Induction of α and β chemokines by intestinal epithelial cells stimulated with Campylobacter jejuni

Bakhiet, Moiz; Al-Salloom, Fajer Subah; Qareiballa, Ahmed; Bindayna, Khalid Mubarak; Farid, Iman A; Botta, Giuseppe

doi:10.1016/j.jinf.2003.11.006

Cited by 32 publications

(22 citation statements)

References 35 publications

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“…Human intestinal epithelial cell transcriptional upregulation and secretion of antimicrobials (␤-defensin) and chemokines (IL-8, monocyte chemoattractant protein 1, and macrophage inflammatory protein 1␤) have been proposed to play a role in C. jejuni-mediated intestinal inflammation (7,23,26,64). Currently, it is believed that C. jejuni stimulates innate immune responses through the activation of NF-B signaling pathways via the mitogen-activated protein kinase family (11,26,42,59).…”

Section: Discussionmentioning

confidence: 99%

Campylobacter jejuni Drives MyD88-Independent Interleukin-6 Secretion via Toll-Like Receptor 2

Friis¹,

Keelan

Taylor³

2009

Infect Immun

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Gastrointestinal disease caused by Campylobacter jejuni is characterized by localized inflammation and the destruction of the epithelial cell barrier that forms host innate protection against pathogens. This can lead to an imbalance in fluid transport across the gastrointestinal tract, resulting in severe diarrhea. The mechanisms of host cell receptor recognition of C. jejuni and downstream immune signaling pathways leading to this inflammatory disease, however, remain unclear. The aim of this study was to analyze the mechanisms involved in C. jejuni induction of the acute-phase inflammatory response regulator interleukin-6 (IL-6). Polarized intestinal epithelial Caco-2 monolayers responded to infections with Salmonella enterica serovar Typhimurium and eight isolates of C. jejuni by an increase in levels of expression and secretion of IL-6. No such IL-6 response, however, was produced upon infection with the human commensal organism Lactobacillus rhamnosus GG. The IL-6 signaling pathway was further characterized using short interfering RNA complexes to block gene expression. The inhibition of myeloid differentiation primary response protein 88 (MyD88) expression in this manner did not affect C. jejuni-induced IL-6 secretion, suggesting a MyD88-independent route to IL-6 signal transduction in C. jejuni-infected human epithelial cells. However, a significant reduction in levels of IL-6 was evident in the absence of Toll-like receptor 2 (TLR-2) expression, implying a requirement for TLR-2 in C. jejuni recognition. Caco-2 cells were also treated with heat-inactivated and purified membrane components of C. jejuni to isolate the factor responsible for triggering IL-6 signaling. The results demonstrate that C. jejuni surface polysaccharides induce IL-6 secretion from intestinal epithelial cells via TLR-2 in a MyD88-independent manner.

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Section: Discussionmentioning

confidence: 99%

Campylobacter jejuni Drives MyD88-Independent Interleukin-6 Secretion via Toll-Like Receptor 2

Friis¹,

Keelan

Taylor³

2009

Infect Immun

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“…Both CKC and HD11 cells showed (23,44), strongly suggests these data can be extrapolated to responses that may occur in the intestine. In humans, bacterial infection of epithelial cells stimulates the production of chemokines which are involved in the attraction of leukocytes (3,21). Campylobacter can traverse human epithelial cells and therefore interact with leukocytes to further stimulate the immune response.…”

Section: Discussionmentioning

confidence: 99%

“…Campylobacter can invade human epithelial cell monolayers (11,12), causing disruption to the epithelium and gaining access to its basal side (41,45). Interleukin-1␤ (IL-1␤), IL-8, and nitric oxide (NO) are produced during human Campylobacter infections (10), and in vitro experiments with human-derived epithelial cell lines have shown that C. jejuni can induce the secretion of a range of cytokines and chemokines (2,3,16,17,19).…”

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confidence: 99%

“…While the production of chemokines by human cells in response to Campylobacter infection has only just been described (3), their role in infection may be crucial to the development of inflammatory disease. The chicken has a reduced chemokine repertoire compared to mammals (18) and possesses two homologues of IL-8, 9E3/CEF4 (also known as IL-8/CAF and referred to as IL-8 in this paper) and K60, both of which are found on chromosome 4 (38).…”

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confidence: 99%

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Campylobacter jejuni-Induced Cytokine Responses in Avian Cells

et al. 2005

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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.

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“…Indeed, experimental infection of several types of human tissue culture cells has demonstrated the potential of Campylobacter to initiate a range of immune responses. For instance, intestinal INT407 and T84 cells respond to C. jejuni by producing cytokines interleukin-8 (IL-8) and/or tumor necrosis factor alpha (TNF-␣) (4,8,20,25,58,60), whereas infected THP-1 monocytes and dendritic cells secrete an even broader range of cytokines (23,26). Although some reports clearly show the requirement of the cytolethal distending toxin and/or bacterial invasion for cytokine responses (21,25), most of the observed responses seem independent of these traits.…”

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confidence: 99%

Activation of Human and Chicken Toll-Like Receptors by Campylobacter spp

et al. 2010

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Campylobacter infection in humans is accompanied by severe inflammation of the intestinal mucosa, in contrast to colonization of chicken. The basis for the differential host response is unknown. Toll-like receptors (TLRs) sense and respond to microbes in the body and participate in the induction of an inflammatory response. Thus far, the interaction of Campylobacter with chicken TLRs has not been studied. Here, we investigated the potential of four Campylobacter strains to activate human TLR1/2/6, TLR4, TLR5, and TLR9 and chicken TLR2t2/16, TLR4, TLR5, and TLR21. Live bacteria showed no or very limited potential to activate TLR2, TLR4, and TLR5 of both the human and chicken species, with minor but significant differences between Campylobacter strains. In contrast, lysed bacteria induced strong NF-B activation through human TLR1/2/6 and TLR4 and chicken TLR2t2/16 and TLR4 but not via TLR5 of either species. Interestingly, C. jejuni induced TLR4-mediated beta interferon in human but not chicken cells. Furthermore, isolated chromosomal Campylobacter DNA was unable to activate human TLR9 in our system, whereas chicken TLR21 was activated by DNA from all of the campylobacters tested. Our data are the first comparison of TLR-induced immune responses in humans and chickens. The results suggest that differences in bacterial cell wall integrity and in TLR responses to Campylobacter LOS and/or DNA may contribute to the distinct clinical manifestation between the species.

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Induction of α and β chemokines by intestinal epithelial cells stimulated with Campylobacter jejuni

Cited by 32 publications

References 35 publications

Campylobacter jejuni Drives MyD88-Independent Interleukin-6 Secretion via Toll-Like Receptor 2

Campylobacter jejuni Drives MyD88-Independent Interleukin-6 Secretion via Toll-Like Receptor 2

Campylobacter jejuni-Induced Cytokine Responses in Avian Cells

Activation of Human and Chicken Toll-Like Receptors by Campylobacter spp

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