Involvement of tumor necrosis factor-α, interleukin-I β, interleukin-8, and interleukin-I receptor antagonist in acute lung injury caused by local Shwartzman reaction
| Autor: | Akihiro Matsukawa, Sumitaka Imamura, Motoko Kagayama, Masaru Yoshinaga, Susumu Ohkawara |
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| Rok vydání: | 1997 |
| Předmět: |
Pathology
medicine.medical_specialty Lung Lipopolysaccharide business.industry medicine.drug_class Inflammation General Medicine respiratory system Lung injury Receptor antagonist Pathology and Forensic Medicine chemistry.chemical_compound Interleukin 1 receptor antagonist medicine.anatomical_structure chemistry medicine Tumor necrosis factor alpha Interleukin 8 medicine.symptom business |
| Zdroj: | Pathology International. 47:16-24 |
| ISSN: | 1440-1827 1320-5463 |
| DOI: | 10.1111/j.1440-1827.1997.tb04430.x |
| Popis: | A local Shwartzman reaction (LSR) was prepared in rabbit lung as a model of acute lung injury. To induce LSR, intratracheal injection of lipopolysaccharide (LPS) 10 micrograms into the lower lobe of the right lung, followed 24 h later by i.v. injection of LPS (10 micrograms/kg). In the lung with the LSR, myeloperoxidase activity, representing neutrophil accumulation, peaked at 1-2 h and was sustained for 48 h after challenge with i.v. LPS. The lung water content peaked at 12 h, and decreased gradually. Histological findings showed diffuse interstitial widening, intra-alveolar leukocyte infiltration with hemorrhage, and alveolar exudate formation. The production of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), interleukin-8 (IL-8), and IL-1 receptor antagonist (IL-1 Ra) in the lung was analyzed. TNF-alpha first elevated and peaked at 0.5 h (66.5 +/- 16.7 ng/g.lung), subsequently, IL-1 beta and IL-8 increased and peaked at 2 h (17.8 +/- 3.4 ng/g.lung and 336.9 +/- 49.6 ng/g.lung, respectively). IL-1Ra was present even before the challenge, and the production increased to show a dual peak (0.5 h, 1.5 +/- 0.2 micrograms/g.lung; and 2 h, 1.6 +/- 0.1 micrograms/g.lung), and a large concentration of IL-1Ra was sustained for 48 h. Immunohistochemistry showed that the cellular source of these cytokines was alveolar macrophages and infiltrating neutrophils. Thus, disclosing the kinetics of the generation of cytokines led to a better understanding of their roles, namely TNF-alpha as an initiator, IL-1 and IL-8 as amplifier and effector, and IL-1Ra as regulator of the intensity of acute inflammation. |
| Databáze: | OpenAIRE |
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