Immuno-modulatory effect of probiotic E. coli Nissle 1917 in polarized human colonic cells against Campylobacter jejuni infection

is among the leading causes of bacterial foodborne illness. Poultry is the major reservoir and source of human campylobacteriosis. Currently, there is no effective and practical method to decrease colonization in chickens or to reduce human infections. Additionally, antibiotic-resistant infections p...

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Bibliographic Details
Published inGut microbes Vol. 13; no. 1; p. 1
Main Authors Helmy, Yosra A, Kassem, Issmat I, Rajashekara, Gireesh
Format Journal Article
LanguageEnglish
Published United States Taylor & Francis 01.01.2021
Taylor & Francis Group
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Summary:is among the leading causes of bacterial foodborne illness. Poultry is the major reservoir and source of human campylobacteriosis. Currently, there is no effective and practical method to decrease colonization in chickens or to reduce human infections. Additionally, antibiotic-resistant infections pose a serious public health concern; therefore, antibiotic-alternative approaches are needed to reduce transmission of including resistant bacteria from chickens to humans. Here, we evaluated the effect of Nissle 1917 (EcN) on innate responses of polarized HT-29 cells and consequently on 81176 infections in HT-29 cells. Pre-treatment of HT-29 cells with EcN for 4 h had a significant effect on the invasion of different strains (2 h post-infection) ( < .05) and no intracellular (24 h post-infection) were recovered. To further understand how EcN mediates its impact on survival inside the cells, we used Human Antibacterial RT Profiler PCR arrays to profile gene expression in HT-29 cells after treatment with EcN with or without 81-176 infection. Our results suggest that pre-treatment of the HT-29 cells with EcN induced the anti-inflammatory cytokines and activated the anti-apoptotic Akt signaling which likely to protect the cells against the proinflammatory and apoptosis responses induced by . EcN also positively affected the expression of genes involved in cellular maintenance, growth, development, and proliferation. Further, EcN modulated the expression of genes involved in protective innate immunity, such as TLRs, ERK1/2, p38 MAPK, Ap1, JNK, IL1B, IL17A, and NF-κB signaling.
ISSN:1949-0976
1949-0984
DOI:10.1080/19490976.2020.1857514