Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2001-6-27
pubmed:abstractText
Previous results from our laboratory using pharmacological approaches suggested a role for nitric oxide (NO) in the host defense against the human filarial parasite, Brugia malayi. We sought to determine whether a complementary genetic approach, using mice homozygous for a targeted mutation in the gene encoding inducible nitric oxide-synthase (NOS2), would confirm our observation. We hypothesized that such mice would exhibit some deficit in their ability to clear B. malayi. Our data show that the course of infection in NOS2-/- mice is the same as in wild-type mice. Thus, peritoneal cellular responses to infection are similar in NOS2-/- and wild-type mice, with the exception that T cells form a higher percentage of total peritoneal cells in the former. We find virtually no serum IgE in NOS2-/- mice, suggesting a less robust Th2 response. In contrast, NOS2-/- mice demonstrate an early rise in IgG2a titers compared to B6 +/+ mice. Our data suggest that NO is not an obligate requirement for the elimination of B. malayi from the peritoneal cavities of mice.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0014-4894
pubmed:author
pubmed:copyrightInfo
Copyright 2001 Academic Press.
pubmed:issnType
Print
pubmed:volume
98
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
35-43
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Course of Brugia malayi infection in C57BL/6J NOS2 +/+ and -/- mice.
pubmed:affiliation
University of Connecticut Health Center, 263 Farmington Avenue, Farmington, Connecticut, 06030-3105, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.