Correlation Between In Vitro Secretion of Virulence-Associated Proteins of Campylobacter jejuni and Colonization of Chickens

Biswas, Debabrata; Fernando, Ursla; Reiman, Carla; Willson, Philip; Townsend, H. G. G.; Potter, Andrew; Allan, Brenda

doi:10.1007/s00284-006-0295-z

Cited by 31 publications

(26 citation statements)

References 31 publications

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“…Flagella‐mediated motility enhances intestinal colonization by C. jejuni (Wassenaar et al ., ; Biswas et al ., ) but is not essential (Wassenaar et al ., ; Biswas et al ., ) as confirmed by colonization of all chicks tested by our nonmotile kpsM :: kan. The flagellar apparatus also serves as a secretion system for C. jejuni invasion antigens (Cia), which facilitate colonization and persistence (Konkel et al ., 1999; 2004).…”

Section: Discussionmentioning

confidence: 99%

Role of capsular modified heptose in the virulence of Campylobacter jejuni

Wong

Lange

Houle³

et al. 2015

Molecular Microbiology

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SummaryThe Campylobacter jejuni capsular polysaccharide is important for virulence and often contains a modified heptose. In strain ATCC 700819 (a.k.a. NCTC 11168), the modified heptose branches off from the capsular backbone and is directly exposed to the environment. We reported previously that the enzymes encoded by wcaG, mlghB and mlghC are involved in heptose modification. Here, we show that inactivation of any of these genes leads to production of capsule lacking modified heptose and alters the transcription of other capsule modification genes differentially. Inactivation of mlghB or mlghC, but not of wcaG, decreased susceptibility to bile salts and abrogated invasion of intestinal cells. All mutants showed increased sensitivity to serum killing, especially wcaG::cat, and had defects in colonization and persistence in chicken intestine, but did not show significant differences in adhesion, phagocytosis and intracellular survival in murine macrophages. Together, our findings suggest that the capsular heptose modification pathway contributes to bacterial resistance against gastrointestinal host defenses and supports bacterial persistence via its role in serum resistance and invasion of intestinal cells. Our data further suggest a dynamic regulation of expression of this pathway in the gastrointestinal tract.

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Section: Discussionmentioning

confidence: 99%

Role of capsular modified heptose in the virulence of Campylobacter jejuni

Wong

Lange

Houle³

et al. 2015

Molecular Microbiology

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“…The flagellar apparatus functions as a type III secretion apparatus for the Campylobacter invasion antigens (Cia proteins) [53], important for in vitro cell invasion [54] and chick colonization [55], and secretion is enhanced upon exposure to chicken mucus [56]. A correlation has been demonstrated between chicken colonization potential and in vitro secretion of Cia proteins [56].…”

Section: C Jejuni Colonization Factors In the Chicken Gutmentioning

confidence: 99%

“…A correlation has been demonstrated between chicken colonization potential and in vitro secretion of Cia proteins [56]. RpoN mutants are completely aflagellated and as such do not secrete Cia proteins, nor do flgK mutants [48], making it clear that the molecular basis behind the colonization mechanism in chickens is complex.…”

Section: C Jejuni Colonization Factors In the Chicken Gutmentioning

confidence: 99%

Colonization factors of Campylobacter jejuni in the chicken gut

Hermans

Deun

Martel

et al. 2011

Vet Res

208

186

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Campylobacter contaminated broiler chicken meat is an important source of foodborne gastroenteritis and poses a serious health burden in industrialized countries. Broiler chickens are commonly regarded as a natural host for this zoonotic pathogen and infected birds carry a very high C. jejuni load in their gastrointestinal tract, especially the ceca. This eventually results in contaminated carcasses during processing. Current intervention methods fail to reduce the colonization of broiler chicks by C. jejuni due to an incomplete understanding on the interaction between C. jejuni and its avian host. Clearly, C. jejuni developed several survival and colonization mechanisms which are responsible for its highly adapted nature to the chicken host. But how these mechanisms interact with one another, leading to persistent, high-level cecal colonization remains largely obscure. A plethora of mutagenesis studies in the past few years resulted in the identification of several of the genes and proteins of C. jejuni involved in different aspects of the cellular response of this bacterium in the chicken gut. In this review, a thorough, up-to-date overview will be given of the survival mechanisms and colonization factors of C. jejuni identified to date. These factors may contribute to our understanding on how C. jejuni survival and colonization in chicks is mediated, as well as provide potential targets for effective subunit vaccine development.

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“…Mucous is known to elicit a specific transcriptional response in C. jejuni, which results in the transcription of virulence-associated cia genes (Biswas et al, 2007). Nothing is known of the capacity of chicken mucous to promote C. jejuni survival and resistance to stress by altering its transcriptome, and it was therefore interesting to notice that mucous had a limited protective effect Figure 1.…”

Section: Discussionmentioning

confidence: 99%

Short-chain fatty acids andl-lactate as feed additives to controlCampylobacter jejuniinfections in broilers

et al. 2008

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The usefulness of butyrate, acetate, propionate and l-lactate for the control of Campylobacter jejuni infections in broilers was assessed. For this purpose, the effect of these acids on the growth of C. jejuni in broth and intestinal mucous was determined, as well as their influence on the invasiveness of C. jejuni in intestinal epithelial cells. From these in vitro obtained results, one acid was retained for use as a feed additive in an in vivo trial. Butyrate was the most successful of the short-chain fatty acids, with 12.5 mM being bactericidal for C. jejuni at pH 6.0. Propionate and acetate had a bacteriostatic effect at 50 mM. None of the short-chain fatty acids had a bactericidal effect at pH 7.5 at a maximum concentration of 50 mM. Mucous increased the minimum bactericidal concentration of butyrate, but not the bacteriostatic concentrations of propionate or acetate. When C. jejuni was incubated in growth subinhibitory concentrations of butyrate, acetate or propionate or 25 mM L-lactate, no alteration in the invasive capabilities of C. jejuni in Caco-2 cells was observed. The addition of butyrate-coated micro-beads to the feed was unsuccessful to reduce C. jejuni caecal colonization in a seeder model using 2-week-old broilers. In conclusion, despite the marked bactericidal effect of butyrate towards C. jejuni in vitro, butyrate-coated micro-beads do not protect broilers from caecal colonization with C. jejuni in the applied test conditions. This might be partially ascribed to the protective effect of mucous and the rapid absorption of butyrate by the enterocytes.

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Correlation Between In Vitro Secretion of Virulence-Associated Proteins of Campylobacter jejuni and Colonization of Chickens

Cited by 31 publications

References 31 publications

Role of capsular modified heptose in the virulence of Campylobacter jejuni

Role of capsular modified heptose in the virulence of Campylobacter jejuni

Colonization factors of Campylobacter jejuni in the chicken gut

Short-chain fatty acids andl-lactate as feed additives to controlCampylobacter jejuniinfections in broilers

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