Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2002-3-21
pubmed:abstractText
Mycoplasma infection is a leading cause of pneumonia worldwide and can lead to other respiratory complications. A component of mycoplasma respiratory diseases is immunopathologic, suggesting that lymphocyte activation is a key event in the progression of these chronic inflammatory diseases. The present study delineates the changes in T cell populations and their activation after mycoplasma infection and determines their association with the pathogenesis of murine Mycoplasma respiratory disease, due to Mycoplasma pulmonis infection. Increases in T cell population numbers in lungs and lower respiratory lymph nodes were associated with the development of mycoplasma respiratory disease. Although both pulmonary Th and CD8(+) T cells increased after mycoplasma infection, there was a preferential expansion of Th cells. Mycoplasma-specific Th2 responses were dominant in lower respiratory lymph nodes, while Th1 responses predominated in spleen. However, both mycoplasma-specific Th1 and Th2 cytokine (IL-4 and IFN-gamma) responses were present in the lungs, with Th1 cell activation as a major component of the pulmonary Th cell response. Although a smaller component of the T cell response, mycoplasma-specific CD8(+) T cells were also a significant component of pulmonary lymphoid responses. In vivo depletion of CD8(+) T cells resulted in dramatically more severe pulmonary disease, while depletion of CD4(+) T cells reduced its severity, but there was no change in mycoplasma numbers in lungs after cell depletion. Thus, mycoplasma-specific Th1 and CD8(+) T cell activation in the lung plays a critical regulatory role in development of immunopathologic reactions in Mycoplasma respiratory disease.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
168
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3493-501
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:11907110-Animals, pubmed-meshheading:11907110-Antibodies, Monoclonal, pubmed-meshheading:11907110-Antigens, Bacterial, pubmed-meshheading:11907110-CD8-Positive T-Lymphocytes, pubmed-meshheading:11907110-Female, pubmed-meshheading:11907110-Immunodominant Epitopes, pubmed-meshheading:11907110-Injections, Intraperitoneal, pubmed-meshheading:11907110-Interferon-gamma, pubmed-meshheading:11907110-Interleukin-4, pubmed-meshheading:11907110-Lung, pubmed-meshheading:11907110-Lymphocyte Count, pubmed-meshheading:11907110-Lymphocyte Depletion, pubmed-meshheading:11907110-Mice, pubmed-meshheading:11907110-Mice, Inbred C3H, pubmed-meshheading:11907110-Mycoplasma, pubmed-meshheading:11907110-Mycoplasma Infections, pubmed-meshheading:11907110-Pneumonia, pubmed-meshheading:11907110-RNA, Messenger, pubmed-meshheading:11907110-Severity of Illness Index, pubmed-meshheading:11907110-T-Lymphocyte Subsets, pubmed-meshheading:11907110-T-Lymphocytes, Helper-Inducer
pubmed:year
2002
pubmed:articleTitle
Depletion of CD8+ T cells exacerbates CD4+ Th cell-associated inflammatory lesions during murine mycoplasma respiratory disease.
pubmed:affiliation
Department of Molecular Biology and Immunology, University of North Texas Health Science Center, Fort Worth, TX 76107, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.