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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.

We investigated the mechanisms that induce atrophy of the chicken bursa of Fabricius (BF) upon lipopolysaccharide (LPS) treatment in young chicks. LPS treatment resulted in ∼36% decrease in bursal weight within 36 h (P < 0.01). Histological analysis showed infiltration of eosinophilic heterophils and nucleated oval shaped RBCs in or near blood vessels of the BF from LPS-treated chicks. Scanning electron micrographs showed severe erosion and breaks in the mucosal membrane at 12 h and complete exuviation of bursal mucosal epithelial cells at 36 h. We observed decreased cell proliferation (low PCNA positivity) and increased apoptosis (high TUNEL and ssDNA positivity) in the BF 12-72 h after LPS treatment. RNA-seq analysis of the BF transcriptome showed 736 differentially expressed genes with most expression changes (637/736) 12 h after LPS treatment. KEGG pathway analysis identified TLR4-MAPK-NF-κB/AP-1 as the key signaling pathway affected in response to LPS stimulation. These findings indicate LPS activates the TLR4-MAPK-NF-κB/AP-1 signaling pathway that mediates acute atrophy of the chicken bursa of Fabricius by inducing inflammation and apoptosis.

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The benefits of selenium (Se) supplementation during pregnancy and lactation in sows on piglet immunocompetence are not yet fully understood. This study aimed to assess piglet immune status when sows were fed Se-deficient or supplemented diets with sodium selenite (SS) or hydroxy-selenomethionine (OH-SeMet). Twelve pregnant sows were randomly assigned to 3 dietary treatments (4 sows each): no supplemental Se (NC), SS at 0.3 mg Se/kg (SS-0.3), OH-SeMet at 0.3 mg Se/kg (SO-0.3). The trial was carried out from gestation day (gd) 84 to weaning on postpartum day (ppd) 21, at which time all the piglets received the same diet having as Se source SS. On gd 98 and 105, sows were vaccinated with hen egg white lysozyme (HEWL). On ppd 0 and 21, 8 piglets/treatment were euthanized to obtain blood and muscle samples for total Se analyses. Serum samples were collected from 8 female piglets/treatment on ppd 0 and 2 to assess antigen-specific antibody titer for HEWL. On ppd 23, 6 weaned female piglets/treatment were intramuscular challenged with E. coli lipopolysaccharide (LPS) and serum IL-10 levels were measured at 24 h pre-challenge and at 2 and 48 h post challenge. At day 21, piglets from sows fed SO-0.3 showed the highest muscle Se deposition (P < 0.001). At ppd 0, no difference for HEWL-specific IgG was found while at ppd 2, SO-0.3 showed the highest HEWL-specific IgG concentration (P < 0.05). At 24 h pre-challenge and 2 h post LPS challenge, SO-0.3 showed a greater IL-10 level as compare to NC and SS-0.3, respectively (P < 0.05); no difference was found for the same parameter at 48 h post challenge. Piglets from SO supplemented sows exhibited stronger early immune response to LPS challenge. This study indicates the importance of sow Se supplementation with a pure organic form of Se such as OH-SeMet to enhance piglets Se and immune status.