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Development of an in vivo ligated loop model reveals new insight into the host immune response against Campylobacter jejuni

ABSTRACT: Development of an in vivo ligated loop model reveals new insight into the host immune response against Campylobacter jejuni

PROVIDER: PRJNA615847 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11433800_1.fastq.gz	Fastqsanger.gz
	SRR11433800_2.fastq.gz	Fastqsanger.gz
	SRR11433801_1.fastq.gz	Fastqsanger.gz
	SRR11433801_2.fastq.gz	Fastqsanger.gz
	SRR11433802_1.fastq.gz	Fastqsanger.gz

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Project description:The symptoms of infectious diarrheal disease are mediated by the interplay between the host and pathogen. Campylobacter jejuni is the leading bacterial cause of diarrhea worldwide due to its near-ubiquitous zoonotic association with poultry. One of the outstanding questions is what factors drive the intestinal inflammation during the development of C. jejuni-mediated disease. Specifically, it is not known the extent to which the bacteria are responsible for the diarrheal symptoms via cell necrosis, or whether there is immune cell recruitment prior to tissue damage. To determine the stepwise process of inflammation that leads to diarrhea, we used a piglet ligated intestinal loop model to study the intestinal environment in response to C. jejuni. Pigs were chosen due to the anatomical similarity of the porcine intestine to the human intestine, as the basis of disease modeling is to understand the process of human disease. Using immunoassays and proteomic approaches, we found that neutrophils are most likely the predominant cell type recruited to the intestines of C. jejuni infected animals. In the lumen of the intestine, a number of neutrophil related proteins increased during C. jejuni infection, including proteins related to neutrophil migration (elastase and MMP9), actin reorganization and bacterial uptake (Cdc42, WAVE-2, and Arp2/3), and antimicrobial proteins (lipocalin-2, myeloperoxidase, S100A8, and S100A9). The appearance of neutrophils also corresponds with increases of both IL-8 and TNF-a. Compared to infection with the C. jejuni wild-type strain, infection with the noninvasive C. jejuni ∆ciaD mutant resulted in a blunted inflammatory response, with less inflammatory cytokines and neutrophil markers. These findings indicate that intestinal inflammation is driven by C. jejuni virulence, and that resident intestinal cells precipitate the inflammatory response. Using this new disease model, we have developed a platform to study the early immune events during C. jejuni infection.

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Development of an in vivo ligated loop model reveals new insight into the host immune response against Campylobacter jejuni

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