Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
32
pubmed:dateCreated
2005-8-8
pubmed:abstractText
Chlamydia pneumoniae is the causative agent of respiratory tract infections and a number of chronic diseases. Here we investigated the involvement of the common TLR adaptor molecule MyD88 in host responses to C. pneumoniae-induced pneumonia in mice. MyD88-deficient mice were severely impaired in their ability to mount an acute early inflammatory response toward C. pneumoniae. Although the bacterial burden in the lungs was comparable 5 days after infection, MyD88-deficient mice exhibited only minor signs of pneumonia and reduced expression of inflammatory mediators. MyD88-deficient mice were unable to up-regulate proinflammatory cytokines and chemokines, demonstrated delayed recruitment of CD8+ and CD4+ T cells to the lungs, and were unable to clear the pathogen from their lungs at day 14. At day 14 the MyD88-deficent mice developed a severe, chronic lung inflammation with elevated IL-1beta and IFN-gamma leading to increased mortality, whereas wild-type mice as well as TLR2- or TLR4-deficient mice recovered from acute pneumonia and did not show delayed bacterial clearance. Thus, MyD88 is essential to recognize C. pneumoniae infection and initiate a prompt and effective immune host response against this organism leading to clearance of bacteria from infected lungs.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
12
pubmed:volume
280
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
29242-9
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:15964841-Adaptor Proteins, Signal Transducing, pubmed-meshheading:15964841-Animals, pubmed-meshheading:15964841-Antigens, Differentiation, pubmed-meshheading:15964841-Body Weight, pubmed-meshheading:15964841-Bone Marrow Cells, pubmed-meshheading:15964841-CD4-Positive T-Lymphocytes, pubmed-meshheading:15964841-CD8-Positive T-Lymphocytes, pubmed-meshheading:15964841-Cell Separation, pubmed-meshheading:15964841-Chlamydophila Infections, pubmed-meshheading:15964841-Chlamydophila pneumoniae, pubmed-meshheading:15964841-Cytokines, pubmed-meshheading:15964841-Disease Models, Animal, pubmed-meshheading:15964841-Enzyme-Linked Immunosorbent Assay, pubmed-meshheading:15964841-Flow Cytometry, pubmed-meshheading:15964841-Inflammation, pubmed-meshheading:15964841-Lung, pubmed-meshheading:15964841-Macrophages, pubmed-meshheading:15964841-Mice, pubmed-meshheading:15964841-Mice, Transgenic, pubmed-meshheading:15964841-Myeloid Differentiation Factor 88, pubmed-meshheading:15964841-Pneumonia, Bacterial, pubmed-meshheading:15964841-Receptors, Immunologic, pubmed-meshheading:15964841-Time Factors, pubmed-meshheading:15964841-Toll-Like Receptor 2, pubmed-meshheading:15964841-Toll-Like Receptor 4, pubmed-meshheading:15964841-Up-Regulation
pubmed:year
2005
pubmed:articleTitle
MyD88 is pivotal for the early inflammatory response and subsequent bacterial clearance and survival in a mouse model of Chlamydia pneumoniae pneumonia.
pubmed:affiliation
Division of Pediatrics Infectious Diseases and Immunology, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA 90048, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, N.I.H., Extramural