Phospholipase A2 activating protein and idiopathic inflammatory bowel disease

Johnny Peterson, W. D. Dickey, S. S. Saini, W. Gourley, G. R. Klimpel, Ashok Chopra

Research output: Contribution to journalArticle

33 Citations (Scopus)

Abstract

Background - Crohn's disease and ulcerative colitis are idiopathic inflammatory bowel diseases (IBD) involving synthesis of eicosanoids from arachidonic acid (AA), which is released from membrane phospholipids by phospholipase A2 (PLA2). A potentially important regulator of the production of these mediators is a protein activator of PLA2, referred to as PLA2 activating protein (PLAP). Aims - The purpose of this investigation was to discover if PLAP values might be increased in the inflamed intestinal tissue of patients with IBD and in intestinal tissue of mice with colitis. Patients - Biopsy specimens were taken from patients with ulcerative colitis and Crohn's disease undergoing diagnostic colonoscopy, and normal colonic mucosa was obtained from patients without IBD after surgical resection. Methods - Immunocytochemistry with affinity purified antibodies to PLAP synthetic peptides was used to locate PLAP antigen in sections of intestinal biopsy specimens from IBD patients compared with that of normal intestinal tissue. Northern blot analysis with a murine [32P] labelled plap cDNA probe was performed on RNA extracted from the colons of mice fed dextran sulphate sodium (DSS) and cultured HT-29 cells exposed to lipopolysaccharide (LPS). Results - PLAP antigen was localised predominantly within monocytes and granulocytes in intestinal tissue sections from IBD patients, and additional deposition of extracellular PLAP antigen was associated with blood vessels and oedema fluid in the inflamed tissues. In contrast, tissue sections from normal human intestine were devoid of PLAP reactive antigen, except for some weak cytoplasmic reaction of luminal intestinal epithelial cells. Similarly, colonic tissue from DSS treated mice contained an increased amount of PLAP antigen compared with controls. The stroma of the lamina propria of the colonic mucosa from the DSS treated mice reacted intensely with antibodies to PLAP synthetic peptides, while no reaction was observed with control mouse colons. These data were supported by northern analysis which showed that PLAP mRNA was increased in the colons of DSS treated mice and cultured HT-29 cells exposed to LPS. Conclusions - As PLAP values were increased in the intestinal mucosa of IBD patients and mice with colitis, as well as in LPS treated cultured HT-29 cells, a role was postulated for PLAP in increasing PLA2 activity, which leads to the increased synthesis of eicosanoids in intestinal tissues of patients with these inflammatory diseases.

Original languageEnglish (US)
Pages (from-to)698-704
Number of pages7
JournalGut
Volume39
Issue number5
StatePublished - 1996

Fingerprint

Inflammatory Bowel Diseases
Dextran Sulfate
Proteins
HT29 Cells
Phospholipases A2
Antigens
Lipopolysaccharides
Cultured Cells
Colon
Mucous Membrane
Eicosanoids
Colitis
Ulcerative Colitis
Crohn Disease
phospholipase A2-activating protein
Biopsy
Peptides
Antibody Affinity
Colonoscopy
Intestinal Mucosa

Keywords

  • Cytokines
  • Dextran sulphate sodium
  • Immunocytochemistry
  • Inflammation
  • Murine colitis
  • PLA
  • PLAP

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Peterson, J., Dickey, W. D., Saini, S. S., Gourley, W., Klimpel, G. R., & Chopra, A. (1996). Phospholipase A2 activating protein and idiopathic inflammatory bowel disease. Gut, 39(5), 698-704.

Phospholipase A2 activating protein and idiopathic inflammatory bowel disease. / Peterson, Johnny; Dickey, W. D.; Saini, S. S.; Gourley, W.; Klimpel, G. R.; Chopra, Ashok.

In: Gut, Vol. 39, No. 5, 1996, p. 698-704.

Research output: Contribution to journalArticle

Peterson, J, Dickey, WD, Saini, SS, Gourley, W, Klimpel, GR & Chopra, A 1996, 'Phospholipase A2 activating protein and idiopathic inflammatory bowel disease', Gut, vol. 39, no. 5, pp. 698-704.
Peterson J, Dickey WD, Saini SS, Gourley W, Klimpel GR, Chopra A. Phospholipase A2 activating protein and idiopathic inflammatory bowel disease. Gut. 1996;39(5):698-704.
Peterson, Johnny ; Dickey, W. D. ; Saini, S. S. ; Gourley, W. ; Klimpel, G. R. ; Chopra, Ashok. / Phospholipase A2 activating protein and idiopathic inflammatory bowel disease. In: Gut. 1996 ; Vol. 39, No. 5. pp. 698-704.
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abstract = "Background - Crohn's disease and ulcerative colitis are idiopathic inflammatory bowel diseases (IBD) involving synthesis of eicosanoids from arachidonic acid (AA), which is released from membrane phospholipids by phospholipase A2 (PLA2). A potentially important regulator of the production of these mediators is a protein activator of PLA2, referred to as PLA2 activating protein (PLAP). Aims - The purpose of this investigation was to discover if PLAP values might be increased in the inflamed intestinal tissue of patients with IBD and in intestinal tissue of mice with colitis. Patients - Biopsy specimens were taken from patients with ulcerative colitis and Crohn's disease undergoing diagnostic colonoscopy, and normal colonic mucosa was obtained from patients without IBD after surgical resection. Methods - Immunocytochemistry with affinity purified antibodies to PLAP synthetic peptides was used to locate PLAP antigen in sections of intestinal biopsy specimens from IBD patients compared with that of normal intestinal tissue. Northern blot analysis with a murine [32P] labelled plap cDNA probe was performed on RNA extracted from the colons of mice fed dextran sulphate sodium (DSS) and cultured HT-29 cells exposed to lipopolysaccharide (LPS). Results - PLAP antigen was localised predominantly within monocytes and granulocytes in intestinal tissue sections from IBD patients, and additional deposition of extracellular PLAP antigen was associated with blood vessels and oedema fluid in the inflamed tissues. In contrast, tissue sections from normal human intestine were devoid of PLAP reactive antigen, except for some weak cytoplasmic reaction of luminal intestinal epithelial cells. Similarly, colonic tissue from DSS treated mice contained an increased amount of PLAP antigen compared with controls. The stroma of the lamina propria of the colonic mucosa from the DSS treated mice reacted intensely with antibodies to PLAP synthetic peptides, while no reaction was observed with control mouse colons. These data were supported by northern analysis which showed that PLAP mRNA was increased in the colons of DSS treated mice and cultured HT-29 cells exposed to LPS. Conclusions - As PLAP values were increased in the intestinal mucosa of IBD patients and mice with colitis, as well as in LPS treated cultured HT-29 cells, a role was postulated for PLAP in increasing PLA2 activity, which leads to the increased synthesis of eicosanoids in intestinal tissues of patients with these inflammatory diseases.",
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AU - Peterson, Johnny

AU - Dickey, W. D.

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AU - Gourley, W.

AU - Klimpel, G. R.

AU - Chopra, Ashok

PY - 1996

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N2 - Background - Crohn's disease and ulcerative colitis are idiopathic inflammatory bowel diseases (IBD) involving synthesis of eicosanoids from arachidonic acid (AA), which is released from membrane phospholipids by phospholipase A2 (PLA2). A potentially important regulator of the production of these mediators is a protein activator of PLA2, referred to as PLA2 activating protein (PLAP). Aims - The purpose of this investigation was to discover if PLAP values might be increased in the inflamed intestinal tissue of patients with IBD and in intestinal tissue of mice with colitis. Patients - Biopsy specimens were taken from patients with ulcerative colitis and Crohn's disease undergoing diagnostic colonoscopy, and normal colonic mucosa was obtained from patients without IBD after surgical resection. Methods - Immunocytochemistry with affinity purified antibodies to PLAP synthetic peptides was used to locate PLAP antigen in sections of intestinal biopsy specimens from IBD patients compared with that of normal intestinal tissue. Northern blot analysis with a murine [32P] labelled plap cDNA probe was performed on RNA extracted from the colons of mice fed dextran sulphate sodium (DSS) and cultured HT-29 cells exposed to lipopolysaccharide (LPS). Results - PLAP antigen was localised predominantly within monocytes and granulocytes in intestinal tissue sections from IBD patients, and additional deposition of extracellular PLAP antigen was associated with blood vessels and oedema fluid in the inflamed tissues. In contrast, tissue sections from normal human intestine were devoid of PLAP reactive antigen, except for some weak cytoplasmic reaction of luminal intestinal epithelial cells. Similarly, colonic tissue from DSS treated mice contained an increased amount of PLAP antigen compared with controls. The stroma of the lamina propria of the colonic mucosa from the DSS treated mice reacted intensely with antibodies to PLAP synthetic peptides, while no reaction was observed with control mouse colons. These data were supported by northern analysis which showed that PLAP mRNA was increased in the colons of DSS treated mice and cultured HT-29 cells exposed to LPS. Conclusions - As PLAP values were increased in the intestinal mucosa of IBD patients and mice with colitis, as well as in LPS treated cultured HT-29 cells, a role was postulated for PLAP in increasing PLA2 activity, which leads to the increased synthesis of eicosanoids in intestinal tissues of patients with these inflammatory diseases.

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