Immune‐related gene expression profiles of hypothermia adipocytes: Implications for Bell's palsy

Abstract

Objective To identify immune‐related gene expression profiles of adipocytes under low temperatures with RNA sequencing as a model for Bell's palsy implications. Methods Adipocytes were harvested from the white adipose tissue of male Sprague‐Dawley rats and cultured under different acute‐grade cold exposure conditions of 30, 20, and 10°C, and their genomes were sequenced for RNA sequencing analysis. The differentially expressed genes (DEGs) were validated with reverse transcription polymerase chain reaction. Results In total, 55 (35 upregulated and 20 downregulated), 121 (76 upregulated and 45 downregulated), and 92 (64 upregulated and 28 downregulated) DEGs were identified under 30, 20, and 10°C compared with the control, respectively. KEGG and GO analysis revealed that the DEGs were considerably enriched in immune‐related pathways (leukocyte transendothelial migration and platelet activation) and infection (bacterial invasion of epithelial cells and Salmonella infection). The levels of key inflammatory chemokines (CSF1, CXCL1, CCL2, and CCL7) were enhanced after cold exposure. Conclusion These findings broaden our understanding of the immune responses to cold exposure in adipocytes. The molecular profiles of adipocyte immune function will help clarify the potential mechanism impacting myelin, which might contribute to the development of strategies to control Bell's palsy.

Influence of cold-stimulated adipocyte supernatant on the expression of adhesion-related molecules in Schwann cell line

“…This finding suggests that temperature changes can affect the expression of adhesion molecules in Schwann cells. In conclusion, adipocytes stimulated by low temperatures may secrete adipokines [ 17 ], which interfere with the function of adhesion molecules in Schwann cells.…”

“…Although the etiology of Bell's palsy is unclear, environmental factors such as atmospheric pressure and drastic temperature changes may play a key role in the occurrence of Bell's palsy [ 1 , 7 ]. Adipocytes subjected to cold exposure exhibit upregulated inflammatory chemokine expression [ 17 ], which dysregulates the adipose tissue immune microenvironment, resulting in possible pathological changes in the myelin sheath. In the present study, we aimed to explore the effect of cold-exposed adipocytes (adipokines) on Schwann cell adhesion factors.…”

“…As facial cold exposure is a risk factor for Bell's palsy, the development of Bell's palsy is associated with metabolic and inflammatory changes in subcutaneous adipose tissue. Cold exposure can cause the upregulation of inflammatory chemokines in adipocytes [ 17 ]. However, whether changes in Schwann cell microenvironment resulting from the effects of cold exposure on adipocytes alter Schwann cell function, is not known.…”

“…This temperature was selected based on pre-experimental grouping. In addition, 30 °C is a critical point in temperature grading, as this point allows the temperature around the facial nerves to remain relatively stable despite changes in ambient temperature, owing to the protective effects of facial adipose tissue [ 17 ]. We investigated how adipocytes subjected to cold exposure affect the expression profile of adhesion molecules in Schwann cells, in order to provide new insights into the etiology of Bell's palsy.…”