TY - JOUR
T1 - The long polar fimbriae of STEC O157
T2 - H7 induce expression of pro-inflammatory markers by intestinal epithelial cells
AU - Farfan, Mauricio J.
AU - Cantero, Lidia
AU - Vergara, Alejandra
AU - Vidal, Roberto
AU - Torres, Alfredo G.
N1 - Funding Information:
This work was supported by grant FONDECYT 11080180 and 1120809 to M.J.F, FONDECYT 1110260 to R.V., and NIH/NIAID 5R01AI079154 to A.G.T. The contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIAID or NIH.
PY - 2013/3/15
Y1 - 2013/3/15
N2 - Infection with Shiga toxin-producing Escherichia coli (STEC) O157:H7 is characterized by acute inflammation of the colonic mucosa. STEC O157:H7 contains two non-identical loci encoding long polar fimbriae (Lpf), which play a role in the STEC colonization of the intestinal epithelial cells. However, no information is available regarding the involvement of Lpf in the STEC-induced host inflammatory response. Hence, in this study we assess the role of Lpf as an inducer of inflammation on intestinal epithelial cells. Secretion of pro-inflammatory cytokines in response to STEC wild type and lpf isogenic mutants was evaluated on intestinal T84 cells. Of the 27 cytokines assayed, IL-6, IL-8, IL-15, FGF, GM-CSF and IP-10 were significantly reduced, when compared to the wild-type strain, in the lpfA1 lpfA2 double mutant. Further, the host intracellular signaling pathways activated in response to Lpf were determined by using an array containing genes representative of 18 different signal transduction pathways. The analysis indicated that the NF-κB pathway is activated in response to Lpf-expressing STEC. Therefore, our study supports the role of Lpf as a STEC factor mediating intestinal inflammation.
AB - Infection with Shiga toxin-producing Escherichia coli (STEC) O157:H7 is characterized by acute inflammation of the colonic mucosa. STEC O157:H7 contains two non-identical loci encoding long polar fimbriae (Lpf), which play a role in the STEC colonization of the intestinal epithelial cells. However, no information is available regarding the involvement of Lpf in the STEC-induced host inflammatory response. Hence, in this study we assess the role of Lpf as an inducer of inflammation on intestinal epithelial cells. Secretion of pro-inflammatory cytokines in response to STEC wild type and lpf isogenic mutants was evaluated on intestinal T84 cells. Of the 27 cytokines assayed, IL-6, IL-8, IL-15, FGF, GM-CSF and IP-10 were significantly reduced, when compared to the wild-type strain, in the lpfA1 lpfA2 double mutant. Further, the host intracellular signaling pathways activated in response to Lpf were determined by using an array containing genes representative of 18 different signal transduction pathways. The analysis indicated that the NF-κB pathway is activated in response to Lpf-expressing STEC. Therefore, our study supports the role of Lpf as a STEC factor mediating intestinal inflammation.
KW - Enterohemorrhagic E. coli
KW - Inflammation
KW - Interleukin-8
KW - Long polar fimbriae
KW - Shiga toxin E. coli
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U2 - 10.1016/j.vetimm.2012.09.017
DO - 10.1016/j.vetimm.2012.09.017
M3 - Article
C2 - 23078900
AN - SCOPUS:84875509647
SN - 0165-2427
VL - 152
SP - 126
EP - 131
JO - Veterinary Immunology and Immunopathology
JF - Veterinary Immunology and Immunopathology
IS - 1-2
ER -