Çмú´ëȸ ¹ßÇ¥ ¿¬Á¦ ÃÊ·Ï
D - -930

Çмú´ëȸ ¹ßÇ¥ ¿¬Á¦ ÃÊ·Ï

Á¢¼ö¹øÈ£ - 270059    5 
SCGB1C1 IS A KEY REGULATOR RESPONSIBLE FOR SUPPRESSING ALLERGIC AIRWAY INFLAMMATION THROUGH ADIPOSE STEM CELLS-DERIVED EXTRACELLULAR VESICLES
1DEPARTMENT OF OTORHINOLARYNGOLOGY AND BIOMEDICAL RESEARCH INSTITUTE, PUSAN NATIONAL UNIVERSITY HOSPITAL, BUSAN, REPUBLIC OF KOREA
SUNG-DONG KIM1, SHIN AE KANG2, SUE-JEAN MUN3, HAK SUN YU2, HWAN-JUNG ROH3, KYU-SUP CHO1
¸ñÀû: The nanosized vesicles secreted from the various cell types into the surrounding extracellular space are called extracellular vesicles (EVs). Although stem cell-derived extracellular vesicles (EVs) are known to have immunomodulatory effects in asthmatic mice, the major genes responsible for suppressing allergic airway inflammation have not been well documented. This study aims to evaluate the immunomodulatory effects of SCGB1C1 on asthmatic mouse model. ¹æ¹ý:C57BL / 6 mice were sensitized to OVA using intraperitoneal injection and intranasal challenged with OVA.To evaluate the effect of SCGB1C1 on allergic airway inflammation, 5¥ìg/50¥ìl of SCGB1C1 were administrated intranasally before OVA challenge. We evaluated airway hyperresponsiveness (AHR), total immune cell and eosinophils in the bronchoalveolar lavage fluid (BALF), lung histology, serum immunoglobulin, cytokine profiles of BALF and lung draining lymph nodes (LLN), and T cell populations in LLNs. °á°ú:Intranasal administration of SCGB1C1 significantly inhibited AHR, total inflammatory cells and eosinophils in BALF, eosinophilic inflammation in the lung, and serum allergen-specific IgE. SCGB1C1 significantly decreased IL-4 in the LLN and IL-5 in the BALF, but significantly increased IL-10 and TGF-¥â in the BALF. Furthermore, SCGB1C1 treatment notably increased the populations of CD4+CD25+Foxp3+ T cells in asthmatic mice. °á·Ð:The induction of SCGB1C1 by ASCs-derived EVs provides a significant reduction of allergic airway inflammation and improvement of lung function through the induction of Treg expansion. Therefore, SCGB1C1 may be the major regulator responsible for suppressing allergic airway inflammation.


[µ¹¾Æ°¡±â]