Abstract

Previous studies have shown a tissue immune phenotype-altering event occurring on days 2 and 4 in the ceca post-Salmonella challenge. To evaluate the involvement of the cecal microbiota in the phenotype reprogramming, we hypothesized that the addition of subtherapeutic bacitracin (BMD) will affect the cecal microbiota. Therefore, the objective of this study was to determine if the antibiotic-mediated changes in the microbiota composition influenced the immune phenotype induced by Salmonella enteritidis infection of the chicken cecum. A total of 112 fertile eggs were obtained for each experiment, repeated for a total of three separate times. The ceca and cecal contents were collected on days 2 and 4 post-infection for mRNA expression TaqMan assay and 16S rRNA gene microbiota sequencing. The results demonstrate the effects of bacitracin on cecal composition and its interaction with Salmonella enteritidis in young chicks. There is a preliminary indication of phenotype change in the Salmonella-challenged group provided subtherapeutic BMD due to the shifting cecal microbiota and cecal immune response, indicating the addition of bacitracin during infection altered the cecal phenotype. These data demonstrate the potential involvement of the microbiota in reprogramming immune phenotype (disease resistance to disease tolerance) induced by Salmonella in the chicken cecum.

Highlights

  • Foodborne illnesses cause health and economic burden in the United States annually, affecting 48 million people every year

  • There was a significant upregulation of pro-inflammatory cytokines, IL-1β and IL-6, in challenged birds fed with normal starter formula (T2), at day 2 post-infection (Figure 1A,B). This upregulation was much less marked in challenged birds fed with the subtherapeutic addition of bacitracin methylene disalicylate (BMD) (T4 vs. T2)

  • On day 2, both IL-10 and TNF-α were expressed in response to Salmonella challenge (T2 and T4), regardless of BMD addition in the feed (Figure 1C,D)

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Summary

Introduction

Foodborne illnesses cause health and economic burden in the United States annually, affecting 48 million people every year. One of the major causes of human gastroenteritis is Salmonella enterica Enteritidis Improved control measures have been implemented, S. enterica still continues to present an issue every year in US livestock [2]. The mechanism of how AGPs improve animal performance is still unclear, Diaz Carrasco et al [4] speculate it is through intestinal microbiota modulation, in the ceca for the chicken, whether it is dietary related or pathogen related. Studies need to focus on identifying the mechanism of how broad-spectrum antibiotics work in the host gut towards improving the overall health of food production animals

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