2026-03-10T03:17:59Z https://air.repo.nii.ac.jp/oai

oai:air.repo.nii.ac.jp:00002288 2024-08-25T08:08:58Z 611:862:863:1003

No Involvement of Acid Sphingomyelinase in the Secretion of IL-6 from Alveolar Macrophages in Rat Ito, Tomoo Oyama, Chikako Arai, Hirokazu Takahashi, Tsutomu open access chronic lung disease of the newborn alveolar macrophage acid sphingomyelinase Chronic lung disease (CLD) of the newborn is a major problem in neonatology. Activation of alveolar macrophages has been implicated in the pathogenesis of CLD. Acid sphingomyelinase (ASM) responds to diverse cellular stressors, including lipopolysaccharide (LPS) stimulation. Recently, functional inhibitors of acid sphingomyelinase (FIASMAs) have been described as a large group of compounds that inhibit ASM. Here, we used maternal intra-peritoneal LPS injection to model CLD in the infant rat lung. Using this model, we studied ASM activity in the infant rat lung and the effects of FIASMAs on release of interleukin-6 (IL-6) from LPS-stimulated alveolar macrophages. Maternal exposure to LPS non-significantly increased ASM activities in the infant rat lung. FIASMAs significantly decreased ASM activity of LPS-stimulated alveolar macrophages. In addition, some FIASMAs suppressed the release of IL-6 from LPS-stimulated alveolar macrophages during the early response phase. However, FIASMAs did not suppress the release of IL-6 from LPS-stimulated alveolar macrophages. From our study, we could not confirm that ASM activation is responsible for LPS-related pathogenesis of CLD and release of IL-6 from LPS-stimulated alveolar macrophages. 秋田医学会 2014-03-31 eng journal article VoR http://hdl.handle.net/10295/2502 https://air.repo.nii.ac.jp/records/2288 03866106 AN00009294 秋田医学 40 3/4 127 134 https://air.repo.nii.ac.jp/record/2288/files/akitai40-3_4(127).pdf application/pdf 1.3 MB 2017-02-16