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The Role of Cytokines in Inflammation and Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 20 June 2026 | Viewed by 2833

Special Issue Editor

Special Issue Information

Dear Colleagues,

Inflammation is one of the largest biological responses resulting from the interaction of organs with the innate and acquired immune systems. Large amounts of inflammatory cytokines are produced, affecting organs throughout the body. Severe and prolonged inflammation can cause functional and organic damage to other organs, including the cerebral cardiovascular system, liver, and kidneys, and can be fatal. Along with a clear understanding of the mechanisms of these inflammations, the development of novel anti-inflammatory agents is eagerly awaited.

Severe inflammatory diseases may be strongly associated with systemic complications, such as atherosclerosis, abnormal lipid metabolism, nonalcoholic fatty liver disease, nephrosclerosis, systemic amyloidosis, and nervous system diseases. Thus, elucidation of the molecular and cellular mechanisms of disease and the close relationship between inflammation and systemic complications may also be an area of research. Against this background, clinical evidence and research findings focusing on the molecular and cellular mechanisms of inflammation and inflammatory diseases are also welcome.

Prof. Dr. Keiichi Yamanaka
Guest Editor

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Keywords

  • inflammation
  • cytokine
  • complication
  • systemic inflammation
  • internal organ

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Published Papers (2 papers)

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Research

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18 pages, 3788 KB  
Article
Mesangial Cells (MES-SV40) Cultured in High Glucose Produce IL-36α, Which Is Associated with Type 2 Diabetes Mellitus
by María Marcela Sánchez-Torres, Cesar G. Pelcastre-Rodríguez, Fernando Gómez-Chávez, Isaí Martínez-Torres, José Martín Murrieta-Coxca, Alma Nelly Diaz-Herreros, Marcelo W. Heredia-Murillo, Juan C. Cancino-Diaz and Mario E. Cancino-Diaz
Int. J. Mol. Sci. 2026, 27(6), 2751; https://doi.org/10.3390/ijms27062751 - 18 Mar 2026
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Abstract
The high concentration of the inflammatory cytokine IL-36 in the serum of patients with type 2 diabetes mellitus (T2DM), along with the reduced renal damage observed in IL-36R knockout mice following ischemia–reperfusion-induced acute kidney injury, suggests a significant association between IL-36 activity and [...] Read more.
The high concentration of the inflammatory cytokine IL-36 in the serum of patients with type 2 diabetes mellitus (T2DM), along with the reduced renal damage observed in IL-36R knockout mice following ischemia–reperfusion-induced acute kidney injury, suggests a significant association between IL-36 activity and diabetic complications such as diabetic nephropathy (DN). It is also known that minor structural alterations in glomerular tissues can lead to changes in blood vessel pressure, potentially contributing to the development of DN, with inflammation acting as a triggering factor. However, further studies are needed to confirm this relationship. In this study, we observed that mesangial (MES-SV40) cells cultured under high-glucose conditions produced IL-36α in a dose-dependent manner. This cytokine production was also detected in mesangial cells from the glomerular tissues of mice with a high-calorie diet-induced T2DM, whereas healthy mice did not show such expression. In addition, we observed that mouse endothelial cells (SVECs) showed increased tubule formation in co-culture with MES-SV40 cells that had been previously exposed to 30 mmol/L glucose, as well as with the supernatant from these cells. IL-36R expression was confirmed in endothelial cells, as well as the angiogenic effect of IL-36α. Given that elevated VEGF levels have been reported in patients with DN by other authors, our results suggest that IL-36 produced by mesangial cells under high-glucose conditions may promote angiogenesis in glomerular tissues, potentially initiating the development of diabetic nephropathy. Full article
(This article belongs to the Special Issue The Role of Cytokines in Inflammation and Diseases)
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Review

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23 pages, 866 KB  
Review
The Role of IL-17 in Periodontitis and Its Systemic Connections
by Tobias Bonsmann, Martyna Mochol, Ewa Bonsmann, Lukasz Jablonowski, Andrzej Pawlik, Joanna Rasławska-Socha, Mariusz Lipski and Małgorzata Mazurek-Mochol
Int. J. Mol. Sci. 2025, 26(22), 10902; https://doi.org/10.3390/ijms262210902 - 10 Nov 2025
Cited by 4 | Viewed by 2103
Abstract
Interleukin 17 (IL-17) is a crucial mediator at the interface of periodontal dysbiosis and host immunity. This review synthesizes current evidence on IL-17 in periodontitis (PD), its systemic connections, and the role of IL-17 gene variants. Clinical and experimental studies show that IL-17 [...] Read more.
Interleukin 17 (IL-17) is a crucial mediator at the interface of periodontal dysbiosis and host immunity. This review synthesizes current evidence on IL-17 in periodontitis (PD), its systemic connections, and the role of IL-17 gene variants. Clinical and experimental studies show that IL-17 rises in periodontal disease and is associated with the severity of PD via action on epithelial, stromal and osteoblastic cells to promote chemokine release, neutrophil recruitment, cyclooxygenase 2 and prostaglandin E2 synthesis, RANKL expression, osteoclastogenesis, and matrix metalloproteinase activity. Periodontopathogens Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans pre-activate the local inflammation-maintaining Th17 response. There is converging evidence linking IL-17-centered signaling with rheumatoid arthritis, diabetes mellitus, and psoriasis in favor of a shared inflammatory network in barrier tissues and synovium. Despite these associations, IL-17 biology is contextually determined with mucosal defense and bone homeostatic roles that caution against unidimensional explanations. Evidence on IL-17A and IL-17F polymorphisms is still heterogeneous across populations with modest and variable risk associations with PD. Clinically, IL-17 in gingival crevicular fluid, saliva, or serum is a potential monitoring biomarker when utilized along with conventional indices. Therapeutically, periodontal therapy that reduces microbial burden may inhibit IL-17 function, and IL-17-targeted therapy has to balance potential benefit to inflammation and bone resorption against safety in oral tissues. The following research must utilize harmonized case definitions, standardized sampling, and multiethnic cohorts, and it must include multiomics to be able to differentiate between causal and compensatory IL-17 signals. Full article
(This article belongs to the Special Issue The Role of Cytokines in Inflammation and Diseases)
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