Phospholipid turnover in the inflamed intestinal mucosa: Arachidonic acid-rich phosphatidyl/plasmenyl-ethanolamine in the mucosa in inflammatory bowel disease
H. Morita et al., Phospholipid turnover in the inflamed intestinal mucosa: Arachidonic acid-rich phosphatidyl/plasmenyl-ethanolamine in the mucosa in inflammatory bowel disease, J GASTRO, 34(1), 1999, pp. 46-53
Cytosolic phospholipase A2 (PLase A2) is activated by low Ca2+ concentratio
ns and translocates from thp cytosol tn the cell membrane releasing arachid
onic acid: the arachidonic acid cascade then leads to the production of man
y inflammatory mediators. The aim of this study, accordingly, was to invest
igate the role of phospholipid metabolism in the intestinal mucosa in infla
mmatory bowel disease (IBD). Surgically resected specimens from patients wi
th Crohn's disease (CD), ulcerative colitis (UC), and colrectal cancer (non
cancerous tissue; as a control) were submitted to phospholipid analysis and
a PLase A2 assay, which measures the degradation of endogenous mucosal pho
spholipids. A high percentage of plasmenylethanolamine (plas.E) was detecte
d in the glycerophospholipid fraction of CD mucosa. The arachidonic acid co
ntent of the phosphatidylethanolamine plus plas.E subfraction was higher in
inflamed than in intact mucosa in CD. PLaseA2 activity, resulting in lysop
hosphatidyl ethanolamine production, was detected only in inflamed mucosa f
rom CD and UC patients, but not in normal mucosa from controls. PLaseA2 act
ivity was highest in moderately inflamed mucosa adjacent to a severely ulce
rated area. The PLasepA2 that reacts with endogenous phosphatidylcholine PL
aseA2 (PC) to form lysoPC was found irrespective of the presence of inflamm
ation. The PLaseA2 that reacts with ethanolamine-containing phospholipids i
s more closely related to inflammation than other PLaseA2 isoenzymes in IBD
mucosa.