Campylobacter jejuni-Induced Cytokine Responses in Avian Cells

Abstract

Campylobacter jejuni is a major cause of human inflammatory enteritis. During the course of human disease numerous proinflammatory cytokines are produced. Little is known, however, about the cytokine responses produced during the interaction of this bacterium with the avian host. Campylobacter has been considered a commensal of the avian host. Any differences in innate responses to this pathogen between the human and avian hosts should lead to a greater understanding of the disease process in humans. We have demonstrated expression of proinflammatory cytokines and chemokines in response to Campylobacter infection in avian primary chick kidney cells and the avian macrophage cell line HD11. The data indicate that Campylobacter can stimulate the avian host in a proinflammatory manner. The data strongly suggest that the lack of pathology in vivo is not due to an inability of Campylobacter to stimulate a proinflammatory response from avian cells.

Campylobacter jejuni adhere to and invade chicken intestinal epithelial cells in vitro

“…Although immature birds challenged by large C. jejuni inocula may get diarrhoea and some reports allude to a form of vibrionic hepatitis, there is no evidence that naturally acquired C. jejuni causes infection in avian intestinal epithelium cells (Newell, 2000;Skirrow, 1994). Recently, Smith et al (2005) used an avian kidney cell model of Campylobacter infection and showed adherence to and invasion of these cells but the interaction of Campylobacter with avian intestinal cells has never been studied directly. In this study we have developed a primary cell model of intestinal campylobacteriosis to investigate the host-specific tropism of these organisms.…”

“…This would have substantial implications for furthering our understanding of the ecology of the intestinal tract. (Smith et al, 2005). These studies raise the possibility that the avian immune system could influence Campylobacter infectivity in vivo.…”

Unique Properties of the Chicken TLR4/MD-2 Complex: Selective Lipopolysaccharide Activation of the MyD88-Dependent Pathway

“…Primers and probes (Table II) were designed as described (40,41) or using the Primer Express software (Applied Biosystems). Probes (Isogen Life Science) were labeled with the reporter dye carboxyfluorescein (FAM) and the quencher tetramethyl-6-carboxyrhodamine (TAMRA).…”

Virulence genes and cytokine profile in systemic murineCampylobacter coliinfection

“…with intestinal epithelial cells result in the production of cytokines, which are regulators of host responses to infection, and which have important roles in the pathogenesis of infectious diseases. [19][20][21] Cytokines are produced by immune cells, and according to their function, they are divided into the pro-inflammatory cytokines, such as interleukin (IL)-1, IL-2, IL-6, IL-8, IL-12, IL-17 and IL-18, tumor necrosis factor (TNF)-a, and interferon (IFN)-g, and the antiinflammatory cytokines, such as IL-4, IL-10 and tumor growth factor-b. 2,22 Both pro-inflammatory and anti-inflammatory cytokines are induced during Campylobacter spp infection, and it is important to determine whether the immune system is successful in providing protection against these specific pathogens.…”

“…5 Some cytokines can be produced in excess, and thus these might contribute strongly to disease pathology. 19 Indeed, it has been reported that macrophages produce IL-1a, IL-1b, IL-6, IL-8 and TNF-a when infected with Campylobacter spp.. 23 However, the pathogenesis of C. coli infection is still poorly understood, which is mainly a consequence of the lack of a suitable animal model that can be used to mimic the course of infection in human. 24 We thus monitored the stability of the virulence and toxin genes (i.e., cadF, virB11, cdtB, cdtC, ceuE) by comparing the sequence data of C. coli 26536 before and after transmission through the host, and their colonisation and cytokine induction in a murine model.…”