title: Preferential recruitment of neutrophils by endothelin-1 in acute lung inflammation induced by lipopolysaccharide or cigarette smoke.
abstract: This study examined the role of endothelin-1 (ET-1) in recruiting inflammatory cells to the lung after induction of injury with either lipopolysaccharide (LPS) or cigarette smoke. Hamsters injected with either ET-1 or its precursor peptide (Big ET-1) prior to treatment with LPS or cigarette smoke had markedly increased concentrations of neutrophils in bronchoalveolar lavage fluid (BALF) despite a reduction in total numbers of BALF leukocytes. Furthermore, the effect of ET-1 on smoke-exposed animals was reversed by addition of an endothelin-A receptor antagonist. These results are consistent with preferential recruitment of neutrophils by ET-1, and suggest that inhibition of this proinflammatory mediator may decrease acute pulmonary inflammation associated with cigarette smoke and other pulmonary toxins.
authors.affiliation: St John's University, School of Pharmacy and Allied Health Sciences, Jamaica, New York 11439, USA.
authors.forename: Tapan
authors.initials: T
authors.lastname: Bhavsar
authors.forename: Xing Jian
authors.initials: XJ
authors.lastname: Liu
authors.forename: Hardik
authors.initials: H
authors.lastname: Patel
authors.forename: Ralph
authors.initials: R
authors.lastname: Stephani
authors.forename: Jerome O
authors.initials: JO
authors.lastname: Cantor
mesh_terms: D055371:Acute Lung Injury / Q000139:chemically induced / Q000276:immunology*; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D006224:Cricetinae; D004195:Disease Models, Animal; D065130:Endothelin A Receptor Antagonists; D019332:Endothelin-1 / Q000096:biosynthesis / Q000494:pharmacology / Q000502:physiology*; D005260:Female; D008070:Lipopolysaccharides; D020556:Neutrophil Infiltration / Q000187:drug effects / Q000502:physiology*; D012906:Smoke
chemical_list: D065130:Endothelin A Receptor Antagonists; D019332:Endothelin-1; D008070:Lipopolysaccharides; D012906:Smoke