Premium
Claudin 2 protein expression is increased in human necrotizing enterocolitis
Author(s) -
De Plaen Isabelle G,
Chou Pauline M,
Weber Christopher R
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1162.1
Subject(s) - occludin , claudin , crypt , immunohistochemistry , necrotizing enterocolitis , small intestine , tight junction , enterocolitis , pathology , biology , andrology , microbiology and biotechnology , medicine , endocrinology
We have previously shown that an increase in intestinal permeability precedes NEC in a neonatal mouse model and this permeability change is associated with increased expression of claudin 2 and internalization of claudins 2, 4 and 7 and occludin. Whether these proteins are altered in human NEC remains unknown. In this study, we examined the expression of claudin 2, 4, occludin, and ZO‐1 in control and NEC tissues by immunohistochemistry. Samples from 11 colon controls, 10 colon NEC, 9 small intestine controls and 10 small intestine NEC cases were used for the study. Staining intensity was scored semi‐quantitatively from 0 to 3 by two separate investigators and average scores determined. Claudin 2 expression was low in the colon of control tissues (crypt expression 1.0 ± 0.1, surface expression 1.0 ± 0.2). In small intestinal tissue, there was a decreasing gradient of expression from the crypts to the surface (crypt expression 1.5 ± 0.3 vs surface expression 0.7 ± 0.1, P <0.05). Compared to control, the expression of claudin 2 was dramatically increased in the crypts of NEC colon (2 ± 0.2 vs 1.0 ± 0.1, p<0.001) and NEC small intestine (2.3 ± 0.2 vs. 1.5 ± 0.3, P <0.05. In contrast, occludin and ZO‐1 expression and distribution were similar in control and NEC tissues. In conclusion, the expression of claudin 2 but not of 4, occludin, and ZO‐1 is increased in human NEC. Alteration in claudin 2 protein might play a role in NEC pathogenesis.