Proinflammatory cytokines and response to molds in mononuclear cells of patients with Meniere disease

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作者
Lidia Frejo
Alvaro Gallego-Martinez
Teresa Requena
Eduardo Martin-Sanz
Juan Carlos Amor-Dorado
Andres Soto-Varela
Sofia Santos-Perez
Juan Manuel Espinosa-Sanchez
Angel Batuecas-Caletrio
Ismael Aran
Jesus Fraile
Marcos Rossi-Izquierdo
Jose Antonio Lopez-Escamez
机构
[1] Department of Genomic Medicine- Centro de Genómica e Investigación Oncológica – Pfizer/Universidad de Granada/Junta de Andalucía (GENYO),Otology & Neurotology Group CTS495
[2] Hospital Universitario de Getafe,Department of Otolaryngology
[3] Hospital Can Misses Ibiza,Deparment of Otolaryngology
[4] Complexo Hospitalario Universitario,Division of Otoneurology, Department of Otorhinolaryngology
[5] Instituto de Investigación Biosanitaria ibs.GRANADA,Department of Otolaryngology
[6] Hospital Virgen de las Nieves,Otoneurology Unit, ENT Department
[7] University Hospital of Salamanca,Department of Otolaryngology
[8] IBSAL,Department of Otolaryngology
[9] Complexo Hospitalario de Pontevedra,Department of Otolaryngology
[10] Hospital Miguel Servet,Luxembourg Centre for Systems Biomedicine (LCSB)
[11] Hospital Universitario Lucus Augusti,undefined
[12] University of Luxembourg,undefined
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摘要
Epidemiological studies have found a higher prevalence of allergic symptoms and positive prick tests in patients with Meniere’s disease (MD); however the effect of allergenic extracts in MD has not been established. Thus, this study aims to determine the effect of Aspergillus and Penicillium stimulation in cytokine release and gene expression profile in MD. Patients with MD showed higher basal levels of IL-1β, IL-1RA, IL-6 and TNF-α when compared to healthy controls. We observed that IL-1β levels had a bimodal distribution suggesting two different subgroups of patients, with low and high basal levels of cytokines. Gene expression profile in peripheral blood mononuclear cells (PBMC) showed significant differences in patients with high and low basal levels of IL-1β. We found that both mold extracts triggered a significant release of TNF-α in MD patients, which were not found in controls. Moreover, after mold stimulation, MD patients showed a different gene expression profile in PBMC, according to the basal levels of IL-1β. The results indicate that a subset of MD patients have higher basal levels of proinflammatory cytokines and the exposure to Aspergillus and Penicillium extracts may trigger additional TNF-α release and contribute to exacerbate inflammation.
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