Linked Life Data

18768887

Source:http://linkedlifedata.com/resource/pubmed/id/18768887

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2008-9-4
pubmed:abstractText
In this study, we have addressed the role of H(2)S in modulating neutrophil migration in either innate (LPS-challenged naive mice) or adaptive (methylated BSA (mBSA)-challenged immunized mice) immune responses. Treatment of mice with H(2)S synthesis inhibitors, dl-propargylglycine (PAG) or beta-cyanoalanine, reduced neutrophil migration induced by LPS or methylated BSA (mBSA) into the peritoneal cavity and by mBSA into the femur/tibial joint of immunized mice. This effect was associated with decreased leukocyte rolling, adhesion, and P-selectin and ICAM-1 expression on endothelium. Predictably, treatment of animals with the H(2)S donors, NaHS or Lawesson's reagent, enhanced these parameters. Moreover, the NaHS enhancement of neutrophil migration was not observed in ICAM-1-deficient mice. Neither PAG nor NaHS treatment changed LPS-induced CD18 expression on neutrophils, nor did the LPS- and mBSA-induced release of neutrophil chemoattractant mediators TNF-alpha, keratinocyte-derived chemokine, and LTB(4). Furthermore, in vitro MIP-2-induced neutrophil chemotaxis was inhibited by PAG and enhanced by NaHS treatments. Accordingly, MIP-2-induced CXCR2 internalization was enhanced by PAG and inhibited by NaHS treatments. Moreover, NaHS prevented MIP-2-induced CXCR2 desensitization. The PAG and NaHS effects correlated, respectively, with the enhancement and inhibition of MIP-2-induced G protein-coupled receptor kinase 2 expression. The effects of NaHS on neutrophil migration both in vivo and in vitro, together with CXCR2 internalization and G protein-coupled receptor kinase 2 expression were prevented by the ATP-sensitive potassium (K(ATP)(+)) channel blocker, glybenclamide. Conversely, diazoxide, a K(ATP)(+) channel opener, increased neutrophil migration in vivo. Together, our data suggest that during the inflammatory response, H(2)S augments neutrophil adhesion and locomotion, by a mechanism dependent on K(ATP)(+) channels.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1550-6606
pubmed:author
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
181
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4287-98
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:18768887-Adjuvants, Immunologic, pubmed-meshheading:18768887-Animals, pubmed-meshheading:18768887-Cattle, pubmed-meshheading:18768887-Cell Adhesion Molecules, pubmed-meshheading:18768887-Endocytosis, pubmed-meshheading:18768887-Gene Expression Regulation, pubmed-meshheading:18768887-Hydrogen Sulfide, pubmed-meshheading:18768887-Immunity, Innate, pubmed-meshheading:18768887-KATP Channels, pubmed-meshheading:18768887-Lipopolysaccharides, pubmed-meshheading:18768887-Male, pubmed-meshheading:18768887-Methylation, pubmed-meshheading:18768887-Mice, pubmed-meshheading:18768887-Mice, Inbred BALB C, pubmed-meshheading:18768887-Mice, Inbred C57BL, pubmed-meshheading:18768887-Mice, Knockout, pubmed-meshheading:18768887-Neutrophil Infiltration, pubmed-meshheading:18768887-Receptors, Interleukin-8B, pubmed-meshheading:18768887-Serum Albumin, Bovine
pubmed:year
2008
pubmed:articleTitle
Hydrogen sulfide augments neutrophil migration through enhancement of adhesion molecule expression and prevention of CXCR2 internalization: role of ATP-sensitive potassium channels.
pubmed:affiliation
Department of Pharmacology, School of Medicine of Ribeirão Preto, Ribeirão Preto, Brazil.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't