Àá½Ã¸¸ ±â´Ù·Á ÁÖ¼¼¿ä. ·ÎµùÁßÀÔ´Ï´Ù.
KMID : 0923620170170040228
Immune Network
2017 Volume.17 No. 4 p.228 ~ p.236
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
Kim Sae-Hae

Jang Yong-Suk
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.
KEYWORD
Complement 5a receptor, Immune evade, M cell, Toll-like receptor, Yersinia enterocolitica
FullTexts / Linksout information
 
Listed journal information
SCI(E) ÇмúÁøÈïÀç´Ü(KCI) KoreaMed ´ëÇÑÀÇÇÐȸ ȸ¿ø