Hydroxytyrosol mitigates Mycoplasma gallisepticum-induced pulmonary injury through downregulation of the NF-kB/NLRP3/IL-1b signaling pathway in chicken

In this study, the anti-inflammatory and antiapoptotic effects of hydroxytyrosol (HT) in Myco-plasma gallisepticum (MG)-infected chicken were investi-gated, and the underlying molecular mechanisms were explored. The results revealed severe ultrastructural patho-logical changes after MG infection in the lung tissue of chicken, including inflammatory cell infiltration, thickening of the lung chamber wall, visible cell swelling, mitochon-drial cristae rupture, and ribosome shedding. MG possibly activated the nuclear factor kB (NF-KB)/nucleotide-bind-ing oligomerization domain-like receptor protein 3 (NLRP3)/interleukin (IL)-1f3 signaling pathway in the lung. However, HT treatment significantly ameliorated MG-induced pathological damage of the lung. HT reduced the magnitude of pulmonary injury after MG infection by reducing apoptosis and releasing the proinflammatory fac-tors. Compared with the MG-infected group, the HT-treated group exhibited significant inhibition of the expres-sion of NF-kB/NLRP3/IL-1f3 signaling-pathway-related genes; for example, the expressions of NF-kB, NLRP3, cas-pase-1, IL-1f3, IL-2, IL-6, IL-18, and TNF-a significantly decreased (P < 0.01 or <0.05). In conclusion, HT effectively inhibited MG-induced inflammatory response and apopto-sis and protected the lung by blocking the activation of NF-kB/NLRP3/IL-1f3 signaling pathway and reducing the damage caused by MG infection in chicken. This study revealed that HT may be a suitable and effective anti-inflammatory drug against MG infection in chicken.

Automated summary

This study investigated the effects of hydroxytyrosol (HT) on inflammation and apoptosis in Mycoplasma gallisepticum (MG)-infected chickens, and explored the underlying molecular mechanisms. The results showed severe pathological changes in the lung tissue of chickens after MG infection, including inflammatory cell infiltration, thickening of the lung chamber wall, cell swelling, mitochondrial cristae rupture, and ribosome shedding. MG possibly activated the NF-KB/NLRP3/IL-1f3 signaling pathway in the lung. However, HT treatment significantly reduced MG-induced lung damage and inflammatory response by inhibiting the activation of this pathway.