Complement C3 production in human intestinal epithelial cells is regulated by interleukin 1β and tumor necrosis factor α

Ryan Moon, Alexander A. Parikh, Csaba Szabo, Josef E. Fischer, Andrew L. Salzman, Per Olof Hasselgren

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Background: Sepsis and endotoxemia are associated with increased mucosal production of complement component C3; the enterocyte may be a source of C3 in these conditions. Objective: To test the hypothesis that interleukin 1β (IL-1β) and tumor necrosis factor α (TNF-α) regulate the production of C3 in the enterocyte at the transcriptional level and that this regulation is potentiated by interferon gamma (IFN-γ). Methods: Cultured Caco-2 cells, a human intestinal epithelial cell line, were treated with various concentrations of human recombinant IL-1β (0.005-1.25 ng/mL) or TNF-α (1- 1000 U/mL) with or without the addition of IFN-γ (250 U/mL). C3 levels in the culture medium were measured by enzyme-linked immunosorbent assay and cellular messenger RNA levels by Northern blot analysis. Results: Treatment of the Caco-2 cells with IL-1β or TNF-α resulted in a time- and dose- dependent increase in C3 production. The use of IFN-γ alone did not affect C3 production but potentiated the effect of IL-1β and TNF-α in a synergistic manner. C3 messenger RNA levels were increased following stimulation with either cytokine. Conclusions: C3 production in the enterocyte is regulated by IL-1β and TNF-α at the transcriptional level, and this response is potentiated by IFN-γ. The results suggest that C3 production in the intestinal mucosa may be regulated locally by cytokines in a paracrine or autocrine manner.

Original languageEnglish (US)
Pages (from-to)1289-1293
Number of pages5
JournalArchives of Surgery
Volume132
Issue number12
StatePublished - Dec 1997
Externally publishedYes

Fingerprint

Complement C3
Interleukin-1
Tumor Necrosis Factor-alpha
Epithelial Cells
Interferon-gamma
Enterocytes
Caco-2 Cells
Cytokines
Messenger RNA
Endotoxemia
Intestinal Mucosa
Northern Blotting
Culture Media
Cultured Cells
Sepsis
Enzyme-Linked Immunosorbent Assay
Cell Line

ASJC Scopus subject areas

  • Surgery

Cite this

Moon, R., Parikh, A. A., Szabo, C., Fischer, J. E., Salzman, A. L., & Hasselgren, P. O. (1997). Complement C3 production in human intestinal epithelial cells is regulated by interleukin 1β and tumor necrosis factor α. Archives of Surgery, 132(12), 1289-1293.

Complement C3 production in human intestinal epithelial cells is regulated by interleukin 1β and tumor necrosis factor α. / Moon, Ryan; Parikh, Alexander A.; Szabo, Csaba; Fischer, Josef E.; Salzman, Andrew L.; Hasselgren, Per Olof.

In: Archives of Surgery, Vol. 132, No. 12, 12.1997, p. 1289-1293.

Research output: Contribution to journalArticle

Moon, R, Parikh, AA, Szabo, C, Fischer, JE, Salzman, AL & Hasselgren, PO 1997, 'Complement C3 production in human intestinal epithelial cells is regulated by interleukin 1β and tumor necrosis factor α', Archives of Surgery, vol. 132, no. 12, pp. 1289-1293.
Moon R, Parikh AA, Szabo C, Fischer JE, Salzman AL, Hasselgren PO. Complement C3 production in human intestinal epithelial cells is regulated by interleukin 1β and tumor necrosis factor α. Archives of Surgery. 1997 Dec;132(12):1289-1293.
Moon, Ryan ; Parikh, Alexander A. ; Szabo, Csaba ; Fischer, Josef E. ; Salzman, Andrew L. ; Hasselgren, Per Olof. / Complement C3 production in human intestinal epithelial cells is regulated by interleukin 1β and tumor necrosis factor α. In: Archives of Surgery. 1997 ; Vol. 132, No. 12. pp. 1289-1293.
@article{55c8e790e54342b9bf47370f9f45c110,
title = "Complement C3 production in human intestinal epithelial cells is regulated by interleukin 1β and tumor necrosis factor α",
abstract = "Background: Sepsis and endotoxemia are associated with increased mucosal production of complement component C3; the enterocyte may be a source of C3 in these conditions. Objective: To test the hypothesis that interleukin 1β (IL-1β) and tumor necrosis factor α (TNF-α) regulate the production of C3 in the enterocyte at the transcriptional level and that this regulation is potentiated by interferon gamma (IFN-γ). Methods: Cultured Caco-2 cells, a human intestinal epithelial cell line, were treated with various concentrations of human recombinant IL-1β (0.005-1.25 ng/mL) or TNF-α (1- 1000 U/mL) with or without the addition of IFN-γ (250 U/mL). C3 levels in the culture medium were measured by enzyme-linked immunosorbent assay and cellular messenger RNA levels by Northern blot analysis. Results: Treatment of the Caco-2 cells with IL-1β or TNF-α resulted in a time- and dose- dependent increase in C3 production. The use of IFN-γ alone did not affect C3 production but potentiated the effect of IL-1β and TNF-α in a synergistic manner. C3 messenger RNA levels were increased following stimulation with either cytokine. Conclusions: C3 production in the enterocyte is regulated by IL-1β and TNF-α at the transcriptional level, and this response is potentiated by IFN-γ. The results suggest that C3 production in the intestinal mucosa may be regulated locally by cytokines in a paracrine or autocrine manner.",
author = "Ryan Moon and Parikh, {Alexander A.} and Csaba Szabo and Fischer, {Josef E.} and Salzman, {Andrew L.} and Hasselgren, {Per Olof}",
year = "1997",
month = "12",
language = "English (US)",
volume = "132",
pages = "1289--1293",
journal = "JAMA Surgery",
issn = "2168-6254",
publisher = "American Medical Association",
number = "12",

}

TY - JOUR

T1 - Complement C3 production in human intestinal epithelial cells is regulated by interleukin 1β and tumor necrosis factor α

AU - Moon, Ryan

AU - Parikh, Alexander A.

AU - Szabo, Csaba

AU - Fischer, Josef E.

AU - Salzman, Andrew L.

AU - Hasselgren, Per Olof

PY - 1997/12

Y1 - 1997/12

N2 - Background: Sepsis and endotoxemia are associated with increased mucosal production of complement component C3; the enterocyte may be a source of C3 in these conditions. Objective: To test the hypothesis that interleukin 1β (IL-1β) and tumor necrosis factor α (TNF-α) regulate the production of C3 in the enterocyte at the transcriptional level and that this regulation is potentiated by interferon gamma (IFN-γ). Methods: Cultured Caco-2 cells, a human intestinal epithelial cell line, were treated with various concentrations of human recombinant IL-1β (0.005-1.25 ng/mL) or TNF-α (1- 1000 U/mL) with or without the addition of IFN-γ (250 U/mL). C3 levels in the culture medium were measured by enzyme-linked immunosorbent assay and cellular messenger RNA levels by Northern blot analysis. Results: Treatment of the Caco-2 cells with IL-1β or TNF-α resulted in a time- and dose- dependent increase in C3 production. The use of IFN-γ alone did not affect C3 production but potentiated the effect of IL-1β and TNF-α in a synergistic manner. C3 messenger RNA levels were increased following stimulation with either cytokine. Conclusions: C3 production in the enterocyte is regulated by IL-1β and TNF-α at the transcriptional level, and this response is potentiated by IFN-γ. The results suggest that C3 production in the intestinal mucosa may be regulated locally by cytokines in a paracrine or autocrine manner.

AB - Background: Sepsis and endotoxemia are associated with increased mucosal production of complement component C3; the enterocyte may be a source of C3 in these conditions. Objective: To test the hypothesis that interleukin 1β (IL-1β) and tumor necrosis factor α (TNF-α) regulate the production of C3 in the enterocyte at the transcriptional level and that this regulation is potentiated by interferon gamma (IFN-γ). Methods: Cultured Caco-2 cells, a human intestinal epithelial cell line, were treated with various concentrations of human recombinant IL-1β (0.005-1.25 ng/mL) or TNF-α (1- 1000 U/mL) with or without the addition of IFN-γ (250 U/mL). C3 levels in the culture medium were measured by enzyme-linked immunosorbent assay and cellular messenger RNA levels by Northern blot analysis. Results: Treatment of the Caco-2 cells with IL-1β or TNF-α resulted in a time- and dose- dependent increase in C3 production. The use of IFN-γ alone did not affect C3 production but potentiated the effect of IL-1β and TNF-α in a synergistic manner. C3 messenger RNA levels were increased following stimulation with either cytokine. Conclusions: C3 production in the enterocyte is regulated by IL-1β and TNF-α at the transcriptional level, and this response is potentiated by IFN-γ. The results suggest that C3 production in the intestinal mucosa may be regulated locally by cytokines in a paracrine or autocrine manner.

UR - http://www.scopus.com/inward/record.url?scp=0031440391&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031440391&partnerID=8YFLogxK

M3 - Article

C2 - 9403532

AN - SCOPUS:0031440391

VL - 132

SP - 1289

EP - 1293

JO - JAMA Surgery

JF - JAMA Surgery

SN - 2168-6254

IS - 12

ER -