Chengcheng Jin

TL;DR: Altered interactions between the gut microbiota and the host, produced by defective NLRP3 and NLRP6 inflammasome sensing, may govern the rate of progression of multiple metabolic syndrome-associated abnormalities, highlighting the central role of the microbiota in the pathogenesis of heretofore seemingly unrelated systemic auto-inflammatory and metabolic disorders.

TL;DR: It is proposed that understanding this microbial influence will be crucial for targeted therapy in modern cancer treatment and the recently suggested role of commensal microorganisms in inflammation-induced cancer is discussed.

TL;DR: In this paper, the authors provide evidence that local microbiota provoke inflammation associated with lung adenocarcinoma by activating lung resident γδ T cells, and link local microbiota-immune crosstalk to lung tumor development and define key cellular and molecular mediators that may serve as effective targets in lung cancer intervention.

TL;DR: This work suggests a model in which the NLRC4 inflammasome is central to colonic inflammation-induced tumor formation through regulation of epithelial cell response to injury and shows that caspase-1–deficient mice have enhanced tumor formation.

TL;DR: Three signaling pathways involving potassium efflux, generation of reactive oxygen species, and cathepsin B release are discussed, which drive innate immune response towards invading pathogens and cellular damage, and regulates adaptive immune response.