Linked Life Data

20065024

Source:http://linkedlifedata.com/resource/pubmed/id/20065024

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2010-2-19
pubmed:abstractText
To define the roles of specific complement activation pathways in host defense against Streptococcus pneumoniae in acute otitis media (AOM), we investigated the susceptibility to AOM in mice deficient in complement factor B and C2 (Bf/C2(-/)(-)), C1qa (C1qa(-/)(-)), and factor B (Bf(-)(/)(-)). Bacterial titers of both S. pneumoniae serotype 6A and 14 in the middle ear lavage fluid samples from Bf/C2(-/)(-), Bf(-)(/)(-), and C1qa(-/)(-) mice were significantly higher than in samples from wild-type mice 24 h after transtympanical infection (P < 0.05) and remained persistently higher in samples from Bf/C2(-/)(-) mice than in samples from wild-type mice. Bacteremia occurred in Bf/C2(-/)(-), Bf(-)(/)(-), and C1qa(-/)(-) mice infected with both strains, but not in wild-type mice. Recruitment of inflammatory cells was paralleled by enhanced production of inflammatory mediators in the middle ear lavage samples from Bf/C2(-/)(-) mice. C3b deposition on both strains was greatest for sera obtained from wild-type mice, followed by C1qa(-)(/)(-) and Bf(-)(/)(-) mice, and least for Bf/C2(-)(/)(-) mice. Opsonophagocytosis and whole-blood killing capacity of both strains were significantly decreased in the presence of sera or whole blood from complement-deficient mice compared to wild-type mice. These findings indicate that both the classical and alternative complement pathways are critical for middle ear immune defense against S. pneumoniae. The reduced capacity of complement-mediated opsonization and phagocytosis in the complement-deficient mice appears to be responsible for the impaired clearance of S. pneumoniae from the middle ear and dissemination to the bloodstream during AOM.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1098-5522
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
78
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
976-83
pubmed:dateRevised
2011-10-17
pubmed:meshHeading
pubmed-meshheading:20065024-Animals, pubmed-meshheading:20065024-Bacteremia, pubmed-meshheading:20065024-Blood Bactericidal Activity, pubmed-meshheading:20065024-Colony Count, Microbial, pubmed-meshheading:20065024-Complement C1q, pubmed-meshheading:20065024-Complement C2, pubmed-meshheading:20065024-Complement Factor B, pubmed-meshheading:20065024-Disease Susceptibility, pubmed-meshheading:20065024-Ear, Middle, pubmed-meshheading:20065024-Female, pubmed-meshheading:20065024-Mice, pubmed-meshheading:20065024-Mice, Inbred C57BL, pubmed-meshheading:20065024-Mice, Knockout, pubmed-meshheading:20065024-Microbial Viability, pubmed-meshheading:20065024-Opsonin Proteins, pubmed-meshheading:20065024-Otitis Media, pubmed-meshheading:20065024-Phagocytosis, pubmed-meshheading:20065024-Pneumococcal Infections, pubmed-meshheading:20065024-Streptococcus pneumoniae
pubmed:year
2010
pubmed:articleTitle
Enhanced susceptibility to acute pneumococcal otitis media in mice deficient in complement C1qa, factor B, and factor B/C2.
pubmed:affiliation
Department of Otolaryngology-Head and Neck Surgery, The Ohio State University, 4024 Cramblett Hall, Columbus, OH 43210, USA. tong.1@osu.edu
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural