Abstract
Infection by Salmonella Enteritidis (SE) causes decreased egg production in laying hens. Immunoresponse, steroidogenesis, and cell proliferation by chicken granulosa cells (cGCs) are of particular interest because these changes are involved in follicular growth, atresia, and ovulation. To elucidate the possible mechanisms underlying these changes, transcriptional alterations 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 vitro SE infection. Results showed that the expression of Toll-like receptor 15 was dependent on the follicular maturity, with mature cells having a more significant and progressively stronger immunoresponse. Attenuated responses to LH and FSH as well as retardant steroidogenesis due to down-regulated LH receptor, FSH receptor, and the P450 side-chain cleavage system were observed and may have led to delayed hierarchical follicular growth. Deteriorated cell viability of prehierarchical follicles may occur, as the proliferation of stimulator heparin-binding epidermal growth factor was reduced significantly. Furthermore, the infection led to a higher probability of cGCs from the smaller follicles undergoing apoptosis than those from F1 follicles. Collectively, the data provide evidence of 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 play essential roles in decreased ovulation rate as well as further decreased egg production during SE infection.
Published Version
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