TY - JOUR
T1 - Immuno-modulatory effect of probiotic E. coli Nissle 1917 in polarized human colonic cells against Campylobacter jejuni infection
AU - Helmy, Yosra A.
AU - Kassem, Issmat I.
AU - Rajashekara, Gireesh
N1 - Publisher Copyright:
© 2020 The Author(s). Published with license by Taylor & Francis Group, LLC.
PY - 2021
Y1 - 2021
N2 - Campylobacter jejuni 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 C. jejuni 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 C. jejuni including resistant bacteria from chickens to humans. Here, we evaluated the effect of E. coli Nissle 1917 (EcN) on innate responses of polarized HT-29 cells and consequently on C. jejuni 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 C. jejuni strains (2 h post-infection) (P < .05) and no intracellular C. jejuni (24 h post-infection) were recovered. To further understand how EcN mediates its impact on C. jejuni’s survival inside the cells, we used Human Antibacterial RT2 ProfilerTM PCR arrays to profile gene expression in HT-29 cells after treatment with EcN with or without C. jejuni 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 C. jejuni. 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.
AB - Campylobacter jejuni 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 C. jejuni 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 C. jejuni including resistant bacteria from chickens to humans. Here, we evaluated the effect of E. coli Nissle 1917 (EcN) on innate responses of polarized HT-29 cells and consequently on C. jejuni 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 C. jejuni strains (2 h post-infection) (P < .05) and no intracellular C. jejuni (24 h post-infection) were recovered. To further understand how EcN mediates its impact on C. jejuni’s survival inside the cells, we used Human Antibacterial RT2 ProfilerTM PCR arrays to profile gene expression in HT-29 cells after treatment with EcN with or without C. jejuni 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 C. jejuni. 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.
KW - Campylobacter
KW - E. coli Nissle 1917
KW - HT-29 cells
KW - innate immune response
KW - intracellular survival
KW - invasion
KW - Probiotic
UR - http://www.scopus.com/inward/record.url?scp=85098655630&partnerID=8YFLogxK
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U2 - 10.1080/19490976.2020.1857514
DO - 10.1080/19490976.2020.1857514
M3 - Article
C2 - 33382951
AN - SCOPUS:85098655630
SN - 1949-0976
VL - 13
SP - 1
EP - 16
JO - Gut Microbes
JF - Gut Microbes
IS - 1
ER -