Campylobacter jejuni colonization promotes the translocation of Escherichia coli to extra-intestinal organs and disturbs the short-chain fatty acids profiles in the chicken gut.

For a long time Campylobacter was only considered as a commensal microorganism in avian hosts restricted to the ceca, without any pathogenic features. The precise reasons for the symptomless chicken carriers are still unknown, but investigations of the gastrointestinal ecology of broiler chickens may improve our understanding of the microbial interactions with the host. Therefore, the current studies were conducted to investigate the effects of Campylobacter jejuni colonization on Escherichia coli translocation and on the metabolic end products (short-chain fatty acids, SCFAs). Following oral infection of 14 day old broiler chickens with 1 × 10(8) CFU of Campylobacter jejuni NCTC 12744 in two independent animal trials, it was found that C. jejuni heavily colonized the intestine and disseminate to extra-intestinal organs. Moreover, in both animal trials, the findings revealed that C. jejuni promoted the translocation of E. coli with a higher number encountered in the spleen and liver at 14 days post infection (dpi). In addition, Campylobacter affected the microbial fermentation in the gastrointestinal tract of broilers by reducing the amount of propionate, isovalerate, and isobutyrate in the cecal digesta of the infected birds at 2 dpi and, at 7 and 14 dpi, butyrate, isobutyrate, and isovalerate were also decreased. However, in the jejunum, the C. jejuni infection lowered only butyrate concentrations at 14 dpi. These data indicated that C. jejuni may utilize SCFAs as carbon sources to promote its colonization in the chicken gut, suggesting that Campylobacter cannot only alter gut colonization dynamics but might also influence physiological processes due to altered microbial metabolite profiles.Finally, the results demonstrated that C. jejuni can cross the intestinal epithelial barrier and facilitates the translocation of Campylobacter itself as well as of other enteric microorganisms such as E. coli to extra-intestinal organs of infected birds. Altogether, our findings suggest that the Campylobacter carrier state in chicken is characterised by multiple changes in the intestinal barrier function, which supports multiplication and survival within the host.

Intestinal epithelial responses to Salmonella enterica serovar Enteritidis: effects on intestinal permeability and ion transport.

Salmonella infection of chickens that leads to potential human foodborne salmonellosis continues to be a major concern. Chickens serve as carriers but, in contrast to humans, rarely show any clinical signs including diarrhea. The present investigations aimed to elucidate whether the absence of diarrhea during acute Salmonella enterica serovar Enteritidis (Salmonella Enteritidis) infection may be linked to specific changes in the electrophysiological properties of the chicken gut. Immediately after slaughter, intestinal pieces of the mid-jejunum and cecum of either commercial broiler or specific pathogen-free (SPF) chickens were mounted in Ussing chambers in 2 separate experimental series. Living Salmonella Enteritidis (3 × 10(9)) or Salmonella Enteritidis endotoxin (20 mg/L), or both, were added to the mucosal side for 1 h. In both experimental series, the Salmonella infection decreased the trans-epithelial ion conductance G(t) (P < 0.05). In the jejunum of SPF chickens, there was also a marked decrease in net charge transfer across the epithelium, evidenced by decreased short-circuit current (I(sc), P < 0.05). Interestingly, the mucosal application of Salmonella endotoxin to the epithelial preparations from jejunum and cecum of SPF chicken had an effect similar to living bacteria. However, the endotoxin had no additional effect on the intestinal function in the presence of bacteria. The decreasing effect of Salmonella and or its endotoxin on G(t) could be partly reversed by serosal addition of histamine. To our knowledge, this is the first study to address the functional response of native intestinal epithelium of chicken to an in vitro Salmonella infection. For the first time, it can be reported that intestinal ion permeability of chicken decreases acutely by the presence of Salmonella. This type of response could counteract ion and fluid secretion and may thus, at least in part, explain why chickens do not develop overt diarrhea after Salmonella infection.