Document Detail


Thymic function is maintained during Salmonella-induced atrophy and recovery.
MedLine Citation:
PMID:  22993205     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Thymic atrophy is a frequent consequence of infection with bacteria, viruses, and parasites and is considered a common virulence trait between pathogens. Multiple reasons have been proposed to explain this atrophy, including premature egress of immature thymocytes, increased apoptosis, or thymic shutdown to prevent tolerance to the pathogen from developing. The severe loss in thymic cell number can reflect an equally dramatic reduction in thymic output, potentially reducing peripheral T cell numbers. In this study, we examine the relationship between systemic Salmonella infection and thymic function. During infection, naive T cell numbers in peripheral lymphoid organs increase. Nevertheless, this occurs despite a pronounced thymic atrophy caused by viable bacteria, with a peak 50-fold reduction in thymocyte numbers. Thymic atrophy is not dependent upon homeostatic feedback from peripheral T cells or on regulation of endogenous glucocorticoids, as demonstrated by infection of genetically altered mice. Once bacterial numbers fall, thymocyte numbers recover, and this is associated with increases in the proportion and proliferation of early thymic progenitors. During atrophy, thymic T cell maturation is maintained, and single-joint TCR rearrangement excision circle analysis reveals there is only a modest fall in recent CD4(+) thymic emigrants in secondary lymphoid tissues. Thus, thymic atrophy does not necessarily result in a matching dysfunctional T cell output, and thymic homeostasis can constantly adjust to systemic infection to ensure that naive T cell output is maintained.
Authors:
Ewan A Ross; Ruth E Coughlan; Adriana Flores-Langarica; Sian Lax; Julia Nicholson; Guillaume E Desanti; Jennifer L Marshall; Saeeda Bobat; Jessica Hitchcock; Andrea White; William E Jenkinson; Mahmood Khan; Ian R Henderson; Gareth G Lavery; Christopher D Buckley; Graham Anderson; Adam F Cunningham
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-09-19
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  189     ISSN:  1550-6606     ISO Abbreviation:  J. Immunol.     Publication Date:  2012 Nov 
Date Detail:
Created Date:  2012-10-22     Completed Date:  2013-01-09     Revised Date:  2014-02-20    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  4266-74     Citation Subset:  AIM; IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Atrophy
CD4-Positive T-Lymphocytes / cytology,  immunology,  microbiology
Cell Differentiation / immunology
Cell Movement / immunology
Mice
Recovery of Function / immunology*
Salmonella Infections / immunology*,  pathology,  physiopathology
Salmonella typhimurium / immunology
Thymus Gland / immunology*,  microbiology,  pathology*
Grant Support
ID/Acronym/Agency:
090244//Wellcome Trust; 090244//Wellcome Trust; BB/F022778/1//Biotechnology and Biological Sciences Research Council; G0401620//Medical Research Council; G0900857//Medical Research Council; G1000213//Medical Research Council; G1001055//Medical Research Council; G1001390//Medical Research Council
Comments/Corrections

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