Puerarin inhibits Mycoplasma gallisepticum (MG-HS)-induced inflammation and apoptosis via suppressing the TLR6/MyD88/NF-κB signal pathway in chicken

• Published in: International immunopharmacology 2020-11, Vol.88, p.106993-106993, Article 106993
• Main Authors: Niu, Lumeng, Luo, Ronglong, Zou, Mengyun, Sun, Yingfei, Fu, Yali, Wang, Yingjie, Peng, Xiuli
• Format: Article
• Language: English
• Subjects: Alveoli; Anti-inflammatory agents; Apoptosis; Cell cycle; Cell proliferation; Chickens; Cytokines; Damage; Etiology; Gene expression; Health services; IL-1β; Infections; Inflammation; Inflammatory diseases; Inflammatory response; Interleukin 6; Lungs; Metastases; Mycoplasma gallisepticum; Mycoplasma gallisepticum (MG-HS strain); MyD88 protein; NF-κB protein; Poultry; Puerarin; Respiratory diseases; Respiratory system; Signal transduction; TLR6/MyD88/NF-κB signaling pathway; Toll-like receptors; Tumor necrosis factor-TNF; Tumor necrosis factor-α
• ISSN: 1567-5769; 1878-1705
• DOI: 10.1016/j.intimp.2020.106993

•Puerarin, like Try, has a significant effect in the treatment of MG infection in chicken.•Puerarin can effectively inhibit inflammation and apoptosis via suppressing the TLR6/MyD88/NF-κB signal pathway.•Puerarin can effectively inhibit the expression of MG adhesion protein pMGA1.2.•Puerarin at appropriate concentrations is not cytotoxic. Mycoplasma gallisepticum (MG) is the primary etiological agent of chicken chronic respiratory disease (CRD), which mainly causes inflammatory damage of the host respiratory system. Previous studies suggest that puerarin (PUE) plays a pivotal regulatory role in inflammatory diseases, whereas the impacts of PUE on MG-induced inflammation remain unclear. This study investigated the effects of PUE on MG-HS infection in vitro and in vivo and indicated its potential therapeutic and preventive value. Experimental results showed that PUE significantly suppressed pMGA1.2 expression, promoted MG-infected cell proliferation and cell cycle process by reducing apoptosis. Histopathological examination of lung tissue showed severe histopathological lesions including thickened alveolar walls, narrowed alveolar cavity, and inflammatory cell infiltration in the MG-infected chicken group. However, PUE treatment significantly ameliorated MG-induced pathological damage in lung. Compared to the MG-infected group, PUE effectively inhibited the expression of MG-induced inflammatory genes, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), cytokines interleukin-6 (IL-6), toll-like receptor 6 (TLR6), myeloid differentiation primary response gene 88 (MyD88) and nuclear factor κB (NF-κB). Moreover, PUE dose-dependently inhibited MG-induced NF-κB p65 to enter the cell nucleus. In conclusion, our findings indicate that PUE treatment can efficiently inhibit MG-induced inflammatory response and apoptosis, and protect the lung from MG infection-induced damage by inhibiting the TLR6/MyD88/NF-κB signaling pathway activation. The study suggests that PUE may be a potential anti-inflammatory agent defense againstMGinfection in chicken.