MyD88-dependent signaling contributes to host defense against ehrlichial infection.
The ehrlichiae are small gram-negative obligate intracellular bacteria in the family Anaplasmataceae. Ehrlichial infection in an accidental host may result in fatal diseases such as human monocytotropic ehrlichiosis, an emerging, tick-borne disease. Although the role of adaptive immune responses in...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2010-07-01
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| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC2909256?pdf=render |
| _version_ | 1811327508470038528 |
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| author | Young-Sang Koh Jung-Eun Koo Amlan Biswas Koichi S Kobayashi |
| author_facet | Young-Sang Koh Jung-Eun Koo Amlan Biswas Koichi S Kobayashi |
| author_sort | Young-Sang Koh |
| collection | DOAJ |
| description | The ehrlichiae are small gram-negative obligate intracellular bacteria in the family Anaplasmataceae. Ehrlichial infection in an accidental host may result in fatal diseases such as human monocytotropic ehrlichiosis, an emerging, tick-borne disease. Although the role of adaptive immune responses in the protection against ehrlichiosis has been well studied, the mechanism by which the innate immune system is activated is not fully understood. Using Ehrlichia muris as a model organism, we show here that MyD88-dependent signaling pathways play a pivotal role in the host defense against ehrlichial infection. Upon E. muris infection, MyD88-deficient mice had significantly impaired clearance of E. muris, as well as decreased inflammation, characterized by reduced splenomegaly and recruitment of macrophages and neutrophils. Furthermore, MyD88-deficient mice produced markedly lower levels of IL-12, which correlated well with an impaired Th1 immune response. In vitro, dendritic cells, but not macrophages, efficiently produced IL-12 upon E. muris infection through a MyD88-dependent mechanism. Therefore, MyD88-dependent signaling is required for controlling ehrlichial infection by playing an essential role in the immediate activation of the innate immune system and inflammatory cytokine production, as well as in the activation of the adaptive immune system at a later stage by providing for optimal Th1 immune responses. |
| first_indexed | 2024-04-13T15:09:08Z |
| format | Article |
| id | doaj.art-9bc2a9f704d34bcdadfeaa5cbb5d1334 |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-04-13T15:09:08Z |
| publishDate | 2010-07-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-9bc2a9f704d34bcdadfeaa5cbb5d13342022-12-22T02:42:04ZengPublic Library of Science (PLoS)PLoS ONE1932-62032010-07-0157e1175810.1371/journal.pone.0011758MyD88-dependent signaling contributes to host defense against ehrlichial infection.Young-Sang KohJung-Eun KooAmlan BiswasKoichi S KobayashiThe ehrlichiae are small gram-negative obligate intracellular bacteria in the family Anaplasmataceae. Ehrlichial infection in an accidental host may result in fatal diseases such as human monocytotropic ehrlichiosis, an emerging, tick-borne disease. Although the role of adaptive immune responses in the protection against ehrlichiosis has been well studied, the mechanism by which the innate immune system is activated is not fully understood. Using Ehrlichia muris as a model organism, we show here that MyD88-dependent signaling pathways play a pivotal role in the host defense against ehrlichial infection. Upon E. muris infection, MyD88-deficient mice had significantly impaired clearance of E. muris, as well as decreased inflammation, characterized by reduced splenomegaly and recruitment of macrophages and neutrophils. Furthermore, MyD88-deficient mice produced markedly lower levels of IL-12, which correlated well with an impaired Th1 immune response. In vitro, dendritic cells, but not macrophages, efficiently produced IL-12 upon E. muris infection through a MyD88-dependent mechanism. Therefore, MyD88-dependent signaling is required for controlling ehrlichial infection by playing an essential role in the immediate activation of the innate immune system and inflammatory cytokine production, as well as in the activation of the adaptive immune system at a later stage by providing for optimal Th1 immune responses.http://europepmc.org/articles/PMC2909256?pdf=render |
| spellingShingle | Young-Sang Koh Jung-Eun Koo Amlan Biswas Koichi S Kobayashi MyD88-dependent signaling contributes to host defense against ehrlichial infection. PLoS ONE |
| title | MyD88-dependent signaling contributes to host defense against ehrlichial infection. |
| title_full | MyD88-dependent signaling contributes to host defense against ehrlichial infection. |
| title_fullStr | MyD88-dependent signaling contributes to host defense against ehrlichial infection. |
| title_full_unstemmed | MyD88-dependent signaling contributes to host defense against ehrlichial infection. |
| title_short | MyD88-dependent signaling contributes to host defense against ehrlichial infection. |
| title_sort | myd88 dependent signaling contributes to host defense against ehrlichial infection |
| url | http://europepmc.org/articles/PMC2909256?pdf=render |
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