Comparative translocation of enteropathogenic Campylobacter spp. and Escherichia coli from the intestinal tract of gnotobiotic mice

Youssef, Mohammad; Corthier, Gérard; Goossens, Herman; Tancrède, C; Henry-Amar, Michel; Andremont, Antoine

doi:10.1128/iai.55.4.1019-1021.1987

Cited by 20 publications

(4 citation statements)

References 22 publications

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“…It is also difficult to assess how extensively these in vitro observations can be applied to the situation in vivo, i.e., in the intestinal epithelium. In particular, we have no findings which help elucidate the mechanism of portal entry of C. jejuni through the intestinal epithelium to the lymph nodes (10,19). Thus, the picture of cellular events which occur during C. jejiuni invasion of HEp-2 cells is far from complete.…”

Section: -mentioning

confidence: 90%

“…The mechanism by which the bacterium produces the disease is not fully understood, but clinical evidence exists for intestinal epithelial invasion in cases of Campylobacter enteritis, with bloody diarrhea and inflammatory cells in the stools. The ability to penetrate into the enterocytes has been confirmed in experimental models in which C. jejuni was orally administered to infant chickens (6), mice (19), and hamsters (10). In addition, invasion potential has been shown in mammalian cell lines (5,13), and this property has been associated with pathogenicity in humans (5).…”

mentioning

confidence: 97%

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Cellular events and intracellular survival of Campylobacter jejuni during infection of HEp-2 cells

Melo¹,

Gabbiani²,

Péchère³

1989

Infect Immun

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Invasion and intracellular survival of Campylobacter jejuni in HEp-2 cells were analyzed by transmission electron microscopy and by viable counts after killing of extracellular bacteria by gentamicin. During the first 30 min after challenge, no bacteria were seen in association with the host cell. After 1 h, campylobacters apparently attached to the cell membrane, with areas of close appositions. In these areas, an intracellular network of actin-like filaments was seen beneath the plasma membrane. Other bacteria were included into endocytic vacuoles. After 3 h, an intense lysosomal response was observed in the host cells, as determined by the presence of myelinic forms and acid phosphatase activity. After 9 h, bacteria still contained in vacuoles showed signs of degradation with a change from spiral to coccal forms. Morphological evidence of phagosome-lysosome fusion was also seen, and these observations by transmission electron microscopy correlated well with a decrease in bacteria viability 9 h after challenge, as determined from separate kinetics studies. Inhibitors of phagocytosis were observed to reduce markedly the entry of C. jejuni into the cells at concentrations which apparently did not affect bacterial viability. These results suggest that the campylobacters were successively attached to the HEp-2 cell membrane, internalized by a phagocytic-like mechanism, and digested after phagosome-lysosome fusion.

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Section: -mentioning

confidence: 90%

mentioning

confidence: 97%

Cellular events and intracellular survival of Campylobacter jejuni during infection of HEp-2 cells

Melo¹,

Gabbiani²,

Péchère³

1989

Infect Immun

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“…The use of germfree animals or mice with a limited gut flora has alleviated these shortcomings with varying degrees of success [10,11]. It was demonstrated earlier that C. jejuni colonized the entire gastrointestinal (GI) tract of isolator-raised germfree mice and induced clinical signs of disease including granulocyte infiltrates, bloody diarrhea, and humoral immune responses, reproducibly occurring after infection [12][13][14][15][16]. However, germfree mice have an abnormal development of gut-associated lymphoid tissue [17,18].…”

Section: Introductionmentioning

confidence: 99%

Correction: Novel Murine Infection Models Provide Deep Insights into the “Ménage à Trois” of Campylobacter jejuni, Microbiota and Host Innate Immunity

Bereswill¹,

Fischer²,

Plickert³

et al. 2011

PLoS ONE

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Background: Although Campylobacter jejuni-infections have a high prevalence worldwide and represent a significant socioeconomic burden, it is still not well understood how C. jejuni causes intestinal inflammation. Detailed investigation of C. jejuni-mediated intestinal immunopathology is hampered by the lack of appropriate vertebrate models. In particular, mice display colonization resistance against this pathogen. Methodology/Principal Findings:To overcome these limitations we developed a novel C. jejuni-infection model using gnotobiotic mice in which the intestinal flora was eradicated by antibiotic treatment. These animals could then be permanently associated with a complete human (hfa) or murine (mfa) microbiota. After peroral infection C. jejuni colonized the gastrointestinal tract of gnotobiotic and hfa mice for six weeks, whereas mfa mice cleared the pathogen within two days. Strikingly, stable C. jejuni colonization was accompanied by a pro-inflammatory immune response indicated by increased numbers of T-and B-lymphocytes, regulatory T-cells, neutrophils and apoptotic cells, as well as increased concentrations of TNF-a, IL-6, and MCP-1 in the colon mucosa of hfa mice. Analysis of MyD88 2/2 , TRIF 2/2 , TLR4 2/2 , and TLR9 2/2 mice revealed that TLR4-and TLR9-signaling was essential for immunopathology following C. jejuni-infection. Interestingly, C. jejuni-mutant strains deficient in formic acid metabolism and perception induced less intestinal immunopathology compared to the parental strain infection. In summary, the murine gut flora is essential for colonization resistance against C. jejuni and can be overcome by reconstitution of gnotobiotic mice with human flora. Detection of C. jejuni-LPS and -CpG-DNA by host TLR4 and TLR9, respectively, plays a key role in immunopathology. Finally, the host immune response is tightly coupled to bacterial formic acid metabolism and invasion fitness. Conclusion/Significance:We conclude that gnotobiotic and ''humanized'' mice represent excellent novel C. jejuni-infection and -inflammation models and provide deep insights into the immunological and molecular interplays between C. jejuni, microbiota and innate immunity in human campylobacteriosis.

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“…The pathogenesis of a Campylobacter jejuni infection, currently one of the leading causes of food-borne bacterial gastroenteritis, is associated with bacterial invasion in and translocation over the intestinal epithelium ( 6 , 7 ) and disruption of tight junctions ( 8 ) . The mechanisms behind C. jejuni translocation are paradoxical: both transcellular and paracellular routes have been observed ( 9 , 10 ) .…”

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confidence: 99%

Butyrate protects Caco-2 cells from Campylobacter jejuni invasion and translocation

et al. 2008

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Invasion in and translocation across enterocytes are major events during Campylobacter jejuni-induced enteritis in humans. C. jejuni in vitro infection of cell monolayers typically results in loss of tight junction integrity, which could contribute to translocation. In the present study, we wanted to investigate whether butyrate is able to confer protection to Caco-2 cells against C. jejuni invasion, thus reducing paracellular permeability and limiting C. jejuni translocation. Protection of Caco-2 cells against C. jejuni invasion was assessed using a gentamicin protection assay. Transwell systems were used to investigate the impact of butyrate on translocation of C. jejuni across a Caco-2 monolayer and its effect on transepithelial resistance during infection. Butyrate protected Caco-2 cells against C. jejuni invasion in a concentration-dependent manner. Differentiated Caco-2 cells were less susceptible to C. jejuni invasion than 3-d-old undifferentiated cells and higher concentrations of butyrate and longer incubation times were needed to become refractive for invasion. C. jejuni translocation over Caco-2 monolayers was reduced when monolayers were treated with butyrate and this was accompanied by an enhanced drop in transepithelial resistance. The present study showed that butyrate is able to protect Caco-2 cells from two major virulence mechanisms of C. jejuni, namely invasion and translocation, but not from a decline in transepithelial resistance.

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Comparative translocation of enteropathogenic Campylobacter spp. and Escherichia coli from the intestinal tract of gnotobiotic mice

Cited by 20 publications

References 22 publications

Cellular events and intracellular survival of Campylobacter jejuni during infection of HEp-2 cells

Cellular events and intracellular survival of Campylobacter jejuni during infection of HEp-2 cells

Correction: Novel Murine Infection Models Provide Deep Insights into the “Ménage à Trois” of Campylobacter jejuni, Microbiota and Host Innate Immunity

Butyrate protects Caco-2 cells from Campylobacter jejuni invasion and translocation

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