{"id":101,"date":"2021-08-30T13:47:28","date_gmt":"2021-08-30T20:47:28","guid":{"rendered":"https:\/\/labs.wsu.edu\/bacteria-host-cell-interactions\/?page_id=101"},"modified":"2025-11-03T09:27:08","modified_gmt":"2025-11-03T17:27:08","slug":"paper-highlights","status":"publish","type":"page","link":"https:\/\/labs.wsu.edu\/bacteria-host-cell-interactions\/paper-highlights\/","title":{"rendered":"Paper Highlights"},"content":{"rendered":"\n

Paper Highlights<\/h1>\n\n\n
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“An in vivo ligated loop model reveals new insight into the host immune response against Campylobacter jejuni”<\/h2>\n\n\n\n

Negretti NM, Ye Y, Malavasi LM, Pokharel SM, Huynh S, Noh S, Klima CL, Gourley CR, Ragle CA, Bose S, Looft T, Parker CT, Clair G, Adkins JN, Konkel ME.<\/p>\n\n\n\n

Gut Microbes. 2020 Nov 9;12(1):1-25. doi: 10.1080\/19490976.2020.1814121.<\/p>\n\n\n\n

A porcine ligated loop model reveals new insight into the host immune response against\u00a0Campylobacter jejuni<\/em><\/a>; PMID: 32887530 (https:\/\/pubmed.ncbi.nlm.nih.gov\/32887530\/)<\/p>\n\n\n\n

\"See
Figure. C. jejuni-mediated intestinal inflammation is driven by epithelial cell invasion. Panels: A: C. jejuni migrate across the intestinal epithelial cell barrier by transiently disputing tight junctions. C. jejuni then invade the epithelial cells and trigger the release of the pro-inflammatory [interleukin 8 (IL-8)] from epithelial cells. Resident monocytes (macrophages) also produce IL-8. B: Elevated levels of IL-8 result in the recruitment of activated neutrophils into the lumen of the intestine. Extracellular C. jejuni are killed by antimicrobial neutrophil-derived proteins (lipocalin-2, myeloperoxidase, S100A8, and S100A9) and reactive oxygen species (ROS). Intestinal barrier disruption permits more C. jejuni to access to the basolateral surface of the intestinal cells where invasion occurs. C: Luminal TNF-\uf061 increases and C. jejuni multiply within intestinal epithelial cells, resulting in cell necrosis. IL-17A, an immune cytokine indicative of compromised intestinal barrier integrity, is produced in response to the infection. Ultimately, these processes lead to the development of clinical symptoms. Cytokines are highlighted in orange boxes.<\/figcaption><\/figure>\n\n<\/div>\r\n\n<\/div>\n\n\n
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Keywords: <\/strong>Disease model; innate immunity; intestinal disease; pathogenesis; proteomics.<\/p>\n\n\n\n

This paper represents the collaborative efforts of the scientists at Washington State University within the School of Molecular Biosciences, Department of Veterinary Microbiology and Pathology, Washington Animal Disease Diagnostic Laboratory, and talented scientists at Pacific Northwest National Laboratory in Richland, WA, Produce Safety and Microbiology at the United States Department of Agriculture-Agricultural Research Service in Albany, CA, and at the National Animal Disease Center in Ames, Iowa.<\/p>\n\n\n\n

One of the hallmarks of C. jejuni<\/em> intestinal infection is a robust host inflammatory response. As such, researchers have been keen to determine whether damage to the intestinal epithelium is initiated from C. jejuni<\/em> invading and replicating within the intestinal epithelial cells or whether the host factors, such as neutrophil infiltration, drive the initial pathology. To summarize the key findings of this paper, we conclude that C. jejuni<\/em> invasion of intestinal epithelial cells triggers the release of the chemokine IL-8, prompting neutrophil recruitment and activation. The infiltration of neutrophils potentiates a leaky gut and inflammatory pathologies, including intestinal epithelial cell loss and blunted villi. In short, we have demonstrated that the recruitment of activated neutrophils, and not the replication of C. jejuni<\/em> within intestinal epithelial cells, drives the initial intestinal pathology.<\/p>\n\n\n\n

Our work critically advances the understanding of interactions occurring at the bacteria-host cell interface. This study provides new information that supports the hypothesis that C. jejuni<\/em> infection and the accompanying pathologies are initially driven by the innate immune system. The mechanistic insights provided by this study will impact future studies of pathogen virulence determinants that elicit neutrophil activation. This study addresses longstanding questions that are fundamental to understanding the basis of C. jejuni<\/em> disease. The use of pigs versus other animals brings significant value to this study, as pigs develop a spectrum of clinical pathologies that mimic human infections. Adding to the novelty of this study is the use of the ligated-intestinal loop model, which permits the application of high-throughput and qualitative LC-MS\/MS. Noteworthy is that the use of this model can be used to study the early immune events of infection with other intestinal pathogens.<\/p>\n\n<\/div>\r\n\n<\/div>","protected":false},"excerpt":{"rendered":"

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