Bovine colostrum inhibits nuclear factor kappaB-mediated proinflammatory cytokine expression in intestinal epithelial cells.
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)-1beta with or without bovine colostrum. The effects of colostrum on nuclear factor kappaB (NF-kappaB) 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-kappaB-dependent reporter gene assay and an electrophoretic mobility shift assay. Furthermore, we assessed the expression levels of inhibitor protein of NF-kappaB-alpha, cyclooxygenase-2, and p65 proteins by Western blotting. Bovine colostrum significantly inhibited IL-1beta-induced IL-8 and intracellar adhesion molecule-1 mRNA expression. Moreover, it suppressed IL-1beta-induced NF-kappaB activation, including NF-kappaB 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-kappaB-alpha degradation, and blocked translocation of p65 into the nucleus. These data demonstrated that bovine colostrum might protect against IEC inflammation by inhibiting the NF-kappaB pathway, suggesting colostrum has a therapeutic potential for intestinal inflammation.
An
Min Ji
MJ
Department of Internal Medicine and Institute of Gastroenterology, Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.
Cheon
Jae Hee
JH
Kim
Seung Won
SW
Park
Jae Jun
JJ
Moon
Chang Mo
CM
Han
Song Yi
SY
Kim
Eun Soo
ES
Kim
Tae Il
TI
Kim
Won Ho
WH
D021581:Active Transport, Cell Nucleus; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002417:Cattle; D015815:Cell Adhesion Molecules / Q000037:antagonists & inhibitors; D002470:Cell Survival / Q000187:drug effects; D003126:Colostrum; D051546:Cyclooxygenase 2 / Q000378:metabolism; D052246:Cyclooxygenase 2 Inhibitors / Q000494:pharmacology; D004847:Epithelial Cells / Q000187:drug effects*; D005260:Female; D015870:Gene Expression / Q000187:drug effects; D019073:HT29 Cells; D006801:Humans; D020672:I-kappa B Proteins / Q000037:antagonists & inhibitors; D007249:Inflammation / Q000235:genetics / Q000378:metabolism*; D053583:Interleukin-1beta / Q000037:antagonists & inhibitors*; D016209:Interleukin-8 / Q000037:antagonists & inhibitors*; D007422:Intestines / Q000166:cytology / Q000187:drug effects; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B / Q000037:antagonists & inhibitors*; D012333:RNA, Messenger / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D051996:Transcription Factor RelA / Q000037:antagonists & inhibitors
D000893:Anti-Inflammatory Agents; D015815:Cell Adhesion Molecules; D052246:Cyclooxygenase 2 Inhibitors; D020672:I-kappa B Proteins; D053583:Interleukin-1beta; D016209:Interleukin-8; D016328:NF-kappa B; C000606204:NFKBIA protein, human; D012333:RNA, Messenger; D051996:Transcription Factor RelA; D000072000:NF-KappaB Inhibitor alpha; D051546:Cyclooxygenase 2