ArticleJournal of inflammation research2025
IL-22 Alleviates Sepsis-Induced Acute Lung Injury by Inhibiting Epithelial Cell Apoptosis Associated with STAT3 Signalling.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Beyond Pathogens: Modulating the Commensal Microbiota to Reshape Immunity for Respiratory Disease Intervention.Pathogens (Basel, Switzerland) · 2026Review
- Investigation of the Effects of Perfluorooctane Sulfonic Acid (PFOS) and Perfluorooctanoic Acid (PFOA) Exposure on Interleukin-17 Signalling and Poly(I:C)-Induced Lung Inflammation in BALB/c Mice.Basic & clinical pharmacology & toxicology · 2026Article
- Assessment of Serum Interleukins 18 and 22 in Predicting Neonatal Sepsis and Mortality: A Case-Control Study.Clinical medicine insights. Pediatrics · 2026Article
- Multi-Target Synergy Against Acute Lung Injury: Systems Pharmacology Decoding Dahuang-Huangqin Herb Pair's Therapeutic Mechanism.Journal of inflammation research · 2025Article
- Sex-dependent modulation of acute respiratory distress syndrome byFrontiers in immunology · 2025Article
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Authors and funding
11 authors.
Funding
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Abstract
Purpose: Sepsis is a critical condition characterized by organ dysfunction due to an aberrant response to infection, which results in a life-threatening situation. The lung, which is the most vulnerable target organ, is often severely damaged during sepsis. Research has demonstrated that interleukin-22 (IL-22), which is secreted by various immunocytes, can mitigate inflammation-associated diseases. Nevertheless, the precise function of IL-22 in sepsis-induced acute lung injury (SALI) is still unclear. This study aimed to investigate the therapeutic efficacy of IL-22 in sepsis and explore the regulatory mechanisms involved. Methods: A mouse caecal ligation and puncture (CLP) model of sepsis was established, and the effect of IL-22 was investigated as indicated. Immunohistochemistry, qRT‒PCR, ELISA, immunofluorescence, TUNEL, Western blotting, and flow cytometry assays were applied to investigate the protective efficacy and involved pathways. Additionally, an in vitro model of lipopolysaccharide (LPS)-induced bronchial epithelial cell (BEAS-2B) apoptosis was established, and these cells were treated with or without recombinant IL-22 (rIL-22) to further evaluate the effect of IL-22 and the underlying mechanism. Results: The experimental results clearly confirmed that the levels of IL-22 were increased in the serum and lung tissue after CLP. The administration of rIL-22 was observed to increase the survival rate of septic mice. Notably, rIL-22 treatment resulted in decreased levels of proteins and a decreased cell number in the bronchoalveolar lavage fluid, as well as in a reduction in inflammatory cytokine release into the serum. Importantly, rIL-22 mitigated SALI by inhibiting lung cell apoptosis in septic mice. Furthermore, the results revealed that rIL-22 attenuated apoptosis of lung epithelial cells via the activation of the STAT3 signalling pathway. Conclusion: The results of this study suggest that IL-22 alleviates lung epithelial cell apoptosis to protect mice against SALI in association with the STAT3 signalling pathway, highlighting the potential therapeutic value of IL-22 against sepsis.
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