscript is 15 April 2026.

Please contact Ashley Ambros at [email protected] with any queries and discount codes regarding this Article Collection.

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Dove Medical Press is pleased to invite you to submit your research to an upcoming Article Collection on "Cellular and Molecular Drivers of Lung Inflammation in Respiratory Diseases", in the Journal of Inflammation Research.

Lung inflammation is a hallmark characteristic feature of many respiratory diseases, from asthma and chronic obstructive pulmonary disease (COPD) to pulmonary fibrosis and acute respiratory distress syndrome (ARDS). While inflammation serves as a protective role in response to infection or injury, dysregulated or persistent inflammatory responses can lead to progressive lung damage and impaired respiratory structure and function. Understanding the cellular and molecular drivers behind lung inflammation is crucial for developing targeted therapies that can modulate these pathways without compromising host defense. This topic explores the intricate network of immune and structural cells, signaling pathways, and other cofounding factors that orchestrate inflammatory responses in the lung. This study will offer valuable insight into both disease mechanisms and potential intervention points.

This topic is important because it establishes the foundational understanding of lung inflammation, a key driver of the onset, progression, and severity of numerous respiratory diseases that together pose a significant global health burden.
Studying this topic also matters as it provides following additional advantages:
• Better Understanding of Disease Mechanisms
• Development of Targeted Therapies
• Early Diagnosis and Biomarkers tools
• Understanding Environmental and Infectious Triggering agent

The subject of this Collection, "Cellular and Molecular Drivers of Lung Inflammation in Respiratory Diseases," explores the complex cellular and molecular processes that drive and regulate lung inflammation. It covers key subtopics including immune cell activation, structural cells dysfunction, cytokine and chemokine signaling, and the impact of environmental and infectious triggers on pulmonary inflammation. Special attention will also be given to emerging therapeutic targets and biomarker discovery. This scope is well-aligned with the Journal of Inflammation Research, which emphasizes cutting-edge studies on inflammation-related processes. The ail of this collection will be to encourage the submission of original research articles, comprehensive reviews, and brief reports that will provide new insights into the cellular and molecular understanding of lung inflammation in both acute and chronic respiratory diseases.

Keywords

1. Lung inflammation
2. Respiratory diseases
3. Immune cell signaling
4. Cytokines and chemokines
5. Biomarkers of lung disease

All manuscripts submitted to this Article Collection will undergo a full peer-review. Please review the journal’s aims and scope and author submission instructions prior to submitting a manuscript.

Please submit your manuscript on our website, using the promo code 5DF61 to indicate that the manuscript is intended for this Article Collection. The deadline for submitting a manuscript is 15 June 2026.

Guest Advisors

Dr. Ashish Kumar, North Dakota State University

[email protected]

I am a Doctoral Graduate Research Assistant in pharmaceutical sciences, specializing in the pathophysiology of asthma. My research explores the dynamic relationship between lung physiology and hormonal influences in disease conditions, aiming to advance respiratory pharmacology and personalized medicine.

Dr. Nilesh Sudhakar Ambhore,University of Minnesota

[email protected]

I am a dedicated and self-motivated research scientist with over 8 years of extensive experience in pharmacology, molecular biology, small molecule drug discovery, and target validation. My proven expertise encompasses the entire preclinical drug development process, including development of in vivo disease models, mechanism of action investigation, endpoint analysis, and disease modelling.

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Dove Medical Press is pleased to invite you to submit your research to an upcoming Article Collection on "Neutrophils in a New Light: Emerging Roles in Inflammation", in the Journal of Inflammation Research.

Neutrophils are among the most abundant and evolutionarily conserved components of the innate immune system, long recognized for their frontline role in microbial defense and acute inflammation. However, our understanding of these cells has significantly evolved. Beyond their classical functions, neutrophils are now appreciated as highly plastic and multifunctional cells with the capacity to influence a wide range of immune responses, including those involved in chronic and sterile inflammation, tissue repair, autoimmunity, and even cancer.

This proposed Article Collection of the Journal of Inflammation Research aims to highlight the growing complexity of neutrophil biology and its implications for understanding and treating inflammatory diseases. By assembling a focused collection of high-quality original research articles, reviews, and short communications, this issue will provide readers with a comprehensive and up-to-date overview of the novel roles of neutrophils across diverse inflammatory contexts.

The field of neutrophil research is currently undergoing a paradigm shift. Advances in single-cell RNA sequencing, in vivo imaging, and functional assays have revealed striking heterogeneity among neutrophil populations, suggesting that they are far from being a homogenous cell type. Moreover, their ability to engage in crosstalk with other immune cells, influence adaptive responses, shedding neutrophil extracellular traps (NETs), and contribute to chronic inflammatory states has far-reaching implications for disease progression and therapy.

Despite this, neutrophils remain understudied compared to other immune cells, particularly in chronic disease settings where their roles are less obvious but no less critical. A dedicated special issue in the Journal of Inflammation Research would provide a much-needed platform for consolidating recent discoveries, showcasing state-of-the-art methodologies, and highlighting clinical relevance. Such an issue is well aligned with the journal’s mission to advance understanding of inflammatory mechanisms and foster translational insights into inflammation-related disorders.

This Article Collection will explore the evolving landscape of neutrophil biology with particular emphasis on novel and disease-relevant functions. The field in which submissions are welcomed address the following (but not limited to) subtopics:
1) Neutrophil heterogeneity and plasticity: Insights from single-cell and spatial profiling.
2) Neutrophil roles in chronic inflammation and autoimmunity: Contributions to diseases such as lupus, rheumatoid arthritis, and vasculitis.
3) NETs in inflammation: Molecular mechanisms, regulation, and pathological consequences.
4) Tissue-specific neutrophil behavior: Adaptation and function in lungs, liver, gut, CNS, and tumors.
5) Neutrophil interactions with adaptive immunity: Mechanisms of T cell modulation and antigen presentation.
6) Neutrophils in infection and viral inflammation: Including roles in COVID-19, sepsis, and chronic infections.

This Article Collection will serve as a comprehensive reference for scientists and clinicians working across immunology, inflammation, infectious disease, and translational medicine. By focusing on neutrophils, a cell type once considered simple but now recognized as highly influential, this issue aims to stimulate further research and innovation in the field of inflammation.

Keywords

1. Neutrophils Biology
2. Innate Immunity
3. Inflammation Resolution
4. Neutrophil Heterogeneity
5. Neutrophil Extracellular Traps (NETs)

All manuscripts submitted to this Article Collection will undergo a full peer-review. Please review the journal’s aims and scope and author submission instructions prior to submitting a manuscript.

Please submit your manuscript on our website, using the promo code 5480B to indicate that the manuscript is intended for this Article Collection. The deadline for submitting a manuscript is 15 June 2026.

Guest Advisor

Dr. Tomasz W Kaminski, Thrombosis and Hemostasis Program, Versiti Blood Research Institute, Milwaukee, WI

[email protected]

Tomasz W. Kaminski earned his doctoral degree from the Medical University of Bialystok, Poland. During his PhD training, he focused on studying hemostasis disturbances in chronic kidney disease. He joined the Sundd Lab as a postdoctoral associate in 2019. Dr. Kaminski’s research centers on innate immune mechanisms in platelets and neutrophils, as well as the pathophysiology of thrombo-inflammation. He employs state-of-the-art intravital microscopy techniques to capture real-time interactions between neutrophils and platelets during the initial phases of immune system activation. His work exhibits a truly interdisciplinary nature, as he investigates the neutrophil and platelet biology in hemophilic arthropathy, sickle cell disease and influenza. Dr. Kaminski has been recognized with numerous awards from both national and international societies and institutions. Furthermore, his research endeavors receive support from external funding sources.

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Dove Medical Press is pleased to invite you to submit your research to an upcoming Article Collection on "Inflammatory Disorders and Diseases of Environmental Etiology", in the Journal of Inflammation Research.

Chronic inflammation is a key pathological feature underlying development and progression of chronic diseases including cardiovascular, respiratory, and neurodegenerative disorders. Inflammation is triggered by various environmental insults such as long-term exposure to toxic particles (PM2.5, ultrafines or nanoparticles), industrial chemicals (immunotoxicants), biological agents and infections, and climate change. On the other hand, occupational exposures to toxic particles or fibers, industrial and agricultural chemicals are among the major factors associated with chronic inflammatory disorders in adults. Certain communities living in the areas with inadequate zonal policies, or working in settings with higher and prolonged exposure to such pollutants, are at a greater risk of developing chronic inflammatory disorders. Additionally, children born in or living in such areas have arrested growth and higher rate of developmental disorders.

Published studies have consistently reported that exposed individuals may suffer chronic inflammation in different organs due to differential modulation of innate or adaptive pathways locally or systematically leading to development or exacerbation of inflammatory and/or developmental disorders. Chronic inflammatory and developmental disorders with environmental origins are poorly characterized in terms of their etiology, underlying mechanisms, potential therapeutic targets and targeted therapeis due to unique pathological manifestations in these disorders.

Environmental etiology of chronic inflammatory and developmental disorders is an important public health concern that needs to be addressed. Vulnerable communities often suffer from greater exposure risks and limited healthcare access leading to underdiagnosis of inflammatory and developmental disorders. Advancements in public health and mechanistic research to address these issues may unravel the causative factor(s), pathological mechanisms, and exposure limits of the key environmental factors responsible for disease burden. Additionally, such research advancements could help unravel potential therapeutic targets and facilitate development of targeted therapies for environmentally-induced chronic disroders. Research in these directions will promote the health equity and minimize the disease burden.

Original Research articles: Original articles may be focused on either mechanistic or epidimiological studies addressing the chronic inflammatory and developmental disorders associated with exposure to pollutants including particulates (natural or engineered) or chemical agents (metals, PFAS, pesticides, etc.), infectious agents or their antigens, climate change, or other environmental factors. Experimental studies using cellular or animal models should define the resemblance of the models with the real-world exposure scenario in human population. Animal studies could be focused on addressing the toxicological aspects, identifying molecular targets, biomarkers of exposure or effect, and/or targeted therapies, and proposing potential intervention/mitigation strategies. Epidimiological studies could focus on identifying the populations at risk of chronic inflammatory or developmental disorders and the associated environmental exposures and risk factors. Besides focusing on the current levels of exposure in the populations at risk, epidemiological studies may also focus on developing/recommending the permissible limits of these toxicants in residential and occupational settings.

Comprehensive Review Articles: Review articles addressing the pathologies of chronic inflammatory or developmental disordrs of environmental origin using experimental models could incorporate source of release of toxicant in the environment, exposure routes, biological effects and organ toxicities, mechanistic aspects, and therapeutic targets. Reviews based on human epidemiological studies may focus on consideration the zonal policies, vulnerable populations, current problem of unequal disease burdern due to toxicants, environmental regulation of the toxicants, and biomonitoring data addressing the level of exposure to humans and the environment. Comprehensive reviews may take into account both experimental and human studies. It is strongly recommended to propose potential strategies to improve the public health and promote health equity.

Keywords:

1. Experimental models of inflammatory effects of pollutant exposures
2. Respiratory, cardiovascular, metabolic, or neurological inflammatory disorders.
3. Developmental immunotoxicity disorders
4. Immune dysfunction in adulthood due to early life environmental exposures
5. Transgenerational immune effects of environmental origin

All manuscripts submitted to this Article Collection will undergo a full peer-review. Please review the journal’s aims and scope and author submission instructions prior to submitting a manuscript.

Please submit your manuscript on our website, using the promo code 874E2 to indicate that the manuscript is intended for this Article Collection. The deadline for submitting a manuscript is 15 June 2026.

Please contact Ashley Ambros at [email protected] with any queries and discount codes regarding this Article Collection.

Guest Advisors:

Afzaal N. Mohammed, University of Arizona COM-Phoenix

[email protected]

Dr. Mohammed is a ResearchScientist III at University of Arizona COM-Phoenix. His research interest centered around broad range or topics including developmental biology, respiratory toxicology and pathogenesis, public health, and drug discovery. His major contribution is in the field of developmental biology where is addressed emerging public health issues related to respiratory and neurological disorders using rodent models. Currently, he is focused 1) Identifying novel drugs and biological agents to treat developmental respiratory disorders. 2) Addressing the respiratory disorders associated with occupational exposure to carbon nanomaterials.

Jagjit S. Yadav, University of Cincinnati College of Medicine 

[email protected]

Dr. Yadav is Professor in the Department of Environmental and Public health, Division of Environmental genetics and Molecular Toxicology, at the University of Cincinnati College of Medicine, Cincinnati, Ohio, USA. He has been serving as a Deputy Director of the NIH’s P30 Center for Environmental Genetics at UC and Director of the Inhalation Toxicology Resource Unit. His research lab focuses on Pulmonary pathogenesis and immunotoxicology research as related to environmental health. He is also interested in understanding the role of host microbiome and genetic background in respiratory toxicity/infections/disease susceptibility from exposure to environmental pollutants (particles/nanoparticles, chemicals, microbial agents/antigens) using in vitro and in vivo (rodent) models and role of Gut-Lung axis in lung inflammatory disorders/disease.

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Dove Medical Press is pleased to invite you to submit your research to an upcoming Article Collection on "Inflammaging in Cardiovascular and Chronic Disease", in the Journal of Inflammation Research.

Inflammaging is a persistent, low-grade sterile inflammation associated with aging. It is characterized by elevated circulation of proinflammatory cytokines, chemokines and other inflammatory mediators in the circulation, reflecting a fundamental imbalance in intercellular communication and inflammatory control. Multiple lines of evidence indicate that inflammaging arises from a convergence of factors including immune cell dysregulation, immunosenescence, chronic infections, cellular senescence and genetic predisposition. Other than this, metabolic and environmental contributors such as central obesity, increased gut permeability, shifts in microbiota composition further exacerbates this process. At the molecular level, excessive production of reactive oxygen species, dysfunctional mitochondria play pivotal role in chronic inflammation. This persistent inflammatory state not only accelerates cellular senescence but also impairs immune system, leading to severe implications in tissue homeostasis. Thus, inflammation is recognized as an intrinsic driver of aging process and key contributor to pathogenesis of multiple chronic diseases.

Inflammaging is the major contributor to cardiovascular disease (CVD), the leading cause of morbidity and mortality worldwide. In 2021 alone, CVDs were responsible for 20.5 million deaths, accounting for roughly one-third of all global deaths. Beyond CVD, inflammaging is also recognized as a risk factor for several chronic conditions including cancer, kidney disease, diabetes mellitus, depression, dementia, sarcopenia, and frailty. Despite its well documented pathologic role across diverse diseases the precise molecular mechanism that regulate inflammaging remains incompletely understood and relatively understudied. Therefore, a comprehensive understanding of these processes holds great promise for the development of novel treatment strategies that could significantly improve the clinical outcome. Targeting inflammaging is a particularly appealing as it offers potential not only to prevent CVD but also to slow the broader health decline associated with ageing. Importantly interventions that modulating inflammation may be most effective if implemented early in the trajectory of age-related physiological decline.

This Article Collection aims to focus on the latest developments in understanding the role of inflammaging in the pathogenesis of cardiovascular and chronic inflammatory diseases. We welcome contributions that explore inflammaging across molecular, cellular and disease levels, with a focus on uncovering its mechanism and identifying innovative therapeutic strategies. By advancing knowledge in this area, the collections seeks to highlight novel targets for preventing and alleviating CVD, chronic inflammation and age-related diseases.

Submissions to this topic may include, but are not limited to, the following potential areas of research:

• Molecular drivers of inflammaging
• Biomarkers of inflammaging for early detection of cardiovascular and age-related diseases
• Emerging signalling pathways linking chronic low-grade inflammation, oxidative stress and mitochondrial dysfunction in aging vascular system
• Interplay between immune cell senescence and inflammaging in chronic disease progression
• Novel animal models and experimental tools for studying inflammaging mechanisms.
• Therapeutic strategies for counteract inflammaging, such as cytokine inhibitors, senolytics or anti-inflammatory drugs aimed at restoring vascular and systemic health
• Dietary and lifestyle interventions including the impact of prebiotics, and probiotics on inflammaging and healthy aging

This Article Collection welcomes submissions of the following article types: Original Research Articles, Brief Research Reports, Case Reports, Reviews and Mini-reviews.

Keywords

• Inflammaging
• Cardiovascular disease (CVD)
• Immunosenescence
• Senolytics
• Chronic inflammatory diseases

All manuscripts submitted to this Article Collection will undergo a full peer-review. Please review the journal’s aims and scope and author submission instructions prior to submitting a manuscript.

Please submit your manuscript on our website, using the promo code 2E6D0 to indicate that the manuscript is intended for this Article Collection. The deadline for submitting a manuscript is 1 June 2026.

Please contact Ashley Ambros at [email protected] with any queries and discount codes regarding this Article Collection.

Guest Advisor

Dr. Vigneshwaran Vellingiri, University of Illinois, Chicago

[email protected]

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Dove Medical Press is pleased to invite you to submit your research to an upcoming Article Collection on "Microbiome-Immune Crosstalk: Mechanisms, Therapeutic Modulation, and Translational Strategies in Chronic Inflammatory and Infectious Diseases", in the Journal of Inflammation Research.

The human microbiome, encompassing the diverse communities of bacteria, viruses, fungi, and other microorganisms inhabiting our body, plays a pivotal role in maintaining immune homeostasis and influencing disease outcomes. Emerging evidence has revealed that the intricate crosstalk between the microbiome and the immune system critically shapes host responses to infection, inflammation, and cancer. Dysbiosis, or imbalance in microbial communities, has been linked to chronic inflammatory diseases, autoimmune disorders, impaired wound healing, and variable responses to immunotherapies.

Understanding the mechanisms underlying microbiome-immune interactions is essential for developing innovative therapeutic strategies. Targeted modulation of microbial communities, whether through probiotics, prebiotics, postbiotics, or fecal microbiota transplantation, offers promising opportunities to enhance immune function and improve patient outcomes. Moreover, advanced multi-omics approaches are enabling a deeper understanding of host–microbe signaling pathways, revealing potential biomarkers and translational targets for precision medicine.

The interplay between the microbiome and the immune system is fundamental to human health, influencing everything from infection susceptibility to chronic inflammation and response to therapy. Dysregulation in this crosstalk can drive disease progression, reduce treatment efficacy, and contribute to poor clinical outcomes. By understanding these interactions, researchers can identify novel therapeutic targets, develop microbiome-based interventions, and enhance the effectiveness of immunotherapies.

Addressing microbiome-immune crosstalk is particularly important for precision medicine, as it enables the tailoring of treatments based on an individual’s microbial and immune profile. This approach has the potential to revolutionize the management of chronic inflammatory diseases, infectious conditions, autoimmune disorders, and cancer, ultimately improving patient outcomes and reducing healthcare burdens.

This Collection welcomes high-impact original research, reviews, mini-reviews, perspectives/commentaries, methodology papers and graphical reviews/visual communications focusing on the diverse scientific and translational innovations microbiome-immune signaling. Key themes include, but are not limited to:

1. Mechanistic insights into microbiome–immune system interactions;

2. Gut–organ axes and systemic immune regulation;

3. Microbiome influence on immunotherapy efficacy and vaccine response;

4. Dysbiosis-driven chronic inflammatory and autoimmune diseases;

5. Host–microbe signaling pathways as therapeutic targets;

6. Microbiome-targeted interventions: probiotics, prebiotics, postbiotics, and fecal microbiota transplantation (FMT);

7. Multi-omics approaches to study microbiome–immune networks;

8. Translational and clinical studies leveraging microbiome modulation.

Keywords

1. Microbiome–Immune Crosstalk

2. Dysbiosis

3. Immunomodulation

4. Chronic Inflammatory Disease

5. Precision Medicine

All manuscripts submitted to this Article Collection will undergo a full peer-review. Please review the journal’s aims and scope and author submission instructions prior to submitting a manuscript.

Please submit your manuscript on our website, using the promo code E6AEE to indicate that the manuscript is intended for this Article Collection. The deadline for submitting a manuscript is 16 November 2026.

Please contact Ashley Ambros at [email protected] with any queries and discount codes regarding this Article Collection.

Guest Advisors

Dr. Vinay Kumar, Penn State University, College of Medicine, 500 University Dr, Hershey, PA-17033, USA

[email protected]

Dr. Vinay Kumar is a Researcher (junior faculty) at the Heart and Vascular Institute, Pennsylvania State University, where his work focuses on dissecting dysregulated innate and adaptive immune networks in myocardial infarction (MI) and chronic heart failure (HF). His research emphasizes understanding the roles of distinct T-cell subsets and the time-dependent phenotypic shifts these cells undergo during chronic HF. Additionally, Dr. Kumar is dedicated to developing innovative immunomodulatory strategies to reverse pathological immune alterations and facilitate their translation from bench to bedside.

Dr. Anuradha Tyagi, Department of cBRN, Institute of Nuclear Medicine & Allied Sciences, Delhi 110054, India

[email protected]

Dr. Anuradha Tyagi is a biomedical researcher specializing in inflammation biology, wound healing, and host–pathogen interactions. Her work demonstrates that timely modulation of the inflammatory phase is crucial for proper wound closure and tissue repair, particularly in conditions like radiation dermatitis. She has highlighted the therapeutic potential of secondary bile acids in chronic wound management, showing their ability to inhibit biofilm formation, neutralize bacterial virulence factors, modulate pro-inflammatory cytokines, and promote angiogenesis. Dr. Tyagi’s research advances our understanding of immune responses, microbial dynamics, and tissue regeneration, with important translational implications for chronic wound therapy.

Dr Yash Gupta, Department of Medicine, Penn State Health Milton S. Hershey Medical Center, Hershey, PA-17033, USA

[email protected]

Dr. Yash Gupta is a leading translational researcher specializing in gut–liver axis disorders, with a primary focus on precision probiotics and endotoxemia in non-alcoholic fatty liver disease (NAFLD). His work includes the development of novel lipid membrane–camouflaged biomimetic nanoparticles for microRNA delivery to intestinal epithelial cells, enabling targeted therapeutic modulation of intestinal tight junction integrity. Dr. Gupta has also conducted seminal studies on microRNA-mediated suppression of kisspeptin receptors in pancreatic cancer, elucidating how comorbidities such as obesity and hypertension influence tumor survival. He has contributed to defining the role of Bifidobacterium bifidum–PPAR-γ signaling pathways, advancing probiotic-based strategies for inflammatory bowel disease. Additionally, Dr. Gupta has served as a key collaborator in multi-institutional research initiatives, including investigations into erythropoietin signaling in vagus nerve Schwann cells and its role in restoring intestinal motility following surgical injury.

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Dove Medical Press is pleased to invite you to submit your research to an upcoming Article Collection on "Bone-Immune System Crosstalk in Musculoskeletal Health and Disease", in the Journal of Inflammation Research.

Acute inflammation is a fundamental reparative response to injury in musculoskeletal tissues, orchestrating the recruitment of immune cells and the coordinated activity of osteoblasts, osteoclasts, and chondrocytes to remodel and restore damaged bone and cartilage. This intricate process is governed by a sophisticated network of immune signaling pathways and immunometabolic cues, maintaining a delicate homeostatic balance. The emerging field of osteoimmunology is dedicated to deciphering this critical crosstalk.

A bidirectional and dynamic dialogue between hematopoietic immune cells and resident skeletal cells is essential for effective tissue repair and the maintenance of musculoskeletal health. Disruption of this communication—whether by genetic predisposition, chronic inflammation, metabolic dysfunction, or pathogen invasion—can tip the balance from regenerative healing to pathological tissue destruction. This dysregulation lies at the heart of numerous debilitating conditions, leading to chronic pain, loss of function, and significant morbidity, underscoring an urgent need for deeper mechanistic understanding.

The goal of this Article Collection is to bring to light the pivotal role that bones and the musculoskeletal system play in health and disease, and the translational implications of osteoimmunology, immunometabolism, and inflammation-mechanobiology. Key topics include, but are not limited to:

• Coordination of inflammatory processes and skeletal/immune cells involved in bone tissue repair
• Conditions such as osteoarthritis and osteoporosis, characterized by inflammation and destruction of bone and cartilaginous tissue
• Bone and joint infections such as septic arthritis and osteomyelitis
• Arthritic conditions such as rheumatoid arthritis, spondyloarthritis (including ankylosing spondylitis), and gout/gouty arthritis

Keywords

• Osteoimmunology
• Bone-Immune Crosstalk
• Musculoskeletal Inflammation
• Arthritis
• Bone tissue repair

All manuscripts submitted to this Article Collection will undergo a full peer-review. Please review the journal’s aims and scope and author submission instructions prior to submitting a manuscript.

Please submit your manuscript on our website. The deadline for submitting a manuscript is 1 February 2027.

Please contact Ashley Ambros at [email protected] with any queries and discount codes regarding this Article Collection.

Guest Advisor

Dr. Chen Yan, The First Affiliated Hospital of Guangxi Medical University

[email protected]

Dr. Yan Chen is an orthopedic surgeon and Associate Editor of the Journal of Inflammation Research. His research focuses on osteoimmunology, bone regeneration, and mechanobiology of the bone marrow microenvironment. He has led multiple translational research projects exploring bone–immune interactions in musculoskeletal diseases and serves as a reviewer and editor for several international journals. His work integrates clinical orthopedics with cutting-edge molecular and spatial technologies to advance understanding of skeletal inflammation and repair.

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