Increased small bowel epithelial turnover in interleukin-1 receptor knockout mice

Steven Wolf, Meelie A. Debroy, Hiroto Ikeda, Marc Jeschke, Sina Matin, Srinivasan Rajaraman, Tien C. Ko, Ella Englander, James G. Norman, James C. Thompson

Research output: Contribution to journalArticle

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Abstract

Objective: To determine whether interleukin-1 (IL-1) affects the cellular homeostasis of small bowel mucosa, the authors studied apoptosis and proliferation in small bowel epithelium in two groups of C57 mice: an IL-1 receptor knockout group, and a control wild-type group. Summary Background Data: Gut mucosal integrity is maintained by a balance of cell proliferation and cell death. Recent reports suggest that IL-1, a proinflammatory cytokine, increases cell death by apoptosis in some epithelial cells. Methods: Twenty-four male C57BL6 IL-1 receptor (type I) knockout mice were killed, and small bowel was removed for study. Twenty-four wild-type mice (C57-BL6) served as controls. Body weights, bowel length, and mucosal morphology were examined for phenotypic differences. Apoptosis was quantified by terminal deoxyuridine nick-end labeling (TUNEL) immunohistochemical staining and cellular proliferation by proliferation cell nuclear antigen staining. Whole mucosal protein was analyzed for nuclear factor-κB expression. Groups were analyzed by t test. Results: The absence of IL-1 type I receptor in knockout mice was verified by reverse transcriptase-polymerase chain reaction. IL-1 receptor null mice were larger than wild-type controls, with a longer small bowel; however, the index of small bowel length to total body weight did not differ between groups. The percentage of apoptotic cells was higher in IL-1 receptor null mice than in wild-type mice; the proliferation index also increased. Mucosal height and other measures of mucosal morphology were not different. Genotypic absence of IL-1 receptors was associated with decreased expression of nuclear factor-κB in whole mucosal protein extracts. Conclusions: Both apoptosis and proliferation increased in gut epithelial cells of mice without IL-1 receptors, suggesting increased cell turnover with no change in net balance. This model represents an opportunity to examine potential mechanisms of gut epithelial turnover in vivo, under both normal conditions and in conditions of mucosal proliferation and atrophy.

Original languageEnglish (US)
Pages (from-to)42-45
Number of pages4
JournalAnnals of Surgery
Volume232
Issue number1
DOIs
StatePublished - Jul 2000

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Interleukin-1 Receptors
Knockout Mice
Interleukin-1 Type I Receptors
Apoptosis
Cell Proliferation
Interleukin-1
Cell Death
Epithelial Cells
Body Weight
Staining and Labeling
Nuclear Antigens
Deoxyuridine
Reverse Transcriptase Polymerase Chain Reaction
Atrophy
Mucous Membrane
Proteins
Homeostasis
Epithelium
Cytokines
Control Groups

ASJC Scopus subject areas

  • Surgery

Cite this

Wolf, S., Debroy, M. A., Ikeda, H., Jeschke, M., Matin, S., Rajaraman, S., ... Thompson, J. C. (2000). Increased small bowel epithelial turnover in interleukin-1 receptor knockout mice. Annals of Surgery, 232(1), 42-45. https://doi.org/10.1097/00000658-200007000-00006

Increased small bowel epithelial turnover in interleukin-1 receptor knockout mice. / Wolf, Steven; Debroy, Meelie A.; Ikeda, Hiroto; Jeschke, Marc; Matin, Sina; Rajaraman, Srinivasan; Ko, Tien C.; Englander, Ella; Norman, James G.; Thompson, James C.

In: Annals of Surgery, Vol. 232, No. 1, 07.2000, p. 42-45.

Research output: Contribution to journalArticle

Wolf, S, Debroy, MA, Ikeda, H, Jeschke, M, Matin, S, Rajaraman, S, Ko, TC, Englander, E, Norman, JG & Thompson, JC 2000, 'Increased small bowel epithelial turnover in interleukin-1 receptor knockout mice', Annals of Surgery, vol. 232, no. 1, pp. 42-45. https://doi.org/10.1097/00000658-200007000-00006
Wolf, Steven ; Debroy, Meelie A. ; Ikeda, Hiroto ; Jeschke, Marc ; Matin, Sina ; Rajaraman, Srinivasan ; Ko, Tien C. ; Englander, Ella ; Norman, James G. ; Thompson, James C. / Increased small bowel epithelial turnover in interleukin-1 receptor knockout mice. In: Annals of Surgery. 2000 ; Vol. 232, No. 1. pp. 42-45.
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abstract = "Objective: To determine whether interleukin-1 (IL-1) affects the cellular homeostasis of small bowel mucosa, the authors studied apoptosis and proliferation in small bowel epithelium in two groups of C57 mice: an IL-1 receptor knockout group, and a control wild-type group. Summary Background Data: Gut mucosal integrity is maintained by a balance of cell proliferation and cell death. Recent reports suggest that IL-1, a proinflammatory cytokine, increases cell death by apoptosis in some epithelial cells. Methods: Twenty-four male C57BL6 IL-1 receptor (type I) knockout mice were killed, and small bowel was removed for study. Twenty-four wild-type mice (C57-BL6) served as controls. Body weights, bowel length, and mucosal morphology were examined for phenotypic differences. Apoptosis was quantified by terminal deoxyuridine nick-end labeling (TUNEL) immunohistochemical staining and cellular proliferation by proliferation cell nuclear antigen staining. Whole mucosal protein was analyzed for nuclear factor-κB expression. Groups were analyzed by t test. Results: The absence of IL-1 type I receptor in knockout mice was verified by reverse transcriptase-polymerase chain reaction. IL-1 receptor null mice were larger than wild-type controls, with a longer small bowel; however, the index of small bowel length to total body weight did not differ between groups. The percentage of apoptotic cells was higher in IL-1 receptor null mice than in wild-type mice; the proliferation index also increased. Mucosal height and other measures of mucosal morphology were not different. Genotypic absence of IL-1 receptors was associated with decreased expression of nuclear factor-κB in whole mucosal protein extracts. Conclusions: Both apoptosis and proliferation increased in gut epithelial cells of mice without IL-1 receptors, suggesting increased cell turnover with no change in net balance. This model represents an opportunity to examine potential mechanisms of gut epithelial turnover in vivo, under both normal conditions and in conditions of mucosal proliferation and atrophy.",
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