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
em En
| WPRIM
| ID: wpr-22202
Biblioteca responsável:
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.
Palavras-chave
Texto completo:
1
Índice:
WPRIM
Assunto principal:
Fenobarbital
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Yersinia
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Yersinia enterocolitica
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Proteínas do Sistema Complemento
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Complemento C5a
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Adenosina
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Camundongos Knockout
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Proteínas Quinases Dependentes de AMP Cíclico
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Receptor da Anafilatoxina C5a
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Receptores Toll-Like
Limite:
Animals
Idioma:
En
Revista:
Immune Network
Ano de publicação:
2017
Tipo de documento:
Article