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Interleukin 1 production by human lung tissue. I. Identification and characterization
B S Bochner1, S D Landy, M Plaut
1Department of Medicine, Johns Hopkins University School of Medicine, Good Samaritan Hospital, Baltimore, MD 21239.
Journal of Immunology (Baltimore, Md. : 1950)
|October 1, 1987
Summary
Human lung fragments release a factor that increases leukocyte adhesion to blood vessel walls. This factor is identified as Interleukin-1 (IL-1), crucial for inflammatory responses in lung tissue.
Area of Science:
- Immunology
- Cell Biology
- Pulmonary Medicine
Background:
- Inflammatory infiltrates depend on leukocyte adhesion to vascular endothelium.
- Previous in vitro studies identified agents promoting leukocyte-endothelial cell adhesion.
Purpose of the Study:
- To investigate if human lung fragments release factors promoting leukocyte-endothelial cell adhesion.
- To characterize the nature of this adherence-promoting factor.
Main Methods:
- Culturing human lung fragments and collecting supernatants.
- Testing supernatants for their ability to promote polymorphonuclear leukocyte adherence to human vascular endothelial cells (VEC).
- Characterizing the factor using heat lability, polymyxin B inactivation, Sephadex G-75 chromatography, IL-1 assay, and antibody neutralization.
Main Results:
- Human lung fragments release a factor that enhances VEC adhesiveness for leukocytes in a time- and dose-dependent manner.
- This factor is identified as Interleukin-1 (IL-1) (alpha and beta forms).
- IL-1 exhibited heat lability, polymyxin B resistance, specific molecular weight distribution, IL-1 assay activity, and neutralization by anti-IL-1 antisera.
Conclusions:
- Interleukin-1 (IL-1) released by lung tissue promotes leukocyte adherence to vascular endothelium.
- IL-1 production in vivo likely contributes to inflammatory infiltrates in human lungs and other tissues.