Yersinia enterocolitica Exploits Signal Crosstalk between Complement 5a Receptor and Toll-like Receptor 1/2 and 4 to Avoid the Bacterial Clearance in M cells.
- Author:
Sae Hae KIM
1
;
Yong Suk JANG
Author Information
- Publication Type:Original Article
- Keywords: Complement 5a receptor; Immune evade; M cell; Toll-like receptor; Yersinia enterocolitica
- MeSH: Adenosine; Animals; Complement C5a*; Complement System Proteins*; Cyclic AMP-Dependent Protein Kinases; Mice; Mice, Knockout; Phenobarbital; Receptor, Anaphylatoxin C5a*; Toll-Like Receptors*; Yersinia enterocolitica*; Yersinia*
- From:Immune Network 2017;17(4):228-236
- CountryRepublic of Korea
- Language:English
- Abstract: In the intestinal mucosal surface, microfold cells (M cells) are the representative gateway for the uptake of luminal antigens. At the same time, M cells are the primary infection site for pathogens invading mucosal surface for their infection. Although it is well recognized that many mucosal pathogens exploit the M cells for their infection, the mechanism to infect M cells utilized by pathogens is not clearly understood yet. In this study, we found that M cells expressing complement 5a (C5a) receptor (C5aR) also express Toll-like receptor (TLR) 1/2 and TLR4. Infection of Yersinia enterocolitica, an M cell-invading pathogen, synergistically regulated cyclic adenosine monophosphate-dependent protein kinase A (cAMP-PKA) signaling which are involved in signal crosstalk between C5aR and TLRs. In addition, Y. enterocolitica infection into M cells was enhanced by C5a treatment and this enhancement was abrogated by C5a antagonist treatment. Finally, Y. enterocolitica infection into M cells was unsuccessful in C5aR knock-out mice. Collectively, we suggest that exploit the crosstalk between C5aR and TLR signaling is one of infection mechanisms utilized by mucosal pathogens to infect M cells.
