ArticleJournal of thoracic disease2026
Inhibition of macrophage pyroptosis protects against sepsis-induced injury to the alveolar epithelial barrier.
Article in Journal of thoracic disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Acute lung injury (ALI) is characterized by alveolar epithelial barrier dysfunction, largely driven by excessive inflammation. This study aimed to elucidate the specific role and mechanism of macrophage pyroptosis in sepsis-induced epithelial injury. Methods: We established an Results: LPS stimulation potently activated the NLRP3 inflammasome in macrophages, leading to robust pyroptosis, as indicated by a significant increase in caspase-1 activity, lactate dehydrogenase (LDH) release, and the secretion of interleukin-1 β (IL-1β) and IL-18. Pre-treatment with MCC950 completely abolished this activation. CM from LPS-activated macrophages (LPS-CM) induced severe epithelial barrier injury, manifesting as a significant increase in epithelial cell death and monolayer permeability, and a marked downregulation of tight junction proteins zonula occludens-1 (ZO-1) and occludin. Crucially, all these aforementioned effects were significantly attenuated when epithelial cells were incubated with CM from macrophages pre-treated with MCC950, demonstrating that inhibiting macrophage pyroptosis preserves epithelial barrier integrity. Conclusions: Macrophage pyroptosis, activated via the LPS/NLRP3 pathway, is a pivotal mechanism in sepsis-induced alveolar epithelial barrier dysfunction. Pharmacological inhibition of this pathway represents a promising therapeutic strategy for ALI.
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