RGD Reference Report - Relationship between interleukin-1 beta and platelet-activating factor in the pathogenesis of acute immune complex alveolitis in the rat. - Rat Genome Database

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Relationship between interleukin-1 beta and platelet-activating factor in the pathogenesis of acute immune complex alveolitis in the rat.

Authors: Warren, JS 
Citation: Warren JS Am J Pathol. 1992 Sep;141(3):551-60.
RGD ID: 7401229
Pubmed: PMID:1519663   (View Abstract at PubMed)
PMCID: PMC1886684   (View Article at PubMed Central)

Intrapulmonary interleukin-1 beta (IL-1 beta) participates in the pathogenesis of acute IgG immune-complex alveolitis through a mechanism involving neutrophil recruitment. We have examined the relationship between intrapulmonary IL-1 beta and locally produced platelet-activating factor (PAF) in the development of acute alveolitis. Instillation of IgG anti-bovine albumin into the lungs of rats, followed immediately by intravenous infusion of bovine serum albumin (BSA), resulted in acute neutrophil-mediated lung injury. Development of IgG immune-complex lung injury was accompanied by three- and five-fold increases in bronchoalveolar lavage (BAL) fluid and whole lung PAF levels, respectively. Intratracheal administration of the PAF antagonists, WEB-2086 (Boehringer) or L-652,731 (Merck, Sharpe, and Dohme, Rahway, NJ), reduced pulmonary vascular leakage. Neutralization of intrapulmonary IL-1 activity with anti-IL-1 beta antibodies reduced pulmonary vascular permeability and whole lung PAF levels. Morphometric analysis and whole lung myeloperoxidase measurements revealed a differential effect between the PAF antagonists and anti-IL-1 beta with respect to pulmonary neutrophil recruitment. Intratracheal instillation of anti-IL-1 beta retarded net pulmonary neutrophil recruitment while the PAF antagonists retarded migration of neutrophils from the interstitial/vascular compartments into the alveolar compartment. Intratracheal instillation of anti-IL-1 beta plus L-652,731 resulted in reduction in lung vascular permeability and retarded net pulmonary neutrophil recruitment. No additive effect was observed. Stimulation of isolated mouse alveolar macrophages with recombinant murine IL-1 beta or IL-1 alpha resulted in rapid, dose-dependent, and cell concentration-dependent increases in PAF secretion. These data suggest that intrapulmonary IL-1 beta amplifies local PAF production and that IL-1 beta and PAF modulate different aspects of pulmonary neutrophil recruitment.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
extrinsic allergic alveolitis  ISOIl1b (Rattus norvegicus)7401229; 7401229 RGD 
extrinsic allergic alveolitis  IMP 7401229 RGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
positive regulation of neutrophil chemotaxis  IMP 7401229 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Il1b  (interleukin 1 beta)

Genes (Mus musculus)
Il1b  (interleukin 1 beta)

Genes (Homo sapiens)
IL1B  (interleukin 1 beta)


Additional Information