Elevated expression of iNOS mRNA and protein in coeliac disease

Clin Chim Acta. 2005 Jun;356(1-2):134-42. doi: 10.1016/j.cccn.2005.01.029. Epub 2005 Apr 7.

Abstract

Background: The role of nitric oxide synthase (NOS) in the pathophysiology of coeliac disease (CD) was investigated.

Methods: We examined mRNA (reverse transcription multiplex polymerase chain reaction) and protein expression (Western blotting) of i,e and nNOS in enterocytes isolated from the duodenum of patients with untreated CD (n=22) and iron deficiency anaemia (IDA, n=22). Expression of IL1beta and TNFalpha, two pivotal "NOS-controlling" cytokines, was also studied.

Results: Enterocytes from both patient groups were negative for eNOS and TNF(alpha) message but positive for n and iNOS. nNOS gene expression was not statistically different between groups (158.38+/-29.11% vs. 114.95+/-24.17%, IDA vs. CD, p=0.07, Mann-Whitney U). iNOS expression was higher in patients with CD when compared to patients with IDA (96.95+/-17.82% vs. 48.76+/-8.07%, p<0.006). Low levels of IL1beta mRNA (15.66+/-3.70%) were detected in nine samples-all of these samples were isolated from patients with CD representing a positive result in 40% of coeliac patients. In support of these observations, patients with CD expressed more iNOS protein than those with IDA (159.7+/-14.9% vs. 69.8+/-20%, p<0.05).

Conclusion: These results suggest that iNOS could be an important mediator in coeliac disease. Expression of this regulatory protein may be under the control of IL1beta.

MeSH terms

  • Adult
  • Aged
  • Anemia, Iron-Deficiency / enzymology
  • Blotting, Western
  • Celiac Disease / enzymology*
  • Electrophoresis
  • Enterocytes / enzymology
  • Female
  • Humans
  • Interleukin-1 / genetics
  • Male
  • Middle Aged
  • Nitric Oxide Synthase / analysis
  • Nitric Oxide Synthase / genetics*
  • Nitric Oxide Synthase Type II
  • Polymerase Chain Reaction
  • RNA, Messenger / analysis*

Substances

  • Interleukin-1
  • RNA, Messenger
  • NOS2 protein, human
  • Nitric Oxide Synthase
  • Nitric Oxide Synthase Type II