Literature DB >> 6338779

Lung inflammation: role of endogenous chemotactic factors in attracting polymorphonuclear granulocytes.

H Y Reynolds.   

Abstract

The inflammatory reaction in the lungs can be considered a mechanism of host defense that augments local alveolar cellular and humoral defense against microorganisms and particulates which challenge the airways. As part of this reaction, the accumulation of blood inflammatory and phagocytic cells, primarily PMNs, and fluid components from plasma may be under control of chemoattractant factors and vasoactive mediators. From the air-side, chemotactic factors originating from alveolar macrophages or through activation of the complement system seem essential in initiating the influx of PMNs into the alveolar space. The kinetics of synthesis and release of chemotactic factors from alveolar macrophages of animals and humans and the status of their immunochemical analysis is the essence of this report. Coupling phagocytosis (afferent function) with its capacity to secrete several kinds of effector molecules (chemotactic factors, complement components, leukotrienes, and platelet activating factor), the alveolar macrophage is considered to have a pivotal role in overall regulation of the inflammatory reaction.

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Year:  1983        PMID: 6338779     DOI: 10.1164/arrd.1983.127.2P2.S16

Source DB:  PubMed          Journal:  Am Rev Respir Dis        ISSN: 0003-0805


  15 in total

1.  In-vivo blockage of neutrophil migration by LPS is mimicked by a factor released from LPS-stimulated macrophages.

Authors:  F Q Cunha; G E Souza; C A Souza; B C Cerqueira; S H Ferreira
Journal:  Br J Exp Pathol       Date:  1989-02

Review 2.  Pathogenesis of silicosis: current concepts and hypotheses.

Authors:  G S Davis
Journal:  Lung       Date:  1986       Impact factor: 2.584

3.  Neutrophil migration induced by inflammatory stimuli is reduced by macrophage depletion.

Authors:  G E Souza; F Q Cunha; R Mello; S H Ferreira
Journal:  Agents Actions       Date:  1988-07

Review 4.  Mechanisms of membrane damage and surfactant depletion in acute lung injury.

Authors:  S Westaby
Journal:  Intensive Care Med       Date:  1986       Impact factor: 17.440

5.  Lymphocyte fluctuation in bronchoalveolar lavage fluid in normal volunteers.

Authors:  M Laviolette
Journal:  Thorax       Date:  1985-09       Impact factor: 9.139

6.  Neutrophil elastase alpha 1-proteinase inhibitor complexes in pleural effusions.

Authors:  H Klech; G Rona; E Knoth; F Kummer; P M Bayer
Journal:  Klin Wochenschr       Date:  1988-04-15

7.  Pulmonary absorption of recombinant methionyl human granulocyte colony stimulating factor (r-huG-CSF) after intratracheal instillation to the hamster.

Authors:  R W Niven; F D Lott; J M Cribbs
Journal:  Pharm Res       Date:  1993-11       Impact factor: 4.200

Review 8.  Changes in pulmonary surfactant during bacterial pneumonia.

Authors:  K A Brogden
Journal:  Antonie Van Leeuwenhoek       Date:  1991-05       Impact factor: 2.271

9.  Blockade by antimacrophage serum of the migration of PMN neutrophils into the inflamed peritoneal cavity.

Authors:  G E de Souza; S H Ferreira
Journal:  Agents Actions       Date:  1985-10

10.  Increased expression of the interleukin-8 gene by alveolar macrophages in idiopathic pulmonary fibrosis. A potential mechanism for the recruitment and activation of neutrophils in lung fibrosis.

Authors:  P C Carré; R L Mortenson; T E King; P W Noble; C L Sable; D W Riches
Journal:  J Clin Invest       Date:  1991-12       Impact factor: 14.808

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