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Does gene expression in laryngeal subsites differ between patients with laryngopharyngeal reflux and controls?
Author(s) -
Wood J.M.,
Hussey D.J.,
Woods C.M.,
Astill D.,
I Watson D.,
Lee B.,
Carney A.S.
Publication year - 2018
Publication title -
clinical otolaryngology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.914
H-Index - 68
eISSN - 1749-4486
pISSN - 1749-4478
DOI - 10.1111/coa.12918
Subject(s) - laryngopharyngeal reflux , medicine , cytokeratin , gerd , pathology , metaplasia , larynx , inflammation , gene expression , gene , gastroenterology , immunohistochemistry , reflux , disease , biology , anatomy , biochemistry
Objective To identify laryngeal mRNA gene changes in patients with laryngopharyngeal reflux ( LPR ). Method Laryngeal biopsies from non‐smoking LPR patients (n=10; Reflux Symptom Index ( RSI ) >12 and a Reflux Finding Score ( RFS ) >6) and controls (n=9; RSI <12 and RFS <6) were collected from four subsites (true vocal cord, false vocal cord, medial arytenoid and posterior commissure) of the larynx. qRT ‐ PCR analyses were conducted on 20 reflux‐ and inflammation‐related genes, including interleukins 6 and 8, cytokeratins 8 and 14, mucin genes MUC 1, MUC 2, MUC 3B, MUC 4, MUC 5B, MUC 6 and MUC 7 and carbonic anhydrase III . Statistical analysis (Mann‐Whitney U test) compared gene expression levels between LPR and control groups at each subsite. Results Site‐specific differences in squamous metaplasia and gene expression were noted in LPR patients, with the majority present in the medial arytenoid region. Significant.differences were noted in genes related to mucosal defence and inflammation, including CRNN , CD 1d , TGF β‐1 , MUC 2 , MUC 5B and CDH 1 . Conclusion Whilst the posterior commissure is commonly identified as the area demonstrating the most significant macroscopic change in LPR , the histological changes and genes assessed here showed more pronounced LPR associated differences in the medial arytenoid. We identified differences in expression of mucin genes, cytokeratin‐14 and molecular markers of inflammation. Whilst some of these changes may be metaplasia‐related, further evaluation of the mRNA expression of these genes may provide a useful biomarker panel for diagnosis and therapeutic monitoring of LPR .