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Methane limit LPS-induced NF-κB/MAPKs signal in macrophages and suppress immune response in mice by enhancing
Xu Zhang1,2,3, Na Li1, Han Shao1,2,3
1Department of Anesthesiology and Intensive Care, Changhai Hospital, The Second Military Medical University, Shanghai, 200433, China (mainland).
Abstract:
Inflammatory diseases such as sepsis and autoimmune colitis, characterized by an overwhelming activation of the immune system and the counteracting anti-inflammatory response, remain a major health problem in worldwide. Emerging evidence suggests that methane have a protective effect on many animal models, like ischaemia reperfusion injury and diabetes-associated diseases. Whether methane could modulating inflammatory diseases remains largely unknown. Here we show that methane-rich saline (MS) ip treatment (16 ml/kg) alleviated endotoxin shock, bacteria-induced sepsis and dextran-sulfate-sodium-induced colitis in mice via decreased production of TNF-α and IL-6. In MS-treated macrophages, LPS-induced activation of NF-κb/MAPKs was attenuated. Interestingly, MS treatment significantly elevated the levels of IL-10 both in vitro and in vivo. Neutralization of IL-10 abrogated the therapeutic effect of MS. Moreover, anti-IL10 blockade partially restored the MS-mediated attenuation of NF-κb/MAPKs phosphorylation. We further found that MS resulted in markedly enhanced phosphorylation of GSK-3β and AKT, which both mediate the release of Il-10. Additionally, inhibition of PI3K attenuated MS-mediated p-GSK-3β and IL-10 production and reversed the suppressed activation of NF-κb/ MAPKs in response to LPS. Our results reveal a novel effect and mechanisms of methane and support the potential value of MS as a therapeutic approach in innate inflammatory diseases.
Insights
Methane-rich saline (MS) alleviates inflammatory diseases like sepsis and colitis in mice. It works by reducing pro-inflammatory cytokines and increasing anti-inflammatory IL-10, offering a potential new therapy.
Area of Science:
- Immunology
- Gastroenterology
- Biochemistry
Background:
- Inflammatory diseases, including sepsis and autoimmune colitis, pose significant global health challenges due to immune system dysregulation.
- Methane has demonstrated protective effects in various animal models, but its role in inflammatory diseases is not well understood.
Purpose of the Study:
- To investigate the therapeutic potential of methane-rich saline (MS) in modulating innate inflammatory diseases.
- To elucidate the underlying molecular mechanisms of MS in controlling inflammation.
Main Methods:
- Mice models of endotoxin shock, bacterial sepsis, and dextran-sulfate-sodium-induced colitis were treated with MS.
- Macrophage activation, cytokine production (TNF-α, IL-6, IL-10), and signaling pathways (NF-κb, MAPKs, PI3K/AKT/GSK-3β) were analyzed in vitro and in vivo.
Main Results:
- MS treatment significantly alleviated inflammatory conditions in mice, reducing TNF-α and IL-6 levels.
- MS attenuated LPS-induced NF-κb/MAPKs activation and increased IL-10 production, which was crucial for its therapeutic effect.
- MS enhanced AKT/GSK-3β phosphorylation, indicating PI3K pathway involvement in IL-10 release and inflammation suppression.
Conclusions:
- Methane-rich saline demonstrates significant therapeutic potential for innate inflammatory diseases.
- The anti-inflammatory effects of MS are mediated through the PI3K/AKT/GSK-3β pathway, leading to increased IL-10 production and suppressed NF-κb/MAPKs activation.
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