Document Detail


Type I IFNs enhance susceptibility to Chlamydia muridarum lung infection by enhancing apoptosis of local macrophages.
MedLine Citation:
PMID:  18641348     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Type I IFNs (IFNIs) have pleiotropic functions in regulating host innate and adaptive immune responses to pathogens. To elucidate the role of IFNIs in host resistance to chlamydial infection in vivo, we compared IFN-alpha/beta receptor knockout (IFNAR(-/-)) and wild-type control mice in susceptibility to Chlamydia trachomatis mouse pneumonitis (Chlamydia muridarum) lung infection. We found that the IFNAR(-/-) mice were significantly more resistant to C. muridarum infection showing less bacterial burden and bodyweight loss, and milder pathological changes. However, IFN-gamma response, which is believed to be critical in host defense against chlamydial infection, was similar between the wild-type and IFNAR(-/-) mice. More importantly, TUNEL analysis showed less macrophage apoptosis in IFNAR(-/-) mice, which was consistent with lower expressions of IFNI-induced apoptotic factors, TRAIL, Daxx, and PKR. Furthermore, depletion of lung macrophages with dichloromethylene diphosphonate-liposome significantly increased the susceptibility of the IFNAR(-/-) mice to C. muridarum, confirming the importance of macrophages. Overall, the data indicate that IFNIs play a promoting role in C. muridarum lung infection, largely through increase of local macrophage apoptosis.
Authors:
Hongyu Qiu; Yijun Fan; Antony George Joyee; Shuhe Wang; Xiaobing Han; Hong Bai; Lei Jiao; Nico Van Rooijen; Xi Yang
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  181     ISSN:  1550-6606     ISO Abbreviation:  J. Immunol.     Publication Date:  2008 Aug 
Date Detail:
Created Date:  2008-07-21     Completed Date:  2008-08-19     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2092-102     Citation Subset:  AIM; IM    
Affiliation:
Department of Medical Microbiology, University of Manitoba, Winnipeg, Manitoba, Canada.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antibodies / immunology
Apoptosis / immunology*
Cell Differentiation / immunology
Cell Movement / immunology
Chemokines / biosynthesis
Chlamydia Infections / genetics,  immunology*,  metabolism,  pathology*
Chlamydia muridarum / immunology*
Dendritic Cells / cytology,  immunology
Disease Susceptibility
Female
Interferon Type I / immunology*
Lung Diseases / genetics,  immunology*,  metabolism,  pathology
Macrophages / cytology,  immunology*,  metabolism
Male
Mice
Mice, Knockout
Receptor, Interferon alpha-beta / deficiency,  genetics,  metabolism
Chemical
Reg. No./Substance:
0/Antibodies; 0/Chemokines; 0/Interferon Type I; 156986-95-7/Receptor, Interferon alpha-beta

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