Tumor necrosis factor alpha and interleukin 1β up-regulate gastric mucosal Fas antigen expression in Helicobacter pylori infection

Jeanmarie Houghton, Lisa S. Macera-Bloch, Lawrence Harrison, Kyung H. Kim, Reju M. Korah

Research output: Contribution to journalArticle

74 Citations (Scopus)

Abstract

Fas-mediated gastric mucosal apoptosis is gaining attention as a cause of tissue damage due to Helicobacter pylori infection. We explored the effects of H. pylori directly, and the effects of the inflammatory environment established subsequent to H. pylori infection, on Fas-mediated apoptosis in a nontransformed gastric mucosal cell line (RGM-1). Exposure to H. pylori-activated peripheral blood mononuclear cells (PBMCs), but not H. pylori itself, induced Fas antigen (Fas Ag) expression, indicating a Fas- regulatory role for inflammatory cytokines in this system. Of various inflammatory cytokines tested, only interleukin 1β and tumor necrosis factor alpha induced Fas Ag expression, and removal of either of these from the conditioned medium abrogated the response. When exposed to Fas ligand, RGM-1 cells treated with PBMC-conditioned medium underwent massive and rapid cell death, interestingly, with a minimal effect on total cell numbers early on. Cell cycle analysis revealed a substantial increase in S phase cells among cells exposed to Fas ligand, suggesting an increase in their proliferative response. Taken together, these data indicate that the immune environment secondary to H. pylori infection plays a critical role in priming gastric mucosal cells to undergo apoptosis or to proliferate based upon their Fas Ag status.

Original languageEnglish (US)
Pages (from-to)1189-1195
Number of pages7
JournalInfection and Immunity
Volume68
Issue number3
DOIs
StatePublished - Mar 4 2000
Externally publishedYes

Fingerprint

CD95 Antigens
Helicobacter Infections
Interleukin-1
Helicobacter pylori
Stomach
Up-Regulation
Tumor Necrosis Factor-alpha
Fas Ligand Protein
Apoptosis
Conditioned Culture Medium
Blood Cells
Cytokines
S Phase
Cell Cycle
Cell Death
Cell Count
Cell Line

All Science Journal Classification (ASJC) codes

  • Parasitology
  • Microbiology
  • Immunology
  • Infectious Diseases

Cite this

Houghton, Jeanmarie ; Macera-Bloch, Lisa S. ; Harrison, Lawrence ; Kim, Kyung H. ; Korah, Reju M. / Tumor necrosis factor alpha and interleukin 1β up-regulate gastric mucosal Fas antigen expression in Helicobacter pylori infection. In: Infection and Immunity. 2000 ; Vol. 68, No. 3. pp. 1189-1195.
@article{09f1d65d3b8e418dafad19ede63444f7,
title = "Tumor necrosis factor alpha and interleukin 1β up-regulate gastric mucosal Fas antigen expression in Helicobacter pylori infection",
abstract = "Fas-mediated gastric mucosal apoptosis is gaining attention as a cause of tissue damage due to Helicobacter pylori infection. We explored the effects of H. pylori directly, and the effects of the inflammatory environment established subsequent to H. pylori infection, on Fas-mediated apoptosis in a nontransformed gastric mucosal cell line (RGM-1). Exposure to H. pylori-activated peripheral blood mononuclear cells (PBMCs), but not H. pylori itself, induced Fas antigen (Fas Ag) expression, indicating a Fas- regulatory role for inflammatory cytokines in this system. Of various inflammatory cytokines tested, only interleukin 1β and tumor necrosis factor alpha induced Fas Ag expression, and removal of either of these from the conditioned medium abrogated the response. When exposed to Fas ligand, RGM-1 cells treated with PBMC-conditioned medium underwent massive and rapid cell death, interestingly, with a minimal effect on total cell numbers early on. Cell cycle analysis revealed a substantial increase in S phase cells among cells exposed to Fas ligand, suggesting an increase in their proliferative response. Taken together, these data indicate that the immune environment secondary to H. pylori infection plays a critical role in priming gastric mucosal cells to undergo apoptosis or to proliferate based upon their Fas Ag status.",
author = "Jeanmarie Houghton and Macera-Bloch, {Lisa S.} and Lawrence Harrison and Kim, {Kyung H.} and Korah, {Reju M.}",
year = "2000",
month = "3",
day = "4",
doi = "10.1128/IAI.68.3.1189-1195.2000",
language = "English (US)",
volume = "68",
pages = "1189--1195",
journal = "Infection and Immunity",
issn = "0019-9567",
publisher = "American Society for Microbiology",
number = "3",

}

Tumor necrosis factor alpha and interleukin 1β up-regulate gastric mucosal Fas antigen expression in Helicobacter pylori infection. / Houghton, Jeanmarie; Macera-Bloch, Lisa S.; Harrison, Lawrence; Kim, Kyung H.; Korah, Reju M.

In: Infection and Immunity, Vol. 68, No. 3, 04.03.2000, p. 1189-1195.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Tumor necrosis factor alpha and interleukin 1β up-regulate gastric mucosal Fas antigen expression in Helicobacter pylori infection

AU - Houghton, Jeanmarie

AU - Macera-Bloch, Lisa S.

AU - Harrison, Lawrence

AU - Kim, Kyung H.

AU - Korah, Reju M.

PY - 2000/3/4

Y1 - 2000/3/4

N2 - Fas-mediated gastric mucosal apoptosis is gaining attention as a cause of tissue damage due to Helicobacter pylori infection. We explored the effects of H. pylori directly, and the effects of the inflammatory environment established subsequent to H. pylori infection, on Fas-mediated apoptosis in a nontransformed gastric mucosal cell line (RGM-1). Exposure to H. pylori-activated peripheral blood mononuclear cells (PBMCs), but not H. pylori itself, induced Fas antigen (Fas Ag) expression, indicating a Fas- regulatory role for inflammatory cytokines in this system. Of various inflammatory cytokines tested, only interleukin 1β and tumor necrosis factor alpha induced Fas Ag expression, and removal of either of these from the conditioned medium abrogated the response. When exposed to Fas ligand, RGM-1 cells treated with PBMC-conditioned medium underwent massive and rapid cell death, interestingly, with a minimal effect on total cell numbers early on. Cell cycle analysis revealed a substantial increase in S phase cells among cells exposed to Fas ligand, suggesting an increase in their proliferative response. Taken together, these data indicate that the immune environment secondary to H. pylori infection plays a critical role in priming gastric mucosal cells to undergo apoptosis or to proliferate based upon their Fas Ag status.

AB - Fas-mediated gastric mucosal apoptosis is gaining attention as a cause of tissue damage due to Helicobacter pylori infection. We explored the effects of H. pylori directly, and the effects of the inflammatory environment established subsequent to H. pylori infection, on Fas-mediated apoptosis in a nontransformed gastric mucosal cell line (RGM-1). Exposure to H. pylori-activated peripheral blood mononuclear cells (PBMCs), but not H. pylori itself, induced Fas antigen (Fas Ag) expression, indicating a Fas- regulatory role for inflammatory cytokines in this system. Of various inflammatory cytokines tested, only interleukin 1β and tumor necrosis factor alpha induced Fas Ag expression, and removal of either of these from the conditioned medium abrogated the response. When exposed to Fas ligand, RGM-1 cells treated with PBMC-conditioned medium underwent massive and rapid cell death, interestingly, with a minimal effect on total cell numbers early on. Cell cycle analysis revealed a substantial increase in S phase cells among cells exposed to Fas ligand, suggesting an increase in their proliferative response. Taken together, these data indicate that the immune environment secondary to H. pylori infection plays a critical role in priming gastric mucosal cells to undergo apoptosis or to proliferate based upon their Fas Ag status.

UR - http://www.scopus.com/inward/record.url?scp=0033975683&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0033975683&partnerID=8YFLogxK

U2 - 10.1128/IAI.68.3.1189-1195.2000

DO - 10.1128/IAI.68.3.1189-1195.2000

M3 - Article

C2 - 10678925

AN - SCOPUS:0033975683

VL - 68

SP - 1189

EP - 1195

JO - Infection and Immunity

JF - Infection and Immunity

SN - 0019-9567

IS - 3

ER -