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Necrotizing enterocolitis leads to increased intestinal permeability mediated through differential expression of tight junction proteins (650.7)
Author(s) -
Ravisankar Srikanth Sankar,
Tatum Rodney,
Garg Parvesh,
Shekhawat Prem,
Chen YanHua
Publication year - 2014
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.28.1_supplement.650.7
Subject(s) - tight junction , necrotizing enterocolitis , intestinal permeability , claudin , western blot , biology , transcellular , barrier function , medicine , andrology , enterocolitis , lumen (anatomy) , pathophysiology , pathology , endocrinology , microbiology and biotechnology , biochemistry , gene
Necrotizing enterocolitis (NEC) is a devastating disease with a prevalence of 7% in premature neonates weighing <1500 grams and an estimated death rate of 20‐30%. The precise etiology remains unknown and it is believed to be caused by a disturbance in the delicate balance of multiple pathophysiological factors. In this study, 4‐day old C57BL/6 mice pups were fed 50 µl of 33% Esbilac formula every 3 hours, asphyxiated twice daily (100% N 2 for 60 sec) followed by cold stress at 4°C for 10 min to induce NEC and study the tight junction (TJ) proteins. Dam‐fed pups from the same litter served as controls. Histopathology results revealed successful induction of NEC up to grade 2, where sloughing of the epithelial cells at the tips of the villi with mild villous necrosis was seen. Western blot showed decreased expression of claudin‐1 and an increased expression of claudin‐7 in the NEC intestines compared to control pups. The TJ permeability assay was performed by injecting biotin tracer into the lumen of the small intestine of both control and NEC pups. Biotin tracer diffused easily through the intercellular space of intestinal epithelial cells in NEC mice, suggesting loss of integrity of the TJ barrier function. We conclude that there is disruption of TJs mediated through differential regulation of TJ proteins in our NEC mouse model. Grant Funding Source : NIH