Hostname: page-component-586b7cd67f-2brh9 Total loading time: 0 Render date: 2024-11-24T01:37:00.413Z Has data issue: false hasContentIssue false

Inflammatory cytokines and mononuclear cells in sudden sensorineural hearing loss

Published online by Cambridge University Press:  11 February 2019

S H Yoon
Affiliation:
Department of Otolaryngology, Chonnam National University Medical School, Gwangju, South Korea
M E Kim
Affiliation:
Department of Life Science, BK21-plus Research Team for Bioactive Control Technology, Department of Biology, College of Natural Science, Chosun University, Gwangju, South Korea
H Y Kim
Affiliation:
Department of Otolaryngology, Chonnam National University Medical School, Gwangju, South Korea
J S Lee*
Affiliation:
Department of Life Science, BK21-plus Research Team for Bioactive Control Technology, Department of Biology, College of Natural Science, Chosun University, Gwangju, South Korea
C H Jang*
Affiliation:
Department of Otolaryngology, Chonnam National University Medical School, Gwangju, South Korea
*
Author for correspondence: Dr Jun-Sik Lee, Department of Life Science, BK 21-plus Research Team for Bioactive Control Technology, Biology, College of Natural Science, Chosun University, Gwangju, South Korea E-mail: [email protected] Fax: +822308850
Dr Chul Ho Jang, Department of Otolaryngology, Chonnam National University Hospital, Hakdong 8, Dongku, Gwangju, South Korea E-mail: [email protected] Fax: +82 6222 06776

Abstract

Objective

This study evaluated tumour necrosis factor-α, interleukins 10 and 12, and interferon-γ levels, peripheral blood mononuclear cells, and clusters of differentiation 17c and 86 expression in unilateral sudden sensorineural hearing loss.

Methods

Twenty-four patients with unilateral sudden sensorineural hearing loss, and 24 individuals with normal hearing and no history of sudden sensorineural hearing loss (who were attending the clinic for other problems), were enrolled. Peripheral blood mononuclear cells, and clusters of differentiation 11c and 86 were isolated and analysed. Plasma and supernatant levels of tumour necrosis factor-α, interferon-γ, and interleukins 10 and 12 were measured.

Results

There were no significant differences with respect to age and gender. Monocyte population, mean tumour necrosis factor-α level and cluster of differentiation 86 expression were significantly increased in the study group compared to the control group. However, interferon-γ and interleukin 12 levels were significantly decreased. The difference in mean interleukin 10 level was not significant.

Conclusion

Increases in tumour necrosis factor-α level and monocyte population might play critical roles in sudden sensorineural hearing loss. This warrants detailed investigation and further studies on the role of dendritic cells in sudden sensorineural hearing loss.

Type
Main Articles
Copyright
Copyright © JLO (1984) Limited, 2019 

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

Footnotes

Dr C H Jang takes responsibility for the integrity of the content of the paper

SH Yoon and ME Kim, both two authors contributed equally to this work.

References

1Wilson, H, Alderson, DJ. Sudden sensorineural hearing loss: when is it idiopathic? J Laryngol Otol 2010;124:690–3Google Scholar
2Yamasoba, T, Kikuchi, S, Higo, R, O'Uchi, T, Tokumaru, A. Sudden sensorineural hearing loss associated with slow blood flow of the vertebrobasilar system. Ann Otol Rhinol Laryngol 1993;102:873–7Google Scholar
3Masuda, M, Kanzaki, S, Minami, S, Kikuchi, J, Kanzaki, J, Sato, H et al. Correlations of inflammatory biomarkers with the onset and prognosis of idiopathic sudden sensorineural hearing loss. Otol Neurotol 2012;33:1142–50Google Scholar
4Merchant, SN, Durand, ML, Adams, JC. Sudden deafness: is it viral? ORL J Otorhinolaryngol Relat Spec 2008;70:5260; discussion 2Google Scholar
5Seo, YJ, Jeong, JH, Choi, JY, Moon, IS. Neutrophil-to-lymphocyte ratio and platelet-to-lymphocyte ratio: novel markers for diagnosis and prognosis in patients with idiopathic sudden sensorineural hearing loss. Dis Markers 2014;2014:702807Google Scholar
6Garcia-Berrocal, JR, Trinidad, A, Ramirez-Camacho, R, Lobo, D, Verdaguer, M, Ibanez, A. Immunologic work-up study for inner ear disorders: looking for a rational strategy. Acta Otolaryngol 2005;125:814–18Google Scholar
7Merchant, SN, Adams, JC, Nadol, JB Jr. Pathology and pathophysiology of idiopathic sudden sensorineural hearing loss. Otol Neurotol 2005;26:151–60Google Scholar
8Xenellis, J, Nikolopoulos, TP, Stavroulaki, P, Marangoudakis, P, Androulakis, M, Tsangaroulakis, M et al. Simultaneous and sequential bilateral sudden sensorineural hearing loss: are they different from unilateral sudden sensorineural hearing loss? ORL J Otorhinolaryngol Relat Spec 2007;69:306–10Google Scholar
9Demirhan, E, Eskut, NP, Zorlu, Y, Cukurova, I, Tuna, G, Kirkali, FG. Blood levels of TNF-alpha, IL-10, and IL-12 in idiopathic sudden sensorineural hearing loss. Laryngoscope 2013;123:1778–81Google Scholar
10Haubner, F, Martin, L, Steffens, T, Strutz, J, Kleinjung, T. The role of soluble adhesion molecules and cytokines in sudden sensorineural hearing loss. Otolaryngol Head Neck Surg 2011;144:575–80Google Scholar
11Keles, E, Sapmaz, E, Godekmerdan, A. The role of allergy in the etiopathogenesis of idiopathic sudden sensorineural hearing loss. Eur Arch Otorhinolaryngol 2013;270:1795–801Google Scholar
12Singh, AK, Dutta, M, Chattopadhyay, R, Chakravarty, B, Chaudhury, K. Intrafollicular interleukin-8, interleukin-12, and adrenomedullin are the promising prognostic markers of oocyte and embryo quality in women with endometriosis. J Assist Reprod Genet 2016;33:1363–72Google Scholar
13Hiramatsu, M, Teranishi, M, Uchida, Y, Nishio, N, Suzuki, H, Kato, K et al. Polymorphisms in genes involved in inflammatory pathways in patients with sudden sensorineural hearing loss. J Neurogenet 2012;26:387–96Google Scholar
14Shi, C, Pamer, EG. Monocyte recruitment during infection and inflammation. Nat Rev Immunol 2011;11:762–74Google Scholar
15Iwamoto, S, Iwai, S, Tsujiyama, K, Kurahashi, C, Takeshita, K, Naoe, M et al. TNF-alpha drives human CD14+ monocytes to differentiate into CD70+ dendritic cells evoking Th1 and Th17 responses. J Immunol 2007;179:1449–57Google Scholar
16Mijovic, T, Zeitouni, A, Colmegna, I. Autoimmune sensorineural hearing loss: the otology-rheumatology interface. Rheumatology (Oxford) 2013;52:780–9Google Scholar
17Suslu, N, Yilmaz, T, Gursel, B. Utility of anti-HSP 70, TNF-alpha, ESR, antinuclear antibody, and antiphospholipid antibodies in the diagnosis and treatment of sudden sensorineural hearing loss. Laryngoscope 2009;119:341–6Google Scholar
18Trinchieri, G. Interleukin-12 and the regulation of innate resistance and adaptive immunity. Nat Rev Immunol 2003;3:133–46Google Scholar
19Joss, A, Akdis, M, Faith, A, Blaser, K, Akdis, CA. IL-10 directly acts on T cells by specifically altering the CD28 co-stimulation pathway. Eur J Immunol 2000;30:1683–90Google Scholar
20Svrakic, M, Pathak, S, Goldofsky, E, Hoffman, R, Chandrasekhar, SS, Sperling, N et al. Diagnostic and prognostic utility of measuring tumor necrosis factor in the peripheral circulation of patients with immune-mediated sensorineural hearing loss. Arch Otolaryngol Head Neck Surg 2012;138:1052–8Google Scholar
21Muzzi, E, Zennaro, B, Visentin, R, Soldano, F, Sacilotto, C. Hyperbaric oxygen therapy as salvage treatment for sudden sensorineural hearing loss: review of rationale and preliminary report. J Laryngol Otol 2010;124:e2Google Scholar
22Narozny, W, Sicko, Z, Przewozny, T, Stankiewicz, C, Kot, J, Kuczkowski, J. Usefulness of high doses of glucocorticoids and hyperbaric oxygen therapy in sudden sensorineural hearing loss treatment. Otol Neurotol 2004;25:916–23Google Scholar
23Ihler, F, Sharaf, K, Bertlich, M, Strieth, S, Reichel, CA, Berghaus, A et al. Etanercept prevents decrease of cochlear blood flow dose-dependently caused by tumor necrosis factor alpha. Ann Otol Rhinol Laryngol 2013;122:468–73Google Scholar