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Inflammation Enhances Resection-Induced Intestinal Adaptive Growth in IL-10 Null Mice

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Inflammation Enhances Resection-Induced Intestinal Adaptive Growth in IL-10 Null Mice. / Speck, Karen E.; Garrison, Aaron P.; Rigby, Rachael J.; von Allmen, Doug C.; Lund, P. Kay; Helmrath, Michael A.

In: Journal of Surgical Research, Vol. 168, No. 1, 01.06.2011, p. 62-69.

Research output: Contribution to journalJournal articlepeer-review

Harvard

Speck, KE, Garrison, AP, Rigby, RJ, von Allmen, DC, Lund, PK & Helmrath, MA 2011, 'Inflammation Enhances Resection-Induced Intestinal Adaptive Growth in IL-10 Null Mice', Journal of Surgical Research, vol. 168, no. 1, pp. 62-69. https://doi.org/10.1016/j.jss.2009.09.051

APA

Speck, K. E., Garrison, A. P., Rigby, R. J., von Allmen, D. C., Lund, P. K., & Helmrath, M. A. (2011). Inflammation Enhances Resection-Induced Intestinal Adaptive Growth in IL-10 Null Mice. Journal of Surgical Research, 168(1), 62-69. https://doi.org/10.1016/j.jss.2009.09.051

Vancouver

Speck KE, Garrison AP, Rigby RJ, von Allmen DC, Lund PK, Helmrath MA. Inflammation Enhances Resection-Induced Intestinal Adaptive Growth in IL-10 Null Mice. Journal of Surgical Research. 2011 Jun 1;168(1):62-69. https://doi.org/10.1016/j.jss.2009.09.051

Author

Speck, Karen E. ; Garrison, Aaron P. ; Rigby, Rachael J. ; von Allmen, Doug C. ; Lund, P. Kay ; Helmrath, Michael A. / Inflammation Enhances Resection-Induced Intestinal Adaptive Growth in IL-10 Null Mice. In: Journal of Surgical Research. 2011 ; Vol. 168, No. 1. pp. 62-69.

Bibtex

@article{4e1ad2cf9c0446849e8bafd039ac2609,
title = "Inflammation Enhances Resection-Induced Intestinal Adaptive Growth in IL-10 Null Mice",
abstract = "Background. Surgical resection of the ileum, cecum, and proximal right colon (ICR) is common in the management of Crohn's disease, yet little is known about the effect of active inflammation on the adaptive response following intestinal loss. We recently developed a surgical model of ICR in germ-free (GF) IL-10 null mice that develop small intestinal inflammation only when mice undergo conventionalization with normal fecal microflora (CONV) before surgical intervention. In this study, we examined the effects of postsurgical small bowel inflammation on adaptive growth after ICR. Methods. GF 129SvEv IL-10 null mice, 8-10 wk old, were allocated to GF or CONV groups. Nonoperated GF and CONV mice provided baseline controls. Two wk later, GF and CONV mice were further allocated to ICR or sham operation. Small intestine and colon were harvested 7 d after surgery for histological analysis. Results. All mice within the gnotobiotic facility maintained GF status and did not develop small intestinal or colonic inflammation. CONV resulted in colitis in all groups, whereas small intestinal inflammation was only observed following ICR. Resection-induced small intestinal inflammation in CONV mice was associated with increases in proliferation, crypt depth, and villus height compared with GF mice after ICR. Resection-induced increases in crypt fission only occurred in CONV mice. Conclusion. ICR-dependent small intestinal inflammation in CONVIL-10 null mice dramatically enhances early adaptive growth of the small intestine. Additional studies utilizing our model may provide clinical insight leading to optimal therapies in managing IBD patients after surgical resection. ",
keywords = "IL-10 null, inflammatory bowel disease, IBD, ileocecal resection, ICR, adaptation, crypt fission, proliferation, microbial effect, conventionalization, SMALL-BOWEL RESECTION, POSTOPERATIVE CROHNS-DISEASE, ILEOCECAL RESECTION, INTERLEUKIN-10-DEFICIENT MICE, STEM-CELLS, ADAPTATION, COLITIS, MODELS, ADENOCARCINOMA, PROLIFERATION",
author = "Speck, {Karen E.} and Garrison, {Aaron P.} and Rigby, {Rachael J.} and {von Allmen}, {Doug C.} and Lund, {P. Kay} and Helmrath, {Michael A.}",
year = "2011",
month = jun,
day = "1",
doi = "10.1016/j.jss.2009.09.051",
language = "English",
volume = "168",
pages = "62--69",
journal = "Journal of Surgical Research",
issn = "0022-4804",
publisher = "Academic Press Inc.",
number = "1",

}

RIS

TY - JOUR

T1 - Inflammation Enhances Resection-Induced Intestinal Adaptive Growth in IL-10 Null Mice

AU - Speck, Karen E.

AU - Garrison, Aaron P.

AU - Rigby, Rachael J.

AU - von Allmen, Doug C.

AU - Lund, P. Kay

AU - Helmrath, Michael A.

PY - 2011/6/1

Y1 - 2011/6/1

N2 - Background. Surgical resection of the ileum, cecum, and proximal right colon (ICR) is common in the management of Crohn's disease, yet little is known about the effect of active inflammation on the adaptive response following intestinal loss. We recently developed a surgical model of ICR in germ-free (GF) IL-10 null mice that develop small intestinal inflammation only when mice undergo conventionalization with normal fecal microflora (CONV) before surgical intervention. In this study, we examined the effects of postsurgical small bowel inflammation on adaptive growth after ICR. Methods. GF 129SvEv IL-10 null mice, 8-10 wk old, were allocated to GF or CONV groups. Nonoperated GF and CONV mice provided baseline controls. Two wk later, GF and CONV mice were further allocated to ICR or sham operation. Small intestine and colon were harvested 7 d after surgery for histological analysis. Results. All mice within the gnotobiotic facility maintained GF status and did not develop small intestinal or colonic inflammation. CONV resulted in colitis in all groups, whereas small intestinal inflammation was only observed following ICR. Resection-induced small intestinal inflammation in CONV mice was associated with increases in proliferation, crypt depth, and villus height compared with GF mice after ICR. Resection-induced increases in crypt fission only occurred in CONV mice. Conclusion. ICR-dependent small intestinal inflammation in CONVIL-10 null mice dramatically enhances early adaptive growth of the small intestine. Additional studies utilizing our model may provide clinical insight leading to optimal therapies in managing IBD patients after surgical resection. 

AB - Background. Surgical resection of the ileum, cecum, and proximal right colon (ICR) is common in the management of Crohn's disease, yet little is known about the effect of active inflammation on the adaptive response following intestinal loss. We recently developed a surgical model of ICR in germ-free (GF) IL-10 null mice that develop small intestinal inflammation only when mice undergo conventionalization with normal fecal microflora (CONV) before surgical intervention. In this study, we examined the effects of postsurgical small bowel inflammation on adaptive growth after ICR. Methods. GF 129SvEv IL-10 null mice, 8-10 wk old, were allocated to GF or CONV groups. Nonoperated GF and CONV mice provided baseline controls. Two wk later, GF and CONV mice were further allocated to ICR or sham operation. Small intestine and colon were harvested 7 d after surgery for histological analysis. Results. All mice within the gnotobiotic facility maintained GF status and did not develop small intestinal or colonic inflammation. CONV resulted in colitis in all groups, whereas small intestinal inflammation was only observed following ICR. Resection-induced small intestinal inflammation in CONV mice was associated with increases in proliferation, crypt depth, and villus height compared with GF mice after ICR. Resection-induced increases in crypt fission only occurred in CONV mice. Conclusion. ICR-dependent small intestinal inflammation in CONVIL-10 null mice dramatically enhances early adaptive growth of the small intestine. Additional studies utilizing our model may provide clinical insight leading to optimal therapies in managing IBD patients after surgical resection. 

KW - IL-10 null

KW - inflammatory bowel disease

KW - IBD

KW - ileocecal resection

KW - ICR

KW - adaptation

KW - crypt fission

KW - proliferation

KW - microbial effect

KW - conventionalization

KW - SMALL-BOWEL RESECTION

KW - POSTOPERATIVE CROHNS-DISEASE

KW - ILEOCECAL RESECTION

KW - INTERLEUKIN-10-DEFICIENT MICE

KW - STEM-CELLS

KW - ADAPTATION

KW - COLITIS

KW - MODELS

KW - ADENOCARCINOMA

KW - PROLIFERATION

UR - http://www.scopus.com/inward/record.url?scp=79955623508&partnerID=8YFLogxK

U2 - 10.1016/j.jss.2009.09.051

DO - 10.1016/j.jss.2009.09.051

M3 - Journal article

VL - 168

SP - 62

EP - 69

JO - Journal of Surgical Research

JF - Journal of Surgical Research

SN - 0022-4804

IS - 1

ER -