Cryptococcus gattii Infection Dampens Th1 and Th17 Responses by Attenuating Dendritic Cell Function and Pulmonary Chemokine Expression in the Immunocompetent Hosts
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- Pornpimon Angkasekwinai
- Department of Medical Technology, Faculty of Allied Health Sciences, Thammasat University, Pathumthani, Thailand
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- Nuntarat Sringkarin
- Department of Medical Technology, Faculty of Allied Health Sciences, Thammasat University, Pathumthani, Thailand
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- Oratai Supasorn
- Department of Medical Technology, Faculty of Allied Health Sciences, Thammasat University, Pathumthani, Thailand
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- Madtika Fungkrajai
- Department of Medical Technology, Faculty of Allied Health Sciences, Thammasat University, Pathumthani, Thailand
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- Yui-Hsi Wang
- Division of Allergy and Immunology, University of Cincinnati, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA
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- Methee Chayakulkeeree
- Division of Infectious Diseases and Tropical Medicine, Department of Medicine, Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkok, Thailand
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- Popchai Ngamskulrungroj
- Department of Microbiology, Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkok, Thailand
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- Nasikarn Angkasekwinai
- Division of Infectious Diseases and Tropical Medicine, Department of Medicine, Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkok, Thailand
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- Kovit Pattanapanyasat
- Center of Excellence for Flow Cytometry, Office for Research and Development, Faculty of Medicine, Siriraj Hospital, Mahidol University, Bangkok, Thailand
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- G. S. Deepe
- editor
Description
<jats:title>ABSTRACT</jats:title><jats:p>Cryptococcal infections are primarily caused by two related fungal species:<jats:named-content content-type="genus-species">Cryptococcus neoformans</jats:named-content>and<jats:named-content content-type="genus-species">Cryptococcus gattii</jats:named-content>. It is well known that<jats:named-content content-type="genus-species">C. neoformans</jats:named-content>generally affects immunocompromised hosts; however,<jats:named-content content-type="genus-species">C. gattii</jats:named-content>infection can cause diseases in not only immunocompromised hosts but also immunocompetent individuals. While recent studies suggest that<jats:named-content content-type="genus-species">C. gattii</jats:named-content>infection could dampen pulmonary neutrophil recruitment and inflammatory cytokine production in immunocompetent hosts, the impact of<jats:named-content content-type="genus-species">C. gattii</jats:named-content>infection on the development of their adaptive T helper cell immune response has not been addressed. Here, we report that<jats:named-content content-type="genus-species">C. neoformans</jats:named-content>infection with highly virulent and less virulent strains preferentially induced pulmonary Th1 and Th17 immune responses in the host, respectively. However, fewer pulmonary Th1 and Th17 cells could be detected in mice infected with<jats:named-content content-type="genus-species">C. gattii</jats:named-content>strains. Notably, dendritic cells (DC) in mice infected with<jats:named-content content-type="genus-species">C. gattii</jats:named-content>expressed much lower levels of surface MHC-II and<jats:italic>Il12</jats:italic>or<jats:italic>Il23</jats:italic>transcripts and failed to induce effective Th1 and Th17 differentiation<jats:italic>in vitro</jats:italic>. Furthermore, the expression levels of<jats:italic>Ip10</jats:italic>and<jats:italic>Cxcl9</jats:italic>transcripts, encoding Th1-attracting chemokines, were significantly reduced in the lungs of mice infected with the highly virulent<jats:named-content content-type="genus-species">C. gattii</jats:named-content>strain. Thus, our data suggest that<jats:named-content content-type="genus-species">C. gattii</jats:named-content>infection dampens the DC-mediated effective Th1/Th17 immune responses and downregulates the pulmonary chemokine expression, thus resulting in the inability to mount protective immunity in immunocompetent hosts.</jats:p>
Journal
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- Infection and Immunity
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Infection and Immunity 82 (9), 3880-3890, 2014-09
American Society for Microbiology
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Details 詳細情報について
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- CRID
- 1361699994665087232
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- ISSN
- 10985522
- 00199567
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- Data Source
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- Crossref