Linked Life Data

9973497

Source:http://linkedlifedata.com/resource/pubmed/id/9973497

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1999-4-13
pubmed:abstractText
Protection against infections with the intracellular bacterium Chlamydia spp. requires Th1-polarized CD4+ T cell immunity. In BALB/c mouse lung infections, immediate innate and nascent Chlamydia-specific immune responses following intranasal inoculation of Chlamydia psittaci strain B577 were modulated by 7-day i.p. administration of murine rIL-12, the initiation cytokine for Th1 immunity. Treatment with IL-12 reduced the severity of chlamydial pneumonia, abolished mortality (37.5% in untreated mice), and significantly reduced numbers of chlamydial organisms in lungs. On day 4 after inoculation, the neutrophil:macrophage ratio in bronchointerstitial pneumonias was 1.96 in untreated mice and 0.51 in IL-12-treated mice. This immediate, IL-12-mediated shift in innate inflammatory phenotype was correlated with a significant reduction of lung concentrations of the neutrophil chemoattractant macrophage inflammatory protein (MIP)-2 (putative murine homologue of human IL-8), monocyte chemotactic protein-1, and TNF-alpha; and a reduction in MIP-1alpha and IFN-gamma, at high-dose infection only, and IL-12-independent IL-10 levels. Chlamydia-specific Ab titers and Ig isotype ratios indicated an IL-12-dependent Th1 shift. Recall responses of IL-12-primed mice to secondary chlamydial lung infection eliminated chlamydiae more effectively and generated a lung cytokine profile conducive to perpetuation of the Th1 memory population. These data support the hypothesis that genetic differences in endogenous IL-12 production and response pathways could determine disease outcomes characterized by poor chlamydial clearance and a purulent inflammatory infiltrate vs effective elimination of chlamydiae in a macrophage-dominated response.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
162
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2217-26
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:9973497-Administration, Intranasal, pubmed-meshheading:9973497-Animals, pubmed-meshheading:9973497-Cell Movement, pubmed-meshheading:9973497-Chemokine CCL2, pubmed-meshheading:9973497-Chemokine CXCL2, pubmed-meshheading:9973497-Chlamydia Infections, pubmed-meshheading:9973497-Chlamydophila psittaci, pubmed-meshheading:9973497-Female, pubmed-meshheading:9973497-Immunization, Secondary, pubmed-meshheading:9973497-Immunoglobulin G, pubmed-meshheading:9973497-Interleukin-12, pubmed-meshheading:9973497-Leukocyte Count, pubmed-meshheading:9973497-Lung, pubmed-meshheading:9973497-Mice, pubmed-meshheading:9973497-Mice, Inbred BALB C, pubmed-meshheading:9973497-Monokines, pubmed-meshheading:9973497-Neutrophils, pubmed-meshheading:9973497-Pneumonia, Bacterial, pubmed-meshheading:9973497-Survival Analysis, pubmed-meshheading:9973497-Th1 Cells, pubmed-meshheading:9973497-Tumor Necrosis Factor-alpha
pubmed:year
1999
pubmed:articleTitle
IL-12 administered during Chlamydia psittaci lung infection in mice confers immediate and long-term protection and reduces macrophage inflammatory protein-2 level and neutrophil infiltration in lung tissue.
pubmed:affiliation
Department of Pathobiology, College of Veterinary Medicine, Auburn University, AL 36849, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.