Physiological Responses in Chicken Cells during Salmonella Enteritidis Infection
Date Issued
2016
Date
2016
Author(s)
Wang, Chia-Lan
Abstract
Salmonella Enteritidis (SE) is one of important public health concerns and infected chickens serve as reservoir which potentially transmits to humans through food. Although SE seldom causes systemic infection in chickens, virulent SE strains can colonize in intestines, invade ovarian follicular cells, and lead a persistent infection of the liver. Infection by SE causes decreased egg production in laying hens clinically. The egg production in laying hens are orchestrated by several organs; therefore, serial experiments were performed to elucidate the possible mechanisms of the decreased egg production in laying hens infected with SE. First, the chicken granulosa cells (cGCs) of ovary is the preferred site for SE infection and it is involved in follicular growth, atresia, and ovulation. The alteration of target genes and steroidogenesis in cGCs at distinct stages of follicular maturity were studied. Luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were applied to the cGCs isolated from hierarchical and prehierarchical follicles, respectively, to imitate the effects of gonadotropin during in vivo SE infection. Attenuated responses to LH and FSH as well as retardant progesterone production due to down-regulated the mRNA expressions of LH receptor, FSH receptor, steroidogenic acute regulatory proteins, P450 side-chain cleavage, and 3beta-Hydroxysteroid dehydrogenase were observed. The progesterone production in cGCs was also significantly reduced during the infection. Moreover, there was a tendency toward pathogen elimination in F1 follicles by induction of a strong immune response and cell apoptosis in smaller follicles to avoid bacterial transovarian infection. It is our speculation that slowed steroidogenesis and impeded follicular growth may result in an increased ovulation interval, and further decreased egg production during SE infection. Secondly, the liver is the primary organ for lipid metabolism in chickens and the site for production and assembly of main components in yolk. We proceeded with a time-course experiment using LMH-2A cells that were infected with SE and co-incubated with β-estradiol to evaluate if SE infection affected lipid metabolism and subsequently changed lipoprotein formation of egg yolk. The results indicated that lipid accumulation significantly increased in infected LMH-2A cells, and 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 (VLDL) II were significantly up-regulated. Moreover, declined lipid transportation of hepatocytes was evidenced by the down-regulation of estrogen receptor alpha which promotes VLDLy formation, increased intra-cellular accumulation of ApoB protein, and decreased cellular excretion of VLDL protein. SE infection probably elevated lipid synthesis and reduce lipid transportation in the chicken liver. These changes of cGCs and LMH-2A may lead excessive lipid accumulation in liver and slower lipoprotein deposition in yolk. Collectively, our study explained that reduced egg production in SE infected laying hens may be associated with the decreased steroidogenesis and the progressive changes in chicken liver lipid metabolism.
Subjects
Salmonella Enteritidis
egg production
steroidogenesis
liver lipid accumulation
chicken granulosa cell
LMH-2A cells
SDGs
Type
thesis
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