Li Li 1,2 , Jun Yan 1,2 , Lin-Qin Ma 1,2 , Wei Bi 1,2 , Cai-Jun Wu 1,2 Show Affiliations »
Abstract
BACKGROUND: To investigate effects of Maxingloushi decoction on lung inflammation and programmed death markers (programmed death-1 [PD-1], programmed death-ligand 1 [PD-L1]) in the lung tissue, peripheral blood, and bronchoalveolar lavage fluid (BLF) in a mouse model of chronic obstructive pulmonary disease (COPD). METHODS: Thirty-six mature male BALB/C mice were randomly divided into normal group (group A, n=6), COPD model group (group B, n=10), Maxingloushi decoction + COPD group (group C, n=10), and PD-1 inhibitor + COPD group (group D, n=10). The COPD model was established by smoke inhalation combined with lipopolysaccharide (LPS). Levels of PD-1 and PD-L1 in plasma and BLF were measured by enzyme-linked immunosorbent assay (ELISA). Histopathological techniques were used to semi-quantitatively analyze the immuno-fluorescence optical density (IOD) value of the lung tissue. RESULTS: In plasma and BLF, the expression of PD-1 in the group B was higher than that in the group A, and the expression of PD-L1 was lower than that in the group A. The expression of PD-1 and PD-L1 in the lung tissue was normalized in the group C in comparison with the group B (P<0.05) and the group D (P<0.05), and inflammatory cell infiltration in the lung tissue was also improved. CONCLUSIONS: These findings reveal that COPD causes an immune imbalance in the peripheral blood and lung tissue, and that both Maxingloushi decoction and PD-1 inhibitor treatment can mitigate lung inflammation in COPD by reducing PD-1 expression and increasing PD-L1 expression. The treatment effect of Maxingloushi decoction may be superior to that of PD-1 inhibitor. Copyright: © World Journal of Emergency Medicine.
BACKGROUND: To investigate effects of Maxingloushi decoction on lung inflammation and programmed death markers (programmed death-1 [PD-1], programmed death-ligand 1 [PD-L1]) in the lung tissue, peripheral blood, and bronchoalveolar lavage fluid (BLF) in a mouse model of chronic obstructive pulmonary disease (COPD). METHODS: Thirty-six mature male BALB/C mice were randomly divided into normal group (group A, n=6), COPD model group (group B, n=10), Maxingloushi decoction + COPD group (group C, n=10), and PD-1 inhibitor + COPD group (group D, n=10). The COPD model was established by smoke inhalation combined with lipopolysaccharide (LPS). Levels of PD-1 and PD-L1 in plasma and BLF were measured by enzyme-linked immunosorbent assay (ELISA). Histopathological techniques were used to semi-quantitatively analyze the immuno-fluorescence optical density (IOD) value of the lung tissue. RESULTS: In plasma and BLF, the expression of PD-1 in the group B was higher than that in the group A, and the expression of PD-L1 was lower than that in the group A. The expression of PD-1 and PD-L1 in the lung tissue was normalized in the group C in comparison with the group B (P<0.05) and the group D (P<0.05), and inflammatory cell infiltration in the lung tissue was also improved. CONCLUSIONS: These findings reveal that COPD causes an immune imbalance in the peripheral blood and lung tissue, and that both Maxingloushi decoction and PD-1 inhibitor treatment can mitigate lung inflammation in COPD by reducing PD-1 expression and increasing PD-L1 expression. The treatment effect of Maxingloushi decoction may be superior to that of PD-1 inhibitor. Copyright: © World Journal of Emergency Medicine.
Entities: Chemical
Keywords:
Chronic obstructive pulmonary disease; Immune; Maxingloushi decoction; Mice; Programmed death-1; Programmed death-ligand 1
Year: 2022
PMID： 35003414 PMCID： PMC8677923 DOI： 10.5847/wjem.j.1920-8642.2022.023
Source DB: PubMed Journal: World J Emerg Med ISSN： 1920-8642