AlphaB-crystallin expression in celiac disease - a preliminary study

To investigate immunohistochemically alphaB-crystallin expression and distribution in biopsy sections of the small intestine of patients with celiac disease, and the relationship, if there is any, between the expression of this heat shock protein and the degree of mucosal atrophy.

Biopsy specimens of 22 subjects (12 celiac patients and 10 "normal" individuals) were investigated by immunoperoxidase screening procedures using monoclonal antibodies to detect the presence of alphaB-crystallin. Sections from each case were stained with hematoxylin and eosin to assess mucosal morphology.

The epithelial cells of the small intestine stained more intensively for alphaB-crystallin in patients with celiac disease than in "normal" patients. The quantity and degree of intensity of immunohistochemically demonstrable alphaB-crystallin and its intracellular distribution in the duodenal mucosa of the patients with celiac disease were closely related to the degree of villus atrophy. There was a strong correlation between the number of patients with celiac disease and percentage staining score of alphaB-crystallin per total score (Pearson's r = 0.754, p = 0.123). The mean percentage score per total score was 20% among the patients with celiac disease. On the other hand, there was a weak negative correlation between the number of normal controls and percentage score per total score (Pearson's r= -0.126, p = 0.437). The mean percentage score per total score was 4.6% among the normal controls. AlphaB-crystallin stained the supra-nuclear region of the enterocytes with a 75% sensitivity and 71% specificity.

AlphaB-crystallin, a stress response protein, is expressed in the small intestinal mucosa of patients with celiac disease, and the degree of mucosal atrophy compares significantly with the intensity of expression of alphaB-crystallin. We therefore conclude that an inappropriate stress response involving this heat-shock protein within the mucosa itself may be crucial as an initiating event in the architectural derangement of the mucosal damage associated with celiac disease.