Enteric permeability and inflammation associated with day of hatch Enterobacteriaceae inoculation

Abstract

Early exposure to Enterobacteriaceae may result in inappropriate microbial colonization of the gastrointestinal ( GI ) tract, induce mild GI inflammation, alter immune system development, and predispose poultry to opportunistic infection. Four experiments were conducted to test Enterobacteriaceae isolates Escherichia coli LG strain ( LG ), E. coli Huff strain (Huff), Salmonella Enteritidis LB ( SE ) and Salmonella Typhimurium ( ST ) on ability to induce GI inflammation. All 4 experiments included a noninoculated control, and day of hatch ( DOH ) oral inoculation of LG, Huff, SE and ST in experiment 1, LG and SE in experiment 2, and LG, Huff, SE, and ST in experiment 3. Experiment 4 included LG, Huff, a noninoculated control ( NIC ), and Clostridium perfringens only ( NCP ) wherein birds received oral C. perfringens challenge on d15-16 to induce necrotic enteritis. Body weight was measured, yolk sacs and spleens were collected, and blood was obtained for serum fluorescein isothiocyanate dextran ( FITC-d ) recovery and alpha-1-acid glycoprotein ( A1GP ) concentrations. Samples were taken weekly through 2 wk of age in experiments 1 and 2, or 4 wk of age in experiments 3 and 4. Increased FITC-d recovery was observed for LG and SE on d13 in experiment 2 ( P < 0.05), and C. perfringens only birds on d27 in experiment 4 ( P < 0.05) as compared to noninoculated controls. Each experiment resulted in notable differences in A1GP serum concentrations over time, with fluctuations in A1GP patterns through d14 based on DOH inoculation ( P < 0.05). Over time, A1GP was increased for DOH inoculated birds from d 22 to 29, the fourth wk of life, and d 2-29, the entire experiment, vs. noninoculated controls in experiment 3 ( P < 0.05). Similarly, NCP and LGCP showed increased A1GP from d 20 to 27 and d 6 to 27, vs. NIC in experiment 4 ( P < 0.05). In experiment 4, C. perfringens challenge resulted in earlier A1GP response in DOH inoculated birds, d 17-20, as compared to NCP birds, d 20-27 ( P < 0.05). These results suggest early Enterobacteriaceae exposure may influence early inflammatory state in the GI tract and may also alter patterns of inflammation and responsiveness to pathogens.

Beneficial effect of ζ-carotene-like compounds on acute UVB irradiation by alleviating inflammation and regulating intestinal flora

“…Enterobacteriaceae may lead to inappropriate colonization of gastrointestinal microorganisms, induce gastrointestinal inflammation, alter immune system development, and make the body vulnerable to opportunistic infections. 54 In contrast, intestinal inflammation destroyed the composition of the microbiota, leading to the expansion of Enterobacteriaceae members. 55 Escherichia – Shigella is a member of Enterobacteriaceae and is proportional to the degree of skin itching and positively correlated with most pro-inflammatory factors in mice, 56 but negatively correlated with the integrity of the colonic barrier.…”

Gastrointestinal response to the early administration of antimicrobial agents in growing turkeys infected with Escherichia coli

“…In addition to the subclinical dose of APEC, another important consideration is that the birds were not challenged on the first day of their lives, but later, on d 15 or d 50. According to the literature, the youngest birds infected with APEC respond with reduced productivity, although a compensatory growth effect is often observed in later rearing stages ( Chasser et al, 2021 ; Christensen et al, 2021 ). However, despite the fact that APEC infection had no influence on the growth performance of turkeys, its effects were noted in the air sac, and in the enzyme and metabolic activity of cecal microbiota.…”

Taxonomic and Metagenomic Analyses Define the Development of the Microbiota in the Chick

“…In agreement with previous reports ( 21 – 23 ), we found that during the first several days posthatch, the diversity of cecal microbiota is very low and composed primarily of Proteobacteria . Exposure of the chicken gut to Enterobacteriaceae at the day of hatch can induce mild, nearly undetectable inflammation leading to immune tolerance of related bacteria, including Salmonella ( 24 – 26 ). Accordingly, the ceca of chickens infected with STm are only mildly inflamed despite a high bacterial burden.…”