Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2009-3-23
pubmed:abstractText
Tuberculosis (TB) remains a global health threat. Although it is generally accepted that TB results from intensive cross-talk between the host and the pathogen Mycobacterium tuberculosis, underlying mechanisms remain elusive. The first evidence of human polymorphisms related to susceptibilities to distinct M. tuberculosis lineages has been gathered. Confrontation of limited host resistance with heightened bacterial virulence forms a most hazardous combination. We investigated extreme combinations, confronting inducible nitric oxide synthase-deficient (iNOS(-/-)) and wild-type (WT) mice with 2 related M. tuberculosis strains that differ markedly in virulence, namely, the M. tuberculosis laboratory strains H37Rv and H37Ra. We provide evidence that deregulated chemokine signaling and excessive neutrophil necrosis contribute to disproportionate neutrophil influx and exacerbated TB in iNOS(-/-) mice infected with virulent M. tuberculosis (strain H37Rv), whereas resistant and susceptible mice controlled attenuated H37Ra equally well. Thus, a combination of host susceptibility and M. tuberculosis virulence determines the role of iNOS in the protection and control of inflammation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0022-1899
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
199
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1222-32
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Combination of host susceptibility and virulence of Mycobacterium tuberculosis determines dual role of nitric oxide in the protection and control of inflammation.
pubmed:affiliation
Department of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't