TGFB1 and infection: Noteworthy, upon infection, TGF-β-dependent signaling of ASJ not only induces activation of adjacent interneurons, but this recognition response might be simultaneously counterbalanced by the pathogenic bacteria through inducing a suppressive neuropeptidergic signaling in both ASJ and AWB via NPR-8, as one key element of the “Trojan horse” mechanism [57,165].