TY - JOUR
T1 - Does gene expression in laryngeal subsites differ between patients with laryngopharyngeal reflux and controls?
AU - Wood, J.M.
AU - Hussey, D.J.
AU - Woods, C.M.
AU - Astill, D.
AU - Watson, D.I.
AU - Lee, B.
AU - Carney, A.S.
PY - 2018/2/1
Y1 - 2018/2/1
N2 - 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 MUC1, MUC2, MUC3B, MUC4, MUC5B, MUC6 and MUC7 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, CD1d, TGFβ-1, MUC2, MUC5B and CDH1. 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.
AB - 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 MUC1, MUC2, MUC3B, MUC4, MUC5B, MUC6 and MUC7 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, CD1d, TGFβ-1, MUC2, MUC5B and CDH1. 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.
KW - biomarker
KW - laryngopharyngeal reflux
KW - larynx
KW - medial arytenoid
KW - posterior commissure
KW - cytokeratins
KW - carbonic anhydrase
KW - mucins
KW - vocal cord
UR - http://www.scopus.com/inward/record.url?scp=85021839080&partnerID=8YFLogxK
U2 - 10.1111/coa.12918
DO - 10.1111/coa.12918
M3 - Article
SN - 0307-7772
VL - 43
SP - 158
EP - 163
JO - Clinical Otolaryngology
JF - Clinical Otolaryngology
IS - 1
ER -