Lipopolysaccharide mediates immuno-pathological alterations in young chicken liver through TLR4 signaling

Abstract

BackgroundLipopolysaccharide (LPS) induces acute liver injury and the complex mechanisms include the activation of toll like receptor 4 (TLR4) signaling pathway in many species. However, immuno-pathological changes during TLR4 signaling under LPS stress in acute liver injury is poorly understood in avian species. The present investigation was therefore carried out to evaluate these alterations in TLR4 signaling pathway during acute liver injury in young chickens.ResultsAfter intraperitoneal injection of LPS or saline, liver samples were harvested at 0, 2, 6, 12, 24, 36, 72 and 120 h (n = 6 at each time point) and the microstructures were analyzed by hematoxylin and eosin (H&E) staining. Alanine aminotransferase (ALT) and caspase-3 enzyme activity was assessed by enzyme-linked immunosorbent assay (ELISA). Proliferative cell nuclear antigen (PCNA), single stranded DNA (ssDNA) and TLR4 protein expressions were determined by immunohistochemistry. Gene expressions of PCNA, caspase-3, caspase-8, TLR4 and its downstream molecules were analyzed by quantitative polymerase chain reaction (qPCR). LPS injection induced significantly higher ALT activity, severe fatty degeneration, necrotic symptoms, ballooning degeneration, congestion, enhanced inflammatory cell infiltration in liver sinusoids, decreased proliferation, increased apoptosis and significant up-regulation in TLR4 and its downstream molecules (MyD88, NF-κB, TNF-α, IL-1β and TGF-β) expression at different time points.ConclusionsThis study indicated that TLR4 signaling and its downstream molecules along with certain cytokines play a key role in acute liver injury in young chickens. Hence, our findings provided novel information about the histopathological, proliferative and apoptotic alterations along with changes in ALT and caspase-3 activities associated with acute liver injury induced by Salmonella LPS in avian species.Electronic supplementary materialThe online version of this article (doi:10.1186/s12865-017-0199-7) contains supplementary material, which is available to authorized users.

Osteocalcin prevents insulin resistance, hepatic inflammation, and activates autophagy associated with high-fat diet–induced fatty liver hemorrhagic syndrome in aged laying hens

“…As proinflammatory factors, IL-1, IL-6, and TNF-α have been used for evaluating inflammatory and infectious reaction and related immunity in humans and various animals including chickens ( Yang et al., 2014 ; Koronowicz et al., 2016 ; Huang et al., 2017 ). Tumor necrosis factor-alpha plays an important role in the pathogenesis of mammals' NAFLD ( Wigg et al., 2001 ) and has a close relationship with the liver damage including steatosis, fibrosis, and apoptosis ( Tomita et al., 2006 ; Zhang et al., 2010 ).…”

Lactobacillus plantarum prevents and mitigates alcohol‐induced disruption of colonic epithelial tight junctions, endotoxemia, and liver damage by an EGF receptor‐dependent mechanism

“…Our data revealed that EtOH feeding elevates plasma LPS and that L. plantarum prevents this effect of EtOH by an EGFR-dependent mechanism. LPS exposure has been shown to increase the expression of its receptor, TLR4, in different tissues, including the liver (19,20). Therefore, we evaluated TLR4 mRNA levels in liver.…”

“…Although the prevention of liver damage by L. plantarum in the gut lumen provides strong support for the role of gut permeability and endotoxin flux in alcoholic liver damage, a direct effect of EtOH on liver cannot be ruled out. To gather further support on LPS-mediated liver damage, we evaluated the effect of EtOH and L. plantarum on the levels of plasma LPS and liver mRNA for TLR4 and MYD88, both known to be up-regulated by LPS exposure (19,20). L. plantarum in the diet attenuated EtOH-induced elevation of plasma LPS in WT and rtTA mice, which was blocked by doxycycline-mediated expression of dominant negative EGFR in rtTA-EGFR*-Tg mice.…”

Osteocalcin prevents insulin resistance, hepatic inflammation and autophagy associated with high-fat diet induced fatty liver hemorrhagic syndrome in aged laying hens

“…As pro-inflammatory factors, IL-1, IL-6, and TNF-α have been used for evaluating infectious and inflammatory reaction-associated immunity in humans and various animals including chickens [52][53][54]. TNF-α plays an important role in the pathogenesis of mammals' NAFLD [55] and has a close relationship with the liver steatosis, fibrosis, and apoptosis [56,57].…”