Bovine colostrum inhibits nuclear factor κB–mediated proinflammatory cytokine expression in intestinal epithelial cells☆
Abstract
Colostrum, a nutrient-rich fluid produced by female mammals immediately after giving birth, is loaded with several immune, growth, and tissue repair factors. However, it remains unknown whether bovine colostrum has anti-inflammatory effects on intestinal epithelial cells (IEC). In this study, we aimed to investigate the anti-inflammatory effects of colostrum on IEC and to elucidate its molecular mechanisms. Human colon cancer HT-29 cells were stimulated with interleukin (IL)–1β with or without bovine colostrum. The effects of colostrum on nuclear factor κB (NF-κB) signaling in HT-29 cells were examined using real-time reverse transcriptase–polymerase chain reaction detect IL-8 and intracellar adhesion molecule-1 mRNA expression using a NF-κB-dependent reporter gene assay and an electrophoretic mobility shift assay. Furthermore, we assessed the expression levels of inhibitor protein of NF-κB–α, cyclooxygenase-2, and p65 proteins by Western blotting. Bovine colostrum significantly inhibited IL-1β-induced IL-8 and intracellar adhesion molecule-1 mRNA expression. Moreover, it suppressed IL-1β-induced NF-κB activation, including NF-κB dependent reporter gene expression in a dose-dependent manner. Finally, Western blotting revealed that colostrum decreased the cyclooxygenase-2 protein expression level, inhibited inhibitor protein of NF-κB–α degradation, and blocked translocation of p65 into the nucleus. These data demonstrated that bovine colostrum might protect against IEC inflammation by inhibiting the NF-κB pathway, suggesting colostrum has a therapeutic potential for intestinal inflammation.
Abbreviations: NF-κB, nuclear factor κB, IEC, intestinal epithelial cell, IL, interleukin, FBS, fetal bovine serum, EMSA, electrophoretic mobility shift assay, IκB, inhibitor of NF-κB, COX-2, cyclooxygenase-2, ICAM-1, intracellar adhesion molecule 1, TNF, tumor necrosis factor
Keywords: Bovine, Colostrum, NF-κB, Intestinal, Inflammation, HT-29 cells
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☆ This study was supported by a grant from the Korea Healthcare Technology R&D Project, Ministry for Health, Welfare & Family Affairs, Republic of Korea (A084943).
PII: S0271-5317(09)00055-4
doi:10.1016/j.nutres.2009.03.011
© 2009 Elsevier Inc. All rights reserved.
