Type III Secretion Needle Proteins Induce Cell Signaling and Cytokine Secretion via Toll-Like Receptors

Interleukin-8, CXCL1, and MicroRNA miR-146a Responses to Probiotic Escherichia coli Nissle 1917 and Enteropathogenic E. coli in Human Intestinal Epithelial T84 and Monocytic THP-1 Cells after Apical or Basolateral Infection

“…That study excluded the potential involvement of the locus of enterocyte effacement (LEE)-encoded Map, EspF, and Tir effectors as well as the intimin membrane protein in this inhibition. More recently, it was revealed that T3SS needle proteins induced cytokine expression and signaling by NF-B and/or AP-1 following interaction with TLR2 or TLR4 in an MyD88-dependent fashion (70).…”

Molecular Mechanisms Used by Salmonella to Evade the Immune System

“…Specific Salmonella virulence factors that enhance NF-κB activity are the T3SS1 effector SopE, which is recognized by NOD1 (Keestra et al, 2013), and the T3SS2 effector SrfA, that promotes NF-κB activation by binding to TOLLIP, an inhibitor of IRAK1 (Lei et al, 2016). This proinflammatory pathway can also be induced by the T3SS needle proteins PrgI and SsaG through TLR2 and TLR4 ( Jessen et al, 2014). In addition, SopE acts as a GTP exchange factor (GEF) for Rho family GTPases Cdc42 and Rac1, leading to activation of the c-Jun N-terminal kinase ( JNK) pathway.…”

The N Terminus of Type III Secretion Needle Protein YscF from Yersinia pestis Functions To Modulate Innate Immune Responses

“…Needle proteins were recently identified as Toll-like receptor 2 (TLR2) and TLR4 ligands that activate expression and secretion of cytokines via an MyD88-dependent pathway (20). Purified needle proteins from different bacteria induced cytokine expression to different magnitudes (20).…”

“…Purified needle proteins from different bacteria induced cytokine expression to different magnitudes (20). YscF comes from a T3S system from pathogens that have an anti-inflammatory infection objective (1,21) and induces lower levels of proinflammatory cytokines.…”