Alveolar hypoxia induces organ‐specific inflammasome‐related inflammation in male mouse lungs.

Autor: Udjus, Camilla, Halvorsen, Bente, Kong, Xiang Yi, Sagen, Ellen Lund, Martinsen, Marita, Yang, Kuan, Løberg, Else Marit, Christensen, Geir, Skjønsberg, Ole Henning, Larsen, Karl‐Otto
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Zdroj: Physiological Reports; Jul2024, Vol. 12 Issue 14, p1-13, 13p
Abstrakt: Inflammation through activation of caspase‐1, seems to play a role in pulmonary hypertension induced by alveolar hypoxia. Whether alveolar hypoxia induces caspase‐1‐mediated inflammation and influx of leukocytes in other organs than the lungs, is not known. Our aim was to explore sites of caspase‐1‐related inflammation in alveolar hypoxia. Wild type (WT) mice were exposed to environmental hypoxia or room‐air, and organs were analyzed. Right heart catheterization was performed after 14 days of alveolar hypoxia in WT mice and mice transplanted with WT or caspase‐1−/− bone marrow. Hypoxia induced leukocyte accumulation and increased caspase‐1 protein in the lungs, not in other organs. WT mice transplanted with WT or caspase‐1−/− bone marrow showed no difference in pulmonary leukocyte accumulation or development of pulmonary hypertension after alveolar hypoxia. Caspase‐1 and IL‐18 were detected in bronchial epithelium in WT mice, and hypoxia induced IL‐18 secretion from bronchial epithelial cells. IL‐18 stimulation generated IL‐6 mRNA in monocytes. Phosphorylated STAT3 was increased in hypoxic lungs, not in other organs. Alveolar hypoxia induces caspase‐1 activation and leukocyte accumulation specific to the lungs, not in other organs. Caspase‐1 activation and IL‐18 secretion from bronchial epithelial cells might initiate hypoxia‐induced inflammation, leading to pulmonary hypertension. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index
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