Our results showed that AvBD1, AvBD3-5, and AvBD9-14 were constitutively expressed at moderate or high levels in the isthmal epithelial cells of laying hens. Our

data differed from previous findings with regard to the expression of several AvBDs. First, one report showed that AvBD1-7 was mainly expressed in bone marrow whereas AvBD8-13 were restricted in the urogenital tract of young hens LBH589 [18]. Second, another study indicated that most AvBDs, except AvBD6 and AvBD13, were expressed in all segments of oviduct of White Leghorn laying hens [23]. Tissue-specific expression of AvBD14, a newly discovered avian β-defensin, has not been previously reported. Given that the adequacy of PCR primers and conditions as well as the specificity of RT-PCR products being https://www.selleckchem.com/products/azd2014.html confirmed in the present study, the discrepancies between

our results and others’ may reflect the differences CYT387 order between the experimental conditions, such as the breeds of hens (Ross versus White Leghorn) and the sources of RNA (cultured oviduct epithelial cells versus oviduct tissue). It is plausible that the different AvBD expression profiles presented by various investigators suggest a complex regulatory mechanism(s) governing the expression of AvBD genes in different types of hosts, tissues, or even cells. AvBDs play significant roles in host resistance to Salmonella colonization as indicated by the correlation between a high level expression of AvBD and a low level of Salmonella load in the caecum [19, 21]. Either LPS treatment or Salmonella infection can induce the expression of certain AvBD genes in chicken reproductive tissues [22, 31, 34]. In this study, SE temporarily

modulated the expression of certain AvBDs in the early stages of infection. Increased apoptosis of COEC may be partially responsible for the decline in SE-induced expression of certain AvBDs, such as AvBD2 and AvBD6, but it does not explain the diminished suppression of AvBD4 and AvBD9-11 by SE in the late stage of infection. We therefore hypothesize Sitaxentan that SE-modulation of AvBD transcription involves tightly controlled signaling events that take place during the initial interaction between COEC and SE. In mammalian hosts, recognition of pathogen-associated molecular pattern (PAMP) by toll-like receptors (TLR) activates nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK), leading to the up-regulation of beta defensin-2 [35]. Thus, it is likely that LPS, flagellin, and/or secreted virulence factors of SE function as PAMP to trigger the expression of AvBDs in COEC. We also observed that inactivation of pipB, a gene encoding a T3SS translocated protein, increases the ability of SE to stimulate AvBD expression in COEC. The differential induction of AvBDs by ZM100 and ZM106 was only observed when AvBDs were maximally induced (or repressed) by the wild type strain at 1 hpi and/or 4 hpi.