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
Immune Network
; : 228-236, 2017.
Article
in En
| WPRIM
| ID: wpr-22202
Responsible library:
WPRO
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.
Key words
Full text:
1
Index:
WPRIM
Main subject:
Phenobarbital
/
Yersinia
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Yersinia enterocolitica
/
Complement System Proteins
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Complement C5a
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Adenosine
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Mice, Knockout
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Cyclic AMP-Dependent Protein Kinases
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Receptor, Anaphylatoxin C5a
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Toll-Like Receptors
Limits:
Animals
Language:
En
Journal:
Immune Network
Year:
2017
Type:
Article