A Potential Role for the Receptor for Advanced Glycation End-Products (RAGE) in the Development of Secondhand Smoke-Induced Chronic Sinusitis
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Published:2024-01-13
Issue:1
Volume:46
Page:729-740
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ISSN:1467-3045
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Container-title:Current Issues in Molecular Biology
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language:en
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Short-container-title:CIMB
Author:
Robin Hannah1, Trudeau Courtney1, Robbins Adam1, Chung Emily1, Rahman Erum1, Gangmark-Strickland Olivia1, Licari Frank W.1, Winden Duane R.1, Orr Dan L.2, Arroyo Juan A.3ORCID, Reynolds Paul R.3ORCID
Affiliation:
1. College of Dental Medicine, Roseman University of Health Sciences, South Jordan, UT 84095, USA 2. Oral & Maxillofacial Surgery, University Medical Center, Las Vegas, NV 89102, USA 3. Lung and Placenta Laboratory, Department of Cell Biology and Physiology, Brigham Young University, Provo, UT 84602, USA
Abstract
Chronic sinusitis (CS) is characterized by sinonasal inflammation, mucus overproduction, and edematous mucosal tissue. CS impacts one in seven adults and estimates suggest up to 15% of the general U.S. population may be affected. This research sought to assess a potential role for receptors for advanced glycation end-products (RAGE), an inflammatory receptor expressed in tissues exposed to secondhand smoke (SHS). Human sinus tissue sections were stained for RAGE and S100s, common RAGE ligands. Wild-type mice and mice that over-express RAGE in sinonasal epithelium (RAGE TG) were maintained in room air (RA) or exposed to secondhand smoke (SHS) via a nose-only delivery system five days a week for 6 weeks. Mouse sections were stained for RAGE and tissue lysates were assayed for cleaved caspase 3, cytokines, or matrix metalloproteases. We discovered increased RAGE expression in sinus tissue following SHS exposure and in sinuses from RAGE TG mice in the absence of SHS. Cleaved caspase-3, cytokines (IL-1β, IL-3, and TNF-α), and MMPs (-9 and -13) were induced by SHS and in tissues from RAGE TG mice. These results expand the inflammatory role of RAGE signaling, a key axis in disease progression observed in smokers. In this relatively unexplored area, enhanced understanding of RAGE signaling during voluntary and involuntary smoking may help to elucidate potential therapeutic targets that may attenuate the progression of smoke-related CS.
Funder
National Institutes of Health Flight Attendant’s Medical Research Institute Daniel L. Orr II Family Charitable Fund
Subject
Microbiology (medical),Molecular Biology,General Medicine,Microbiology
Reference60 articles.
1. Adams, P.F., Hendershot, G.E., and Marano, M.A. (1996). Current Estimates from the National Health Interview Survey, Centers for Disease Control and Prevention, National Center for Health Statistics. 2. Epidemiology and Economic Impact of Rhinosinusitis;Anand;Ann. Otol. Rhinol. Laryngol.,2004 3. Summary health statistics for U.S. adults: National health interview survey, 2012;Blackwell;Vital Health Stat.,2014 4. Murine complement deficiency ameliorates acute cigarette smoke-induced nasal damage;Davis;Otolaryngol. Neck Surg.,2010 5. Adult Chronic Rhinosinusitis: Definitions, Diagnosis, Epidemiology, and Pathophysiology;Benninger;Otolaryngol. Head Neck Surg.,2003
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