Newborn piglet model for campylobacteriosis

Babakhani, Farah; Bradley, Gregory A.; Joens, Lynn A.

doi:10.1128/iai.61.8.3466-3475.1993

Cited by 91 publications

(46 citation statements)

References 29 publications

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“…Both in vivo and in vitro studies have demonstrated that C. jejuni both adheres to and invades the cells of the intestinal epithelium (Newell and Pearson, 1984;De Melo et al ., 1989;Konkel and Joens, 1989;Wassenaar et al ., 1991;Babakhani et al ., 1993;Oelschlaeger et al ., 1993). Mutants defective in their ability to be internalized into cultured epithelial cells have reduced virulence in animal models (Yao et al ., 1997) suggesting that bacterial internalization is important in campylobacter pathogenesis.…”

Section: Introductionmentioning

confidence: 99%

Signal transduction in Campylobacter jejuni-induced cytokine production

Watson¹,

Galán²

2005

Cellular Microbiology

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SummaryCampylobacter jejuni is the leading cause of foodborne illness in the USA and one of the most common causes of diarrhoea worldwide. Central to its pathogenicity is its ability to induce the production of proinflammatory cytokines such as interleukin (IL)-8 in intestinal epithelial cells. Here, we demonstrated that C. jejuni infection of intestinal epithelial cells results in the activation of the ERK and p38 mitogen-activated protein kinases and that the ERK kinase pathway is essential for IL-8 production. We found that MAP kinase stimulation leading to IL-8 secretion requires C. jejuni gene products whose production is stimulated upon contact with epithelial cells. We also found that C. jejuni flagellin is a very poor stimulator of Toll-like receptor (TLR)-5 and therefore does not play a significant role in the stimulation of cytokine production.

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Section: Introductionmentioning

confidence: 99%

Signal transduction in Campylobacter jejuni-induced cytokine production

Watson¹,

Galán²

2005

Cellular Microbiology

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“…Indeed, intracellular organisms have been observed by electron microscopic examination of C. jejuni-infected individuals with colitis (Van Spreeuwel et al, 1985). Intracellular bacteria have also been observed in infected infant macaque monkeys (Russell et al, 1993) and newborn piglets (Babakhani et al, 1993). Both animal models closely mimic human C. jejuni infections with the development of self-limiting diarrhoeal disease with acute colitis.…”

Section: Introductionmentioning

confidence: 99%

Bacterial secreted proteins are required for the internalization of Campylobacter jejuni into cultured mammalian cells

Konkel

Kim

Rivera‐Amill

et al. 1999

Molecular Microbiology

258

225

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Presented here is the first evidence that Campylobacter jejuni secrete proteins upon co‐cultivation with host cells and in INT 407 cell‐conditioned medium. A C. jejuni gene designated ciaB for Campylobacter invasion antigen B was identified, using a differential screening technique, which is required for this secretion process and the efficient entry of this bacterium into a host cell. The C. jejuni ciaB gene encodes a protein of 610 amino acids with a calculated molecular mass of 73 154 Da. The deduced amino acid sequence of the CiaB protein shares similarity with type III secreted proteins associated with the invasion of host cells from other more extensively characterized bacterial pathogens. In vitro binding and internalization assays revealed that the binding of C. jejuni ciaB null mutants was indistinguishable from that of the parental isolate, whereas a significant reduction was noted in internalization. Confocal microscopic examination of C. jejuni‐infected cells revealed that CiaB was translocated into the cytoplasm of the host cells. Culturing C. jejuni with INT 407 cells or in INT 407‐conditioned medium resulted in the secretion of at least eight proteins, ranging in size from 12.8 to 108 kDa, into the culture medium. C. jejuni ciaB null mutants were deficient in the secretion of all eight proteins, indicating that CiaB is required for the secretion process. The identification of the C. jejuni ciaB gene represents a significant advance in understanding the molecular mechanism of C. jejuni internalization and the pathogenesis of C. jejuni‐mediated enteritis.

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“…Several animal models, such as Galleria mellonella larvae [102], colostrum-deprived piglets [103], gnotobiotic piglet [104], naïve swines [105], and ferrets [106] were successfully used for the study of numerous aspects of C. jejuni pathogenesis. However, each animal model showed strong limitations in terms of employing or comparing with human conditions upon C. jejuni infection [54].…”

Section: Generation Of Secondary Abiotic Mice To Overcome Colonizatiomentioning

confidence: 99%

Novel Clinical Campylobacter jejuni Infection Models Based on Sensitization of Mice to Lipooligosaccharide, a Major Bacterial Factor Triggering Innate Immune Responses in Human Campylobacteriosis

2020

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: Human Campylobacter jejuni infections inducing campylobacteriosis including post-infectious sequelae such as Guillain-Barré syndrome and reactive arthritis are rising worldwide and progress into a global burden of high socioeconomic impact. Intestinal immunopathology underlying campylobacteriosis is a classical response of the innate immune system characterized by the accumulation of neutrophils and macrophages which cause tissue destruction, barrier defects and malabsorption leading to bloody diarrhea. Clinical studies revealed that enteritis and post-infectious morbidities of human C. jejuni infections are strongly dependent on the structure of pathogenic lipooligosaccharides (LOS) triggering the innate immune system via Toll-like-receptor (TLR)-4 signaling. Compared to humans, mice display an approximately 10,000 times weaker TLR-4 response and a pronounced colonization resistance (CR) against C. jejuni maintained by the murine gut microbiota. In consequence, investigations of campylobacteriosis have been hampered by the lack of experimental animal models. We here summarize recent progress made in the development of murine C. jejuni infection models that are based on the abolishment of CR by modulating the murine gut microbiota and by sensitization of mice to LOS. These advances support the major role of LOS driven innate immunity in pathogenesis of campylobacteriosis including post-infectious autoimmune diseases and promote the preclinical evaluation of novel pharmaceutical strategies for prophylaxis and treatment.

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Newborn piglet model for campylobacteriosis

Cited by 91 publications

References 29 publications

Signal transduction in Campylobacter jejuni-induced cytokine production

Signal transduction in Campylobacter jejuni-induced cytokine production

Bacterial secreted proteins are required for the internalization of Campylobacter jejuni into cultured mammalian cells

Novel Clinical Campylobacter jejuni Infection Models Based on Sensitization of Mice to Lipooligosaccharide, a Major Bacterial Factor Triggering Innate Immune Responses in Human Campylobacteriosis

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