“…The mice exhibit an altered microbiota associated with metabolic disorders characterized by insulin resistance, hyperlipidaemia and increased fat deposition, and all these markers were also observed in WT mice colonized with the gut microbiota of Tlr5-deficient mice [171]. By describing the key role of the local immune system in controlling the composition and activity of the microbiota, these data support the idea that the strong interactions [122,[126][127][128] ↗ expression of TLR (TLR3, TLR4, TLR7 and TLR10) [126,128] ↗ naïve T cells [122] Cytotoxicity and inflammation [122,123,125,129] ↗ pro-inflammatory cytokines (IL-6, TNF-α, IL1-β) [121-123, 127, 130-132] ↗ mature DC [122,131,132] Adjuvant [121,[130][131][132] ↗ chemokines secretion (IL-8 and CXCL1) ↙ activity (IL-8) [122,133] ↗ mast cell activation [134] Allergic response [134,135] ↗ co-stimulatory molecules (CD80 and CD86) [122,123,131,132] ↙ neutrophil and μɸ mobility [133] Tissue damage [124,133] ↗ MPO, MMP-9 and NET [124,136] ↗ neutrophil activity [124,136] NETosis: inflammation, necrosis and apoptosis [124] ↗ β-hexosaminidase release [134] inflammasome activation …”