作者: Milagros Griet , Hortensia Zelaya , Melina Valeria Mateos , Susana Salva , Guillermo Esteban Juarez
DOI: 10.1371/JOURNAL.PONE.0110027
关键词: In vivo 、 Lipopolysaccharide 、 Peripheral blood mononuclear cell 、 Lung injury 、 Inflammation 、 Immunology 、 PI3K/AKT/mTOR pathway 、 Medicine 、 Lactobacillus reuteri 、 CD14
摘要: We have previously demonstrated that Lactobacillus reuteri CRL1098 soluble factors were able to reduce TNF-α production by human peripheral blood mononuclear cells. The aims of this study determine whether L. modulate in vitro the inflammatory response triggered LPS murine macrophages, gain insight into molecular mechanisms involved immunoregulatory effect, and evaluate vivo its capacity exert anti-inflammatory actions acute lung injury induced mice. In assays significantly reduced pro-inflammatory mediators (NO, COX-2, Hsp70) cytokines (TNF-α, IL-6) caused stimulation macrophages with LPS. NF-kB PI3K inhibition contributed these inhibitory effects. Inhibition PI3K/Akt pathway diminished expression CD14 could be effect. addition, our data proved LPS-induced secretion cytokines, cells recruitment airways tissue damage treated mice, providing a new way excessive pulmonary inflammation.