@article{oai:air.repo.nii.ac.jp:00002288,
 author = {Ito, Tomoo and Oyama, Chikako and Arai, Hirokazu and Takahashi, Tsutomu},
 issue = {3/4},
 journal = {秋田医学},
 month = {Mar},
 note = {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.},
 pages = {127--134},
 title = {No Involvement of Acid Sphingomyelinase in the Secretion of IL-6 from Alveolar Macrophages in Rat},
 volume = {40},
 year = {2014}
}