Association of Interleukin-38 levels with gut microbiota dysbiosis in Type 2 Diabetes Mellitus patients | ||||
| Microbes and Infectious Diseases | ||||
| Articles in Press, Accepted Manuscript, Available Online from 27 May 2025 | ||||
| Document Type: Original Article | ||||
| DOI: 10.21608/mid.2025.376615.2714 | ||||
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| Authors | ||||
Muhammed Mutlak Awad  ; Nadia Ibrahim Salih
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| Department of Microbiology, College of Medicine, University of Tikrit, Iraq | ||||
| Abstract | ||||
| Background: Type 2 Diabetes Mellitus (T2DM) is a chronic metabolic condition characterized by insulin resistance, decreased insulin production, and persistent inflammation. Emerging evidence reveals a relation between gut microbial composition, interleukin 38 (IL-38), and T2DM pathogenesis. Dysbiosis in gut microbiota can influence metabolic and immune processes, potentially contributing to insulin resistance and systemic inflammation. Additionally, IL-38, a member of the IL-1 cytokine family, has been implicated in immune regulation and inflammation control, which may have relevance in T2DM progression. The aim of the study is to elucidate the complex association between gut microbiota and T2DM inflammation, metabolism, and immune disorders. Methods: This study reviews current literature and analyzes clinical and experimental findings on the relationship between gut microbiota, IL-38 expression, and T2DM.The research comprised 100 type 2 diabetes mellitus patients individuals with 40 individuals control, Blood and stool sample were obtained from all participants in Kirkuk city, all samples diagnosed by using microbiological and immunological methods. Also, statistical analysis programs were used for explaining the results. A systematic search of relevant studies was conducted, focusing on microbial composition shifts, IL-38 levels, and their combined impact on metabolic dysfunction. Results: Research indicates that gut microbiota dysbiosis in T2DM patients is linked to increased intestinal permeability, leading to systemic inflammation and metabolic disturbances. IL-38 has demonstrated potential anti-inflammatory properties that may counteract these effects by modulating immune responses. Correlations between reduced IL-38 expression and heightened inflammation in T2DM suggest a possible protective role of this cytokine. Conclusions: Understanding the relationship between gut microbiota, IL-38, and T2DM offers novel insights into metabolic disease mechanisms. IL-38, plays a crucial role in modulating inflammatory responses that are often implicated in the development and progression of T2DM. Its anti-inflammatory properties may help mitigate chronic low-grade inflammation associated with insulin resistance and metabolic dysregulation. Targeting gut microbiota composition and IL-38 signaling may therefore provide new avenues for therapeutic intervention, potentially improving outcomes for individuals with T2DM by addressing underlying inflammatory pathways and restoring metabolic balance. | ||||
| Keywords | ||||
| Gut Microbiota; Dysbiosis; Interleukin 38; Immune Regulation; Intestinal Permeability | ||||
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