Cow’s Milk Protein May Induce Allergy and Inflammation in Intestinal Epithelial Cells Through Regulating HOTAIR Expression and NF-κB Signaling Pathway

Abstract

Background: Cow’s milk protein allergy (CMPA) is associated with activation of proinflammatory signaling pathways and overexpression of inflammatory mediators. Long noncoding RNA (LncRNA) HOX transcript antisense intergenic RNA (HOTAIR) is a LncRNA, which is involved in the occurrence and development of many biological processes and diseases. HOTAIR can prevent necrotizing enterocolitis. This study aims to explore the effect of milk protein on NCM-460 cells and its mechanism of action with HOTAIR.

Methods: NCM-460 cells were induced by cow’s milk protein to establish in vitro cell models. CCK-8 and EdU staining were used for evaluating the effects of cow’s milk protein on the viability and proliferation. ELISA was used for comparing the levels of inflammatory cytokines. TUNEL staining was conducted for evaluating the apoptosis. Expression levels of HOTAIR were detected by RT-qPCR. The expression of NF-κB signaling pathway–related molecules in cells was explored to evaluate the mechanism of HOTAIR in improving ALI.

Results: Cow’s milk protein decreased the viability NCM-460 cells and also decreased the expression of HOTAIR. Moreover, it can induce the antiproliferative and proapoptotic effects on NCM-460 cells, and overexpression of LncRNA HOTAIR can partially reverse the effects of cow’s milk protein. In addition, overexpression of LncRNA HOTAIR reversed the effects of cow’s milk protein on NF-κB signaling.

Conclusions: Cow’s milk protein may induce the allergy and inflammation in intestinal epithelial cells through regulating HOTAIR expression and NF-κB signaling pathways.