240 https://oamjms.eu/index.php/mjms/index Scientifc Foundation SPIROSKI, Skopje, Republic of Macedonia Open Access Macedonian Journal of Medical Sciences. 2021 Jun 03; 9(T3):240-243. https://doi.org/10.3889/oamjms.2021.6358 eISSN: 1857-9655 Category: T3 - Thematic Issue “Neuroscience, Neurology, Psychiatry and General Medicine” Section: Oncology Expression of CCL27 in Middle Ear Cholesteatoma Yan Edward 1 * , Eva Decroli 1 , Hirowati Ali 1 , Djong Hon Tjong 2 1 Department of Otorhinolaryngology, Faculty of Medicine, Andalas University, Padang, Indonesia; 2 Department of Otorhinolaryngology, Faculty of Mathematics and Natural Sciences, Andalas University, Padang, Indonesia Abstract BACKGROUND: Cholesteatoma is a lesion of the temporal bone lined by stratifed squamous epithelium that contains desquamated keratin. Cholesteatoma is considered more aggressive during childhood. The molecular mechanism of the pathogenesis of cholesteatoma formation is still unclear. Previous studies reported on immunohistochemical examination and quantitative polymerase chain reaction (PCR) found that TCN1 and CCL27 were involved in the process of cholesteatoma keratinocytes and dermal endothelial cells. In skin tumors derived from keratinocytes, there is a protective mechanism of antitumor T cell-mediated by reducing CCL27 expression. AIM: The objective of this study was to investigate the expression of chemokine ligand 27 (CCL27) in cholesteatoma. METHODS: This is a cross-sectional comparative study. Cholesteatoma specimens were obtained from 15 patients who underwent surgery and 15 normal retroauricular skin as control. The specimen’s gene expression was examined with real-time PCR (RT-PCR). RESULTS: The expression of CCL27 was 36.215 ± 45.848 ng/ul in cholesteatoma, while it is 9.692 ± 15.760 ng/ul in normal retroauricular skin. The expression of CCL 27 in cholesteatoma was higher than in normal retroauricular skin, but it was not signifcant (p > 0.05) CONCLUSION: The expression of CCL27 in cholesteatoma was higher than in normal retroauricular skin. Edited by: Ksenija Bogoeva-Kostovska Keywords: Expression; CCL27; Cholesteatoma Citation: Edward Y, Decroli E, Ali H, Tjong DH. Expression of CCL27 in Middle Ear Cholesteatoma. Open Access Maced J Med Sci. 2021 Jun 03; 9(T3):240-243. https://doi.org/10.3889/oamjms.2021.6358 *Correspondence: Yan Edward. Faculty of Medicine, Andalas University, Padang, Indonesia. E-mail: dr.yanedward@gmail.com Received: 17-Nov-2020 Revised: 22-Nov-2020 Accepted: 19-May-2021 Copyright: © 2021 Yan Edward, Eva Decroli, Hirowati Ali, Djong Hon Tjong Funding: This research did not receive any fnancial support Competing Interest: The authors have declared that no competing interest exists Open Access: This is an open-access article distributed under the terms of the Creative Commons Attribution- NonCommercial 4.0 International License (CC BY-NC 4.0) Introduction Chronic suppurative otitis media (CSOM) is a chronic middle ear infection characterized by a history of continuous ear discharge from the middle ear through the perforated tympanic membrane [1], [2], [3]. Secretions in OMSK either disappear or occur continuously for more than 2 months [4]. The prevalence of CSOM in the world is 65–330 million people, especially in developing countries. The prevalence of CSOM in Indonesia, according to the national survey of sight and hearing health in 1994–1996, ranges from 3 to 5.2% [1], [4]. Cholesteatoma is a lesion of the temporal bone lined by stratifed squamous epithelium that contains desquamated keratin. Cholesteatoma is considered more aggressive during childhood. The molecular mechanism of the pathogenesis of cholesteatoma formation is still unclear [5], [6], [7]. The incidence of cholesteatoma ranges from 9 to 12.6 cases per 100,000 adults and 3 to 15 cases per 100,000 children with male versus female 1.4: 1 [8]. The etiopathogenesis of cholesteatoma cannot be explained with certainty. The mechanisms underlying cholesteatoma etiopathogenesis are still under study. Four dominant theories are still under debate, namely invagination theory, migration, squamous metaplasia, and basal cell hyperplasia. However, there is no single theory that explains the clinical characteristics of cholesteatoma [9], [10], [11]. Biomolecular-level etiopathogenesis research has developed in understanding pathological mechanisms that form the basis for further research [8], [11]. Various studies have reported on the biology of cholesteatoma, but many questions remain unanswered. Cholesteatoma is hyperproliferative but does not show typical symptoms of neoplasia in the absence of metastases and the absence of genetic instability [6], [12]. The mechanisms for the destruction of the temporal bone by cholesteatoma are complex and still not fully understood. Bone destruction by cholesteatoma is caused by several factors, namely mechanical, biochemical, and cellular. CCL27 is also known as a cutaneous T cell attracting chemokine (CTACK), which will accelerate skin regeneration. CCL27 is a keratinocyte-specifc cytokine that mediates lymphocytes to skin sites through the CCR10-specifc surface receptor. CCL27 plays an important role in T cell-mediated skin infammation. CCL27 is a cytokine that belongs to the CC chemokine family, also known as IL-11 R-alpha-locus chemokine (ILC), Skinkine, ESkine, and CTACK. CCL27 is expressed in various tissues, including gonads, thymus, placenta, and skin [13].