Document Detail


CD3+ cells transfer the hypersensitive granulomatous response to mycobacterial glycolipid trehalose 6,6'-dimycolate in mice.
MedLine Citation:
PMID:  17159227     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The granulomatous response is the characteristic histological feature of Mycobacterium tuberculosis infection that is essential for organism containment. Trehalose 6,6-dimycolate (TDM), a cell-wall glycolipid present on most mycobacterial species, has been implicated in the pathogenesis of M. tuberculosis infection. TDM has potent immunoregulatory and inflammatory properties, and can be used to model granulomatous reactions that mimic, in part, pathology caused during active infection. This study examined the hypersensitive granulomatous response, focusing on cellular responses specific to TDM. Lungs from mice immunized with TDM emulsion demonstrated exacerbated histological damage, inflammation, and lymphocytic infiltration upon subsequent challenge with TDM. Splenocytes recovered from these mice demonstrated significant interferon (IFN)-gamma production during recall response to TDM, as well as increased production of proinflammatory mediators (tumour necrosis factor-alpha, interleukin-6 and macrophage inflammatory protein-1alpha). The exacerbated response could be adoptively transferred to naïve mice. Administration of non-adherent lymphocytes or purified CD3(+) cells from TDM-immunized mice led to increased inflammation, lymphocytic infiltration, and vascular endothelial cell damage upon challenge with TDM. Recipient mice that received immunized CD3(+) lymphocytes demonstrated significant increases in Th1-type cytokines and proinflammatory mediators in lung tissue following TDM challenge. When CD1d(-/-) mice were immunized with TDM, they failed to generate a specific IFN-gamma response, suggesting a role for this molecule in the generation of hypersensitivity. These experiments provide further evidence for the involvement of TDM-specific CD3(+) T cells in pathological damage elicited during M. tuberculosis infection.
Authors:
Tera V Guidry; Robert L Hunter; Jeffrey K Actor
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Microbiology (Reading, England)     Volume:  152     ISSN:  1350-0872     ISO Abbreviation:  Microbiology (Reading, Engl.)     Publication Date:  2006 Dec 
Date Detail:
Created Date:  2006-12-12     Completed Date:  2007-03-27     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  9430468     Medline TA:  Microbiology     Country:  England    
Other Details:
Languages:  eng     Pagination:  3765-75     Citation Subset:  IM    
Affiliation:
University of Texas-Houston Health Science Center, Graduate School of Biomedical Sciences, Houston, TX 77030, USA.
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MeSH Terms
Descriptor/Qualifier:
Adoptive Transfer
Animals
Antigens, CD3 / analysis*
Bacterial Proteins / immunology
Chemokine CCL4
Cord Factors / immunology*
Granuloma / immunology*,  pathology
Hypersensitivity, Delayed / pathology
Interferon-gamma / biosynthesis
Interleukin-6 / biosynthesis
Lung / pathology
Lymphocyte Subsets / immunology*
Macrophage Inflammatory Proteins / biosynthesis
Mice
Mice, Inbred BALB C
Mice, Knockout
Mycobacterium tuberculosis / immunology*
Tuberculosis / immunology*,  pathology
Tumor Necrosis Factor-alpha / biosynthesis
Grant Support
ID/Acronym/Agency:
1R21AI058247-1/AI/NIAID NIH HHS; R01HL068537/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Antigens, CD3; 0/Bacterial Proteins; 0/Chemokine CCL4; 0/Cord Factors; 0/Interleukin-6; 0/Macrophage Inflammatory Proteins; 0/Tumor Necrosis Factor-alpha; 82115-62-6/Interferon-gamma

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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