Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2000-3-15
pubmed:abstractText
Control of mycobacterial growth depends on the concerted activity of different cytokines acting in different stages of the development of innate and adaptive immune responses. Tumour necrosis factor-alpha (TNF-alpha) has been shown to play a protective role in Mycobacterium avium infections. Here we assessed the growth of this mycobacterial species in wild-type mice and in mice with a genetically engineered disruption of the type I receptor for TNF-alpha (p55-KO mice). p55-KO mice infected with a low-virulence strain of M. avium exhibited a slightly delayed capacity to eliminate the micro-organisms from the liver as compared with wild-type animals. However, either the growth of this strain in the other organs studied (spleen and lung) or the growth of two other strains of M. avium with intermediate or high virulence, failed to be affected by mutation of the TNF-alpha receptor. p55-KO mice were also as protected by the administration of recombinant interleukin-12 as the heterozygous p55 +/- mice. We conclude that signalling through the type I TNF receptor plays a small role in vivo in the induction of mycobacteriostasis during M. avium infection but may improve survival during infection with virulent mycobacteria, independently of the extent of their proliferation.
pubmed:commentsCorrections
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pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0019-2805
pubmed:author
pubmed:issnType
Print
pubmed:volume
99
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
203-7
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Minor role played by type I tumour necrosis factor receptor in the control of Mycobacterium avium proliferation in infected mice.
pubmed:affiliation
Laboratory of Microbiology and Immunology of Infection, Institute for Molecular and Cell Biology, University of Porto, Portugal.
pubmed:publicationType
Journal Article