Linked Life Data

11086082

Source:http://linkedlifedata.com/resource/pubmed/id/11086082

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2000-12-7
pubmed:abstractText
Macrophage inflammatory protein-1alpha (MIP-1alpha/CCL3) is a CC chemokine required for optimal recruitment of leukocytes in response to cryptococcal Ags. MIP-1alpha is expressed in the lungs by day 6 post Cryptococcus neoformans infection and could play a role in the development of cell-mediated immunity. To address this possibility, wild-type (MIP-1alpha(+/+)) mice and MIP-1alpha knockout (MIP-1alpha(-/-)) mice were infected intratracheally with a highly virulent strain of C. neoformans (145A). MIP-1alpha message was detected in the lungs on days 3, 7, and 14 in MIP-1alpha(+/+) mice, but it was undetectable in MIP-1alpha(-/-) mice. On day 16, MIP-1alpha(-/-) mice had a 7-fold increase in C. neoformans burden in the lungs, but no decrease in pulmonary leukocyte recruitment. MIP-1alpha(+/+) and MIP-1alpha(-/-) mice had similar numbers of recruited lymphocytes and monocytes/macrophages. Notably, MIP-1alpha(-/-) mice had a significantly greater number of eosinophils. MIP-1alpha(-/-) mice had extremely high levels of serum IgE. This switch of immune response to a T(2) phenotype was associated with enhanced IL-4 and IL-13 expression in the lungs of MIP-1alpha(-/-) mice compared with MIP-1alpha (+/+) mice. Progression of pulmonary cryptococcosis in the presence of nonprotective T(2) immunity resulted in profound lung damage in MIP-1alpha(-/-) mice (eosinophilic crystal deposition, destruction of lung parenchyma, and pulmonary hemorrhage). Twelve-week survival was dramatically decreased in MIP-1alpha(-/-) mice. These studies, together with our previous studies, demonstrate that MIP-1alpha plays a role in both the afferent (T(1)/T(2) development) and efferent (T(1)-mediated leukocyte recruitment) phases of cell-mediated immunity to C. neoformans.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
165
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6429-36
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:11086082-Animals, pubmed-meshheading:11086082-Cell Movement, pubmed-meshheading:11086082-Chemokine CCL3, pubmed-meshheading:11086082-Chemokine CCL4, pubmed-meshheading:11086082-Chemokines, CC, pubmed-meshheading:11086082-Cryptococcosis, pubmed-meshheading:11086082-Cryptococcus neoformans, pubmed-meshheading:11086082-Gene Deletion, pubmed-meshheading:11086082-Immune Sera, pubmed-meshheading:11086082-Immunity, Cellular, pubmed-meshheading:11086082-Immunoglobulin E, pubmed-meshheading:11086082-Injections, Intraperitoneal, pubmed-meshheading:11086082-Interferon-gamma, pubmed-meshheading:11086082-Interleukin-12, pubmed-meshheading:11086082-Interleukin-13, pubmed-meshheading:11086082-Interleukin-4, pubmed-meshheading:11086082-Leukocytes, pubmed-meshheading:11086082-Lung, pubmed-meshheading:11086082-Lung Diseases, Fungal, pubmed-meshheading:11086082-Macrophage Inflammatory Proteins, pubmed-meshheading:11086082-Mice, pubmed-meshheading:11086082-Mice, Inbred C57BL, pubmed-meshheading:11086082-Mice, Knockout, pubmed-meshheading:11086082-Phenotype, pubmed-meshheading:11086082-Pulmonary Eosinophilia, pubmed-meshheading:11086082-Survival Analysis, pubmed-meshheading:11086082-T-Lymphocytes
pubmed:year
2000
pubmed:articleTitle
The role of macrophage inflammatory protein-1 alpha/CCL3 in regulation of T cell-mediated immunity to Cryptococcus neoformans infection.
pubmed:affiliation
Veterans Affairs Hospital and Division of Pulmonary and Critical Care Medicine, The University of Michigan Medical School, Ann Arbor, MI 48109, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't