The effect of cortex eucommiae on alleviating lung injury induced by Haemophilus paragallinarum

TL;DR

Cortex Eucommiae may help reduce lung damage in chickens caused by a bacterial infection by boosting autophagy and reducing inflammation.

Contribution

This study identifies Cortex Eucommiae as a potential therapeutic agent for bacterial-induced lung injury by promoting autophagy and suppressing NLRP3.

Findings

Cortex Eucommiae reduced pro-inflammatory cytokine secretion and inhibited NLRP3, Caspase-1, and IL-1β protein expression.

CE upregulated key autophagy genes and proteins, promoting autophagy in chick lung tissue.

CE alleviated Haemophilus paragallinarum-induced lung injury in chicks.

Abstract

To analyze whether Cortex Eucommiae (CE) can inhibit pathological lung injury by regulating autophagy levels in chicks lung tissue and identify potential targets, thereby alleviating pneumonia damage caused by Haemophilus paragallinarum (Hp) infection. Experimental groups were established: Control group, Hp infection group, Hp+CE group, Hp+Rapamycin (Hp+Rapa) group, and HP+(NLR family, pyrin domain-containing 3, NLRP3) inhibitor (INF39) group. Assessments included: HE staining and pathological scoring of chick lungs, ELISA measurement of inflammatory cytokine expression, RT-PCR analysis of key autophagy genes and NLRP3/Caspase-1/IL-1β inflammatory pathway genes, Immunohistochemistry and Western blot analysis of autophagy protein (microtubule-associated protein 1 chain 3, LC3) and inflammatory proteins NLRP3, Caspase-1, and IL-1β. CE reduced pro-inflammatory cytokine secretion, inhibited NLRP3, Caspase-1, and IL-1β protein expression, and upregulated key autophagy genes and proteins, thereby promoting autophagy and subsequently alleviating Hp-induced pneumonia damage in chicks. CE alleviates Hp-induced acute lung injury in chickens by promoting autophagy and suppressing NLRP3 inflammasome expression. CE may represent a potential therapeutic agent for treating bacterial-induced acute lung injury.

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