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The immune imbalance of Treg/Th17 in secretory otitis media patients may be related to PI3K/Akt/mTOR signaling activation in the middle ear mucosa
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  • Zhiyuan Tang,
  • Xianhai Zeng,
  • Juanjuan Li,
  • Hua Zhang,
  • Hancheng Wu,
  • Suqing Zhuang,
  • Yiqing Zheng
Zhiyuan Tang
Shenzhen Longgang E.N.T hospital & Shenzhen Key Laboratory of E.N.T, Institute of E.N.T
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Xianhai Zeng
Shenzhen Longgang E.N.T hospital & Shenzhen Key Laboratory of E.N.T, Institute of E.N.T
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Juanjuan Li
Shenzhen Longgang E.N.T hospital & Shenzhen Key Laboratory of E.N.T, Institute of E.N.T
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Hua Zhang
Shenzhen Longgang E.N.T hospital & Shenzhen Key Laboratory of E.N.T, Institute of E.N.T
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Hancheng Wu
Shenzhen Longgang E.N.T hospital & Shenzhen Key Laboratory of E.N.T, Institute of E.N.T
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Suqing Zhuang
Shenzhen Longgang E.N.T hospital & Shenzhen Key Laboratory of E.N.T, Institute of E.N.T
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Yiqing Zheng
Sun Yat-Sen Memorial Hospital
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Abstract

Objective: To assess whether secretory otitis media may be caused by immune imbalance of Treg/Th17 mediated by PI3K/Akt/mTOR signaling, so as to find new therapeutic target. Methods: IL-17, TGF- and IL-6, IL-10 and Th17 cytokines were detected in peripheral blood of OME patients (PC group) and healthy people (NC group) by ELISA. The expression of ROR t mRNA and Foxp3mRNA in PBMC was detected by RT-PCR. OME rat model was established and the changes of lymphocytes in middle ear mucosa and spleen and PI3K/Akt/mTOR signaling in middle ear mucosa were detected by HE staining, IHC, WB and flow cytometry. Results: The immune imbalance of Treg/Th17 in secretory otitis media (OME) was confirmed by the expression of cytokines in OME serum and analysis of ROR T and Foxp3 mRNA which was Th17 and Treg specific transcription respectively. OME rat model further confirmed that Treg/Th17 imbalance could lead to OME as demonstrated by staining of MIDDLE ear mucosa and expression of ROR T and Foxp3. PI3K, Akt, and mTOR proteins were expressed in the MIDDLE ear mucosa of OME group and CON group, respectively. Compared with CON group, the expression of P-MTOR and P-PI3K proteins in the middle ear mucosa of OME group was significantly increased. Conclusions: Treg/Th17 imbalances are found in OME patients and OME animal model and the pathogenic mechanism may be due to systemic abnormal immune response, activated PI3K/Akt/mTOR signaling, abnormal T cell differentiation, leading to middle ear mucosal hyperemia, edema and subsequent occurrence of OME.