ArticleExperimental and therapeutic medicine2019
Function and mechanism of pyrin and IL-10 in the regulation of the inflammasome in pulmonary vascular endothelial cells following hemorrhagic shock.
Article in Experimental and therapeutic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The present study aimed to evaluate the function of pyrin and interleukin-10 (IL-10) and the potential mechanisms underlying the regulation of inflammation in pulmonary vascular endothelial cells (ECs) following hemorrhagic shock (HS). Adult female Sprague-Dawley rats were divided into 4 groups (n=6 in each group) to examine the changes in pyrin expression following HS-lipopolysaccharide (LPS) administration, including the following groups: A sham operation (SM) + tracheal injection of saline (SAL) group; a HS + SAL group; a SM + LPS group (with a tracheal injection of endotoxin); and a HS + LPS group. An additional 4 groups were used to evaluate the function of IL-10, by the additional intratracheal injection of recombinant IL-10. Western blot analysis and immunofluorescence were performed in order to investigate the changes to pyrin and IL-10 expression in pulmonary vascular ECs. The expression levels of pyrin in the SM + LPS group were significantly increased in comparison with the SM + SAL group (P<0.01). Additionally, the expression levels of pyrin were significantly increased in the HS + LPS group compared with the HS + SAL group (P<0.01). The expression levels of caspase-1 were significantly increased in the HS + LPS group compared with those in the other three groups (P<0.01). The expression levels of pyrin in the HS + LPS + IL-10 group were significantly increased compared with the HS + LPS group (P<0.01). The expression levels of caspase-1 were significantly decreased following IL-10 treatment compared with those in the HS + LPS group (P<0.01). Therefore, HS attenuated LPS-induced pyrin expression in pulmonary vascular ECs and may also inhibit the expression of IL-10, resulting in the activation of caspase-1 subsequent to a second LPS insult.
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