Linked Life Data

8891197

Source:http://linkedlifedata.com/resource/pubmed/id/8891197

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1997-2-4
pubmed:abstractText
The objective of these studies was to present an overview of our studies of the cytokine network and cellular interactions responsible for the T-cell-mediated inflammatory response in the lungs following infection by Cryptococcus neoformans. In a resistant strain of mice, moderately virulent cryptococci were progressively cleared from the lungs after week 1. Characterization of mitogen-induced cytokine production demonstrated that the T cells in the lungs during the first 3 weeks of infection resembled Th0 rather than Th1 cells. In addition, the production of IL-10 (by mitogen-stimulated leukocytes) could promote an increase in the ratio of Th2:Th1 cytokines in short-term in vitro cultures. In vivo, there were increases in the alveolar levels of tumor necrosis factor-alpha and IL-6 at weeks 1-3 and the chemokines monocyte chemoattractant protein-1 at weeks 1-2 followed by macrophage inflammatory protein-1 alpha and ENA-78 at week 3. Overall, the pulmonary inflammatory response to C. neoformans evolved over 5 weeks from granulocytic to mononuclear, suggesting a maturation to a Th1-type response by week 5.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1016-0922
pubmed:author
pubmed:issnType
Print
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
215-22
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:articleTitle
Role of cytokines in T cell immunity to a pulmonary Cryptococcus neoformans infection.
pubmed:affiliation
Department of Internal Medicine, University of Michigan, Ann Arbor, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't