The impact ofSalmonellaEnteritidis on lipid accumulation in chicken hepatocytes

Abstract

Salmonella enterica serovar Enteritidis (SE) is a public health concern and infected chickens serve as a reservoir that potentially transmits to humans through food. Although SE seldom causes systemic disease in chickens, virulent SE strains can colonize in intestines and lead a persistent infection of the liver. The liver is the primary organ for lipid metabolism in chickens and the site for production and assembly of main components in yolk. We performed a time-course experiment using LMH-2A cells that were infected with SE and co-incubated with β-oestradiol to evaluate if SE infection affected lipid metabolism and subsequently changed lipoprotein formation for egg yolk. The results indicated that lipid accumulation significantly increased in infected LMH-2A cells while the viability of these cells was only slightly decreased. The mRNA expressions of lipid transportation and most lipogenetic genes including sterol regulatory element binding protein 1, acetyl-CoA carboxylase, fatty-acid synthase, long-chain-fatty-acid-CoA ligase 1, peroxisome proliferator-activated receptor-γ, and very-low-density lipoproteins (VLDLs) II were significantly up-regulated while the expression of lipogenetic-related stearoyl-CoA denaturase 1 was down-regulated. Moreover, decline in lipid transportation of hepatocytes was evidenced by the down-regulation of oestrogen receptor α which promotes VLDLy formation, an increase of intra-cellular accumulation of Apoprotein B (ApoB) protein, and a decrease of cellular excretion of VLDL protein. Conclusively, SE infection could elevate lipid synthesis and reduce lipid transportation in the chicken hepatocytes. These changes may lead excessive lipid accumulation in liver and slower lipoprotein deposition in yolk.

Intestinal Mucosal Immunity-Mediated Modulation of the Gut Microbiome by Oral Delivery of Enterococcus faecium Against Salmonella Enteritidis Pathogenesis in a Laying Hen Model

“…reported that salmonella can persist in the liver as a chronic infection for up to 5 weeks after the oral inoculation of hens ( 43 ). It is well known that the liver is an important organ for lipid metabolism and the de novo fatty acid synthesis ( 44 ). Importantly, lipid metabolism in the liver has also been regarded as having an important role in egg maturation and production ( 44 ).…”

“…It is well known that the liver is an important organ for lipid metabolism and the de novo fatty acid synthesis ( 44 ). Importantly, lipid metabolism in the liver has also been regarded as having an important role in egg maturation and production ( 44 ). The induction and maintenance of egg productivity are dependent upon the expression of genes related to lipid metabolism and the generation of egg yolk lipid that is mostly composed of low-density lipoproteins (LDLs) ( 45 ).…”

Infection Heterogeneity and Microbiota Differences in Chicks Infected by Salmonella enteritidis

“…In this study, 1-d-old female AA female chicks, with Salmonella infection excluded by cloacal swab testing, were reared and challenged under the same conditions, therefore eliminating the influence of genetic background and environment on the experimental results to the greatest extent, and ensured that all the phenotypic results obtained in this study were due to individual differences. S. enteritidis mainly colonizes the liver, spleen, and intestine of poultry after infection [ 41 , 42 ], leading to intestinal damage, a decline in growth performance, and even death. Growth performance, pathological changes in organs, Salmonella loads, and intestinal morphology are important indicators of the severity of S. enteritidis infection.…”

Lipid droplet accumulation occurs early following Salmonella infection and contributes to intracellular bacterial survival and replication

“…Despite the evidence of the LD participation in Salmonella infection (Arena et al., 2011; Guo et al., 1986; Nawabi et al., 2008; Wang et al., 2016), the mechanisms of formation and roles of LDs in Salmonella pathogenicity are still poorly understood. The present study investigated the mechanism involved in LD biogenesis in Salmonella ‐infected macrophages and the role of this organelle in bacterial pathogenicity.…”