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Translational research into the effects of cigarette smoke on inflammatory mediators and epithelial TRPV1 in Crohn’s disease

Liesbeth Allais, Stephanie Verschuere, Tania Maes (UGent) , Rebecca De Smet (UGent) , Sarah Devriese, Bryan Gonzales (UGent) , Harald Peeters, Koen Van Crombruggen, Claus Bachert (UGent) , Martine De Vos (UGent) , et al.
(2020) PLOS ONE. 15(8).
Author
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Abstract
Crohn's disease is a pathological condition of the gastro-intestinal tract, causing severe transmural inflammation in the ileum and/or colon. Cigarette smoking is one of the best known environmental risk factors for the development of Crohn's disease. Nevertheless, very little is known about the effect of prolonged cigarette smoke exposure on inflammatory modulators in the gut. We examined the effect of cigarette smoke on cytokine profiles in the healthy and inflamed gut of human subjects and in the trinitrobenzene sulphonic acid mouse model, which mimics distal Crohn-like colitis. In addition, the effect of cigarette smoke on epithelial expression of transient receptor potential channels and their concurrent increase with cigarette smoke-augmented cytokine production was investigated. Active smoking was associated with increasedIL-8transcription in ileum of controls (p < 0,001; n = 18-20/group). In the ileum, TRPV1 mRNA levels were decreased in never smoking Crohn's disease patients compared to healthy subjects (p <0,001; n = 20/group). In the colon, TRPV1 mRNA levels were decreased (p = 0,046) in smoking healthy controls (n = 20/group). Likewise, healthy mice chronically exposed to cigarette smoke (n = 10/group) showed elevated ilealCxcl2(p = 0,0075) and colonicKcmRNA levels (p = 0,0186), whereas TRPV1 mRNA and protein levels were elevated in the ileum (p = 0,0315). Although cigarette smoke exposure prior to trinitrobenzene sulphonic acid administration did not alter disease activity, increased pro-inflammatory cytokine production was observed in the distal colon (Kc: p = 0,0273; Cxcl2: p = 0,104; Il1-beta: p = 0,0796), in parallel with the increase ofTrpv1mRNA (p < 0,001). We infer that CS affects pro-inflammatory cytokine expression in healthy and inflamed gut, and that the simultaneous modulation of TRPV1 may point to a potential involvement of TRPV1 in cigarette smoke-induced production of inflammatory mediators.
Keywords
General Biochemistry, Genetics and Molecular Biology, General Agricultural and Biological Sciences, General Medicine, INDUCED PULMONARY INFLAMMATION, BOWEL-DISEASE, EXPERIMENTAL COLITIS, RECEPTOR, CELLS, MECHANISMS, NICOTINE, MICE, EXPOSURE, TOBACCO

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MLA
Allais, Liesbeth, et al. “Translational Research into the Effects of Cigarette Smoke on Inflammatory Mediators and Epithelial TRPV1 in Crohn’s Disease.” PLOS ONE, edited by Mathilde Body-Malapel, vol. 15, no. 8, 2020, doi:10.1371/journal.pone.0236657.
APA
Allais, L., Verschuere, S., Maes, T., De Smet, R., Devriese, S., Gonzales, B., … Laukens, D. (2020). Translational research into the effects of cigarette smoke on inflammatory mediators and epithelial TRPV1 in Crohn’s disease. PLOS ONE, 15(8). https://doi.org/10.1371/journal.pone.0236657
Chicago author-date
Allais, Liesbeth, Stephanie Verschuere, Tania Maes, Rebecca De Smet, Sarah Devriese, Bryan Gonzales, Harald Peeters, et al. 2020. “Translational Research into the Effects of Cigarette Smoke on Inflammatory Mediators and Epithelial TRPV1 in Crohn’s Disease.” Edited by Mathilde Body-Malapel. PLOS ONE 15 (8). https://doi.org/10.1371/journal.pone.0236657.
Chicago author-date (all authors)
Allais, Liesbeth, Stephanie Verschuere, Tania Maes, Rebecca De Smet, Sarah Devriese, Bryan Gonzales, Harald Peeters, Koen Van Crombruggen, Claus Bachert, Martine De Vos, Guy Brusselle, Ken Bracke, Claude Cuvelier, and Debby Laukens. 2020. “Translational Research into the Effects of Cigarette Smoke on Inflammatory Mediators and Epithelial TRPV1 in Crohn’s Disease.” Ed by. Mathilde Body-Malapel. PLOS ONE 15 (8). doi:10.1371/journal.pone.0236657.
Vancouver
1.
Allais L, Verschuere S, Maes T, De Smet R, Devriese S, Gonzales B, et al. Translational research into the effects of cigarette smoke on inflammatory mediators and epithelial TRPV1 in Crohn’s disease. Body-Malapel M, editor. PLOS ONE. 2020;15(8).
IEEE
[1]
L. Allais et al., “Translational research into the effects of cigarette smoke on inflammatory mediators and epithelial TRPV1 in Crohn’s disease,” PLOS ONE, vol. 15, no. 8, 2020.
@article{8672605,
  abstract     = {{Crohn's disease is a pathological condition of the gastro-intestinal tract, causing severe transmural inflammation in the ileum and/or colon. Cigarette smoking is one of the best known environmental risk factors for the development of Crohn's disease. Nevertheless, very little is known about the effect of prolonged cigarette smoke exposure on inflammatory modulators in the gut. We examined the effect of cigarette smoke on cytokine profiles in the healthy and inflamed gut of human subjects and in the trinitrobenzene sulphonic acid mouse model, which mimics distal Crohn-like colitis. In addition, the effect of cigarette smoke on epithelial expression of transient receptor potential channels and their concurrent increase with cigarette smoke-augmented cytokine production was investigated. Active smoking was associated with increasedIL-8transcription in ileum of controls (p < 0,001; n = 18-20/group). In the ileum, TRPV1 mRNA levels were decreased in never smoking Crohn's disease patients compared to healthy subjects (p <0,001; n = 20/group). In the colon, TRPV1 mRNA levels were decreased (p = 0,046) in smoking healthy controls (n = 20/group). Likewise, healthy mice chronically exposed to cigarette smoke (n = 10/group) showed elevated ilealCxcl2(p = 0,0075) and colonicKcmRNA levels (p = 0,0186), whereas TRPV1 mRNA and protein levels were elevated in the ileum (p = 0,0315). Although cigarette smoke exposure prior to trinitrobenzene sulphonic acid administration did not alter disease activity, increased pro-inflammatory cytokine production was observed in the distal colon (Kc: p = 0,0273; Cxcl2: p = 0,104; Il1-beta: p = 0,0796), in parallel with the increase ofTrpv1mRNA (p < 0,001). We infer that CS affects pro-inflammatory cytokine expression in healthy and inflamed gut, and that the simultaneous modulation of TRPV1 may point to a potential involvement of TRPV1 in cigarette smoke-induced production of inflammatory mediators.}},
  articleno    = {{e0236657}},
  author       = {{Allais, Liesbeth and Verschuere, Stephanie and Maes, Tania and De Smet, Rebecca and Devriese, Sarah and Gonzales, Bryan and Peeters, Harald and Van Crombruggen, Koen and Bachert, Claus and De Vos, Martine and Brusselle, Guy and Bracke, Ken and Cuvelier, Claude and Laukens, Debby}},
  editor       = {{Body-Malapel, Mathilde}},
  issn         = {{1932-6203}},
  journal      = {{PLOS ONE}},
  keywords     = {{General Biochemistry,Genetics and Molecular Biology,General Agricultural and Biological Sciences,General Medicine,INDUCED PULMONARY INFLAMMATION,BOWEL-DISEASE,EXPERIMENTAL COLITIS,RECEPTOR,CELLS,MECHANISMS,NICOTINE,MICE,EXPOSURE,TOBACCO}},
  language     = {{eng}},
  number       = {{8}},
  pages        = {{20}},
  title        = {{Translational research into the effects of cigarette smoke on inflammatory mediators and epithelial TRPV1 in Crohn’s disease}},
  url          = {{http://doi.org/10.1371/journal.pone.0236657}},
  volume       = {{15}},
  year         = {{2020}},
}
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