Ovarian laying hen follicular maturation and in vitro Salmonella internalization

Howard, Zoe; Moore, R. W.; Zabala-Díaz, Irene B.; Landers, K.L.; Byrd, J. A.; Kubena, L. F.; Nisbet, David J.; Birkhold, S. G.; Ricke, Steven C.

doi:10.1016/j.vetmic.2005.03.002

Cited by 23 publications

(14 citation statements)

References 21 publications

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“…Because samples in this study were only taken at 4 and 7 days postinfection, and bacteria were still persistent in the peripheral blood, it cannot be concluded, however, that SE displays a stronger interaction with follicles than other serotypes. Studies comparing invasion of the serotypes Enteritidis and Typhimurium in ovarian follicles in vitro yielded conflicting results (Howard et al, 2005;Mizumoto et al, 2005). The fact that SE and Salmonella Typhimurium may be equally capable of colonizing the ovary is in accordance with the data obtained by Keller et al (1997).…”

Section: Colonization Of the Ovarymentioning

confidence: 83%

“…It has been noticed that in vitro attachment of SE to granulosa cells may involve binding to fibronectin (Thiagarajan et al, 1996a). Howard et al (2005) compared the ability of Salmonella to invade ovarian follicles at different stages of follicular maturity in vitro: the small white follicles (immature) were more susceptible to Salmonella invasion than the more mature small and large yellow ones. There are also indications that Salmonella can invade and multiply in granulosa cells (Thiagarajan et al, 1996a).…”

Section: Colonization Of the Ovarymentioning

confidence: 99%

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Mechanisms of egg contamination bySalmonellaEnteritidis

et al. 2009

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Salmonella Enteritidis (SE) has been the major cause of the food-borne salmonellosis pandemic in humans over the last 20 years, during which contaminated hen's eggs were the most important vehicle of the infection. Eggs can be contaminated on the outer shell surface and internally. Internal contamination can be the result of penetration through the eggshell or by direct contamination of egg contents before oviposition, originating from infection of the reproductive organs. Once inside the egg, the bacteria need to cope with antimicrobial factors in the albumen and vitelline membrane before migration to the yolk can occur. It would seem that serotype Enteritidis has intrinsic characteristics that allow an epidemiological association with hen eggs that are still undefined. There are indications that SE survives the attacks with the help of antimicrobial molecules during the formation of the egg in the hen's oviduct and inside the egg. This appears to require a unique combination of genes encoding for improved cell wall protection and repairing cellular and molecular damage, among others.

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Section: Colonization Of the Ovarymentioning

confidence: 83%

Section: Colonization Of the Ovarymentioning

confidence: 99%

Mechanisms of egg contamination bySalmonellaEnteritidis

et al. 2009

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“…Such a mechanism could contribute to the prevention of transovarian transmission of S. serovar spp. This mechanism may be of importance, as S. enteritidis has been demonstrated to preferentially invade prehierarchal follicles (Howard et al 2005).…”

Section: Discussionmentioning

confidence: 99%

Toll-like receptor signaling in hen ovarian granulosa cells is dependent on stage of follicle maturation

2009

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The recent identification of toll-like receptor (TLR) signaling within ovarian granulosa cells has broad implications for ovarian physiology. Functions of TLRs within granulosa cells of the laying hen are of particular interest due to the method of transovarian transmission of Salmonella enteritidis, which results in egg contamination. This study utilized hen granulosa cells to evaluate the expression and function of Gallus TLR-signaling at distinct stages of follicular maturity. Data presented herein demonstrate the presence of TLR2, TLR4, and TLR15 mRNAs in undifferentiated granulosa cells from prehierarchal follicles and differentiated granulosa cells from preovulatory follicles, together with mRNAs encoding adaptor proteins and signaling components required for TLR signaling gene. Treatment with lipopolysaccharide (LPS) or LH, in vitro, led to the differential regulation of TLRs based on the stage of follicle maturation, with the largest (F1) follicle granulosa cells having the most rapid response. Furthermore, treatment with LPS resulted in attenuation of agonistinduced progesterone synthesis in undifferentiated, but not differentiated, granulosa cells. Additionally, undifferentiated granulosa cells were significantly more sensitive to LPS-induced apoptosis than differentiated granulosa cells from the F1 follicle. Together, these data provide evidence for a complete and functional TLR signaling pathway in hen granulosa cells, with effects on steroidogenesis and cell viability dependent upon stage of maturation. These differences may reflect the susceptibility of granulosa cells at early stages of maturation to undergo apoptosis in response to select pathogenic stimuli, thus attenuating transovarian transmission, whereas granulosa cells from preovulatory follicles are comparably resistant to LPS-mediated apoptosis. Reproduction (2009) 137 987-996

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“…Attachment of S. Enteritidis to follicular granulosa cells has been observed (Thiagarajan, Saeed, & Asem, 1994), and the organism may be able to invade and multiply in these cells (Thiagarajan, Saeed, Turek, & Asem, 1996). Howard et al (2005) found that the immature small white follicles were more susceptible to invasion than were the small and large yellow follicles, perhaps leading to continuous infection of eggs throughout the reproductive cycle. Dawoud et al (2011) used a similar in vitro invasion assay to evaluate follicle invasion by different strains of S. Enteritidis.…”

Section: Colonization Of the Ovarymentioning

confidence: 97%