Yingge Wang1,2, Guohao Chen1,2, Chang Lin1,2, Ying Chen1,2, Min Huang1,2, Shengnan Ye3,4. 1. Department of Otorhinolaryngology, The First Affiliated Hospital of Fujian Medical University, 350000, Fuzhou, Fujian, China. 2. Fujian Institute of Otorhinolaryngology, The First Affiliated Hospital, Fujian Medical University, 350000, Fuzhou, Fujian, China. 3. Department of Otorhinolaryngology, The First Affiliated Hospital of Fujian Medical University, 350000, Fuzhou, Fujian, China. Yeshengnan63@qq.com. 4. Fujian Institute of Otorhinolaryngology, The First Affiliated Hospital, Fujian Medical University, 350000, Fuzhou, Fujian, China. Yeshengnan63@qq.com.
Abstract
BACKGROUND: The typical characteristic of pediatric obstructive sleep apnea syndrome (OSAS) is systemic inflammation and adenotonsillar hypertrophy (ATH), but the inflammatory markers and mechanism of adenotonsillar proliferation are unclear. METHODS: IHC, qPCR, and western blotting were used to identify the expression of CHI3L1 in the tonsils of children with OSAS. The primary tonsil lymphocytes (PTLCs) from children with OSAS were cultured and recombinant human CHI3L1 protein was added to culture media. After the stimulation with CHI3L1 protein of different concentrations and time points, lymphocyte proliferation was assessed by CCK-8 kits and flow cytometry. The activation of ERK1/2 and the effects on the proliferation of PTLCs were observed by western blotting. RESULTS: The expression of CHI3L1 was higher in the OSAS group than in the PS group. CHI3L1 (100 ng/mmol for 24 h) resulted in a significant increase in the proliferation rate. The ERK1/2 activator (PMA) promoted the proliferation of PTLCs and inhibitor AG126 significantly inhibited proliferation. CONCLUSIONS: CHI3L1 can promote the proliferation of tonsil lymphocytes via ERK1/2 pathways. This result indicates that CHI3L1 may play an important role in the pathogenesis of OSAS in children. Inhibition of CHI3L1 or ERK1/2 may be potential therapeutic targets for CHI3L1-induced proliferation in childhood OSAS. IMPACT: CHI3L1 may be an inflammatory marker in childhood OSAS. CHI3L1 can promote the proliferation of PTLCs in a concentration and time-dependent condition. CHI3L1 can promote the proliferation of tonsil lymphocytes via ERK1/2 pathways.
BACKGROUND: The typical characteristic of pediatric obstructive sleep apnea syndrome (OSAS) is systemic inflammation and adenotonsillar hypertrophy (ATH), but the inflammatory markers and mechanism of adenotonsillar proliferation are unclear. METHODS: IHC, qPCR, and western blotting were used to identify the expression of CHI3L1 in the tonsils of children with OSAS. The primary tonsil lymphocytes (PTLCs) from children with OSAS were cultured and recombinant human CHI3L1 protein was added to culture media. After the stimulation with CHI3L1 protein of different concentrations and time points, lymphocyte proliferation was assessed by CCK-8 kits and flow cytometry. The activation of ERK1/2 and the effects on the proliferation of PTLCs were observed by western blotting. RESULTS: The expression of CHI3L1 was higher in the OSAS group than in the PS group. CHI3L1 (100 ng/mmol for 24 h) resulted in a significant increase in the proliferation rate. The ERK1/2 activator (PMA) promoted the proliferation of PTLCs and inhibitor AG126 significantly inhibited proliferation. CONCLUSIONS: CHI3L1 can promote the proliferation of tonsil lymphocytes via ERK1/2 pathways. This result indicates that CHI3L1 may play an important role in the pathogenesis of OSAS in children. Inhibition of CHI3L1 or ERK1/2 may be potential therapeutic targets for CHI3L1-induced proliferation in childhood OSAS. IMPACT: CHI3L1 may be an inflammatory marker in childhood OSAS. CHI3L1 can promote the proliferation of PTLCs in a concentration and time-dependent condition. CHI3L1 can promote the proliferation of tonsil lymphocytes via ERK1/2 pathways.