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Cigarette smoke and the terminal ileum: increased autophagy in murine follicle-associated epithelium and Peyer's patches

STEPHANIE VERSCHUERE UGent, Liesbeth Allais UGent, Ken Bracke UGent, Saskia Lippens UGent, Rebecca De Smet UGent, Peter Vandenabeele UGent, Guy Brusselle UGent and Claude Cuvelier UGent (2012) HISTOCHEMISTRY AND CELL BIOLOGY. 137(3). p.293-301
abstract
Cigarette smoke (CS) exposure is associated with increased autophagy in several cell types, such as bronchial epithelial cells. Smoking is also an environmental risk factor in Crohn's disease, in which impairment of the autophagy-mediated anti-bacterial pathway has been implicated. So far, it is unknown whether CS induces autophagy in the gut. Here, we examined the effect of chronic CS exposure on autophagy in the follicle-associated epithelium (FAE) of murine Peyer's patches. Transmission electron microscopy revealed that the proportion of cell area occupied by autophagic vesicles significantly increased in the FAE after CS exposure. An increased number of autophagic vesicles was observed in the FAE, whereas the vesicle size remained unaltered. Besides enterocytes, also M-cells contain more autophagic vesicles upon CS exposure. In addition, the mRNA level of the autophagy-related protein Atg7 in the underlying Peyer's patches is increased after CS exposure, which indicates that the autophagy-inducing effect of CS is not limited to the FAE. In conclusion, our results demonstrate that CS exposure induces autophagy in murine FAE and in the underlying immune cells of Peyer's patches, suggesting that CS exposure increases the risk for Crohn's disease by causing epithelial oxidative damage, which needs to be repaired by autophagy.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
Crohn’s disease, Electron microscopy, Peyer’s patches, M-cells, Follicle-associated epithelium, Smoking, Autophagy, OBSTRUCTIVE PULMONARY-DISEASE, M-CELLS, CROHNS-DISEASE, DENDRITIC CELLS, INFLAMMATION, APOPTOSIS, IMMUNITY, ATG16L1, STRESS, PATHOGENESIS
journal title
HISTOCHEMISTRY AND CELL BIOLOGY
Histochem. Cell Biol.
volume
137
issue
3
pages
293 - 301
Web of Science type
Article
Web of Science id
000300326100003
JCR category
MICROSCOPY
JCR impact factor
2.613 (2012)
JCR rank
1/9 (2012)
JCR quartile
1 (2012)
ISSN
0948-6143
DOI
10.1007/s00418-011-0902-3
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
2003360
handle
http://hdl.handle.net/1854/LU-2003360
date created
2012-01-25 16:19:29
date last changed
2012-08-07 15:19:31
@article{2003360,
  abstract     = {Cigarette smoke (CS) exposure is associated with increased autophagy in several cell types, such as bronchial epithelial cells. Smoking is also an environmental risk factor in Crohn's disease, in which impairment of the autophagy-mediated anti-bacterial pathway has been implicated. So far, it is unknown whether CS induces autophagy in the gut. Here, we examined the effect of chronic CS exposure on autophagy in the follicle-associated epithelium (FAE) of murine Peyer's patches. Transmission electron microscopy revealed that the proportion of cell area occupied by autophagic vesicles significantly increased in the FAE after CS exposure. An increased number of autophagic vesicles was observed in the FAE, whereas the vesicle size remained unaltered. Besides enterocytes, also M-cells contain more autophagic vesicles upon CS exposure. In addition, the mRNA level of the autophagy-related protein Atg7 in the underlying Peyer's patches is increased after CS exposure, which indicates that the autophagy-inducing effect of CS is not limited to the FAE. In conclusion, our results demonstrate that CS exposure induces autophagy in murine FAE and in the underlying immune cells of Peyer's patches, suggesting that CS exposure increases the risk for Crohn's disease by causing epithelial oxidative damage, which needs to be repaired by autophagy.},
  author       = {VERSCHUERE, STEPHANIE and Allais, Liesbeth and Bracke, Ken and Lippens, Saskia and De Smet, Rebecca and Vandenabeele, Peter and Brusselle, Guy and Cuvelier, Claude},
  issn         = {0948-6143},
  journal      = {HISTOCHEMISTRY AND CELL BIOLOGY},
  keyword      = {Crohn{\textquoteright}s disease,Electron microscopy,Peyer{\textquoteright}s patches,M-cells,Follicle-associated epithelium,Smoking,Autophagy,OBSTRUCTIVE PULMONARY-DISEASE,M-CELLS,CROHNS-DISEASE,DENDRITIC CELLS,INFLAMMATION,APOPTOSIS,IMMUNITY,ATG16L1,STRESS,PATHOGENESIS},
  language     = {eng},
  number       = {3},
  pages        = {293--301},
  title        = {Cigarette smoke and the terminal ileum: increased autophagy in murine follicle-associated epithelium and Peyer's patches},
  url          = {http://dx.doi.org/10.1007/s00418-011-0902-3},
  volume       = {137},
  year         = {2012},
}

Chicago
VERSCHUERE, STEPHANIE, Liesbeth Allais, Ken Bracke, Saskia Lippens, Rebecca De Smet, Peter Vandenabeele, Guy Brusselle, and Claude Cuvelier. 2012. “Cigarette Smoke and the Terminal Ileum: Increased Autophagy in Murine Follicle-associated Epithelium and Peyer’s Patches.” Histochemistry and Cell Biology 137 (3): 293–301.
APA
VERSCHUERE, S., Allais, L., Bracke, K., Lippens, S., De Smet, R., Vandenabeele, P., Brusselle, G., et al. (2012). Cigarette smoke and the terminal ileum: increased autophagy in murine follicle-associated epithelium and Peyer’s patches. HISTOCHEMISTRY AND CELL BIOLOGY, 137(3), 293–301.
Vancouver
1.
VERSCHUERE S, Allais L, Bracke K, Lippens S, De Smet R, Vandenabeele P, et al. Cigarette smoke and the terminal ileum: increased autophagy in murine follicle-associated epithelium and Peyer’s patches. HISTOCHEMISTRY AND CELL BIOLOGY. 2012;137(3):293–301.
MLA
VERSCHUERE, STEPHANIE, Liesbeth Allais, Ken Bracke, et al. “Cigarette Smoke and the Terminal Ileum: Increased Autophagy in Murine Follicle-associated Epithelium and Peyer’s Patches.” HISTOCHEMISTRY AND CELL BIOLOGY 137.3 (2012): 293–301. Print.