Neutrophil response toward the microbiota. (A) Under steady state, the microbiota induces a regulatory network that suppresses neutrophil recruitment to prevent inflammatory responses toward the epithelium and commensals. (B) SFB and other commensals can induce Th17 cells, which secrete IL-17 to recruit neutrophils to the intestinal epithelium, resulting in a negative feedback control of the microbiota by neutrophils. Neutrophils also produce IL-22, which can elicit AMP secretion from the epithelium and IgA production from intestinal B cells. (C) Macrophages and dendritic cells in the mucosal system constitutively produce large amounts of pro-IL1β, the inactive form of the pleiotropic cytokine IL-1β. Signals from pathogenic microorganisms trigger the conversion through the NLRC4 inflammasome pathway, which induces robust neutrophil recruitment. Recruited neutrophils can migrate into the lumen of intestine to form an organized intraluminal structure that prevents translocation and expansion of both commensal and pathogenic species. (D) Certain pathogenic species, such as Salmonella, can take advantage of neutrophil-mediated defense mechanisms to acquire growth advantages by using S₄O₆²⁻ as an electron acceptor. S₂O₃²⁻, thiosulfate; S₄O₆²⁻, tetrathionate; Th, T helper.