Cytology in COVID-19 and Laryngopharyngeal Reflux Disease| Book Publisher International

 

Introduction: SARS-CoV-2 infection and laryngopharyngeal reflux (LPR) both expose the upper aerodigestive tract to injurious biological agents—viral particles and gastric refluxate, respectively. These exposures can trigger mucosal inflammation, oxidative stress, and genotoxic changes detectable through cytological and immunohistochemical evaluation.

 

Aim: This study aimed to assess genotoxicity and oxidative DNA damage in exfoliated mucosal cells of individuals with suspected COVID-19 and patients with LPR, and to evaluate epithelial–mesenchymal transition (EMT)–related markers to understand early mucosal remodelling.

 

Settings and Design: A cross-sectional study conducted at AIIMS, Mangalagiri, between August 2022 and February 2024.

 

Methods: Exfoliated buccal or pharyngeal mucosal samples were collected from 86 COVID-19-suspected individuals (18–45 years) undergoing RT-PCR testing and from clinically diagnosed LPR patients with healthy controls. Smears were stained using the Papanicolaou technique for cytological analysis, and immunohistochemistry was performed to evaluate oxidative DNA damage (8-OHdG) and EMT markers (E-cadherin, N-cadherin). Micronucleated cells, inflammatory infiltrates, and oxidative marker expression were quantified. Statistical analysis was done using independent t-tests and ANOVA, with significance set at p < 0.05.

 

Results: COVID-19 RT-PCR–positive subjects showed significantly elevated micronucleated cells, total micronuclei, and inflammatory cell counts compared to RT-PCR–negative individuals, along with intense 8-OHdG expression indicating marked oxidative DNA damage. LPR patients similarly demonstrated increased oxidative stress with strong 8-OHdG staining and higher micronucleated cell frequencies than healthy controls. While E-cadherin expression remained largely preserved, N-cadherin showed moderate upregulation in LPR patients, suggesting an early EMT-related cadherin shift. Both conditions exhibited a reduced epithelial-to-inflammatory cell ratio, reflecting ongoing mucosal injury and remodelling.

 

Conclusion: Both SARS-CoV-2 infection and chronic laryngopharyngeal reflux exert measurable genotoxic and oxidative effects on mucosal epithelial cells. The increased micronuclei formation, heightened 8-OHdG expression, and early EMT-associated changes indicate genomic instability and mucosal remodelling driven by persistent inflammation and oxidative stress. These findings underscore the importance of early detection and targeted interventions to prevent progression toward long-term mucosal damage and potential malignant transformation.

Author(s) Details

Yogita Poojari
All India Institute of Medical Sciences, Mangalagiri, India.

 

Ambati Gowtham Sai
All India Institute of Medical Sciences, Mangalagiri, India.

 

B Vishnu
All India Institute of Medical Sciences, Mangalagiri, India.

 

Pranav Donkada
All India Institute of Medical Sciences, Mangalagiri, India.

 

Hemanth Bonamsetty
All India Institute of Medical Sciences, Mangalagiri, India.

 

Senthil Murugan
Department of Antomy, All India Institute of Medical Sciences, Mangalagiri, India.

 

P K Sankaran
Department of Antomy, All India Institute of Medical Sciences, Mangalagiri, India.

 

Please see the book here :- https://doi.org/10.9734/bpi/mono/978-93-47485-50-3

The Role of Cadmium Induced EGFR/STAT5 Pathway Activation in Epithelial to Mesenchymal Transition | Chapter 4 | Current Innovations in Disease and Health Research Vol. 7

 Cadmium (Cd) is a poisonous and carcinogenic heavy metal about cigarette fume, air and drinking water, due to land and industrial endeavors, posing a health risk to the inexact population. Prolonged, depressed-dose Cd exposure by way of inhalation or ingestion induces alveolus and kidney cancers in two together humans and animal models. While exposure to extreme-dose Cd is cytotoxic and is equated with the occupational background, low-dose Cd uncovering is carcinogenic and mainly correlated with the inexact population. Even though Cd is classification as a group 1 “human carcinogen” by IARC, the means by which Cd-unprotected cells overcome calcium chelation and induce diseased transformation remains imprecise. This study examines the system by which cells unprotected to low doses of Cd live the loss of E-cadherin cell-cell grip and induce epithelial-to-mesenchymal change (EMT). Two epithelial cell lines, BEAS-2B and HEK293, were exposed to 0.4 µM and 1.6 µM of Cadmium chloride hemipentahydrate (CdCl2.2.5H2O) for 24 hours (h) and 9 weeks (wks). The preferred doses are environmentally relevant to levels of Cd found in bread and cigarettes. A dose-helpless decrease in E-cadherin and an increase in N-cadherin protein expression was observed in containers treated accompanying low-dose Cd. Moreover, Cd medicated cells exhibited a faster increase rate when compared accompanying control cells. This observation surpassed to the examination of the EGFR/STAT5 road activation, which has again been noticed to be activated in studies exhausted cancer cells. Our results accompanied a dose-weak and time-dependent increase in two together total EGFR and phosphorylated EGFR (p-EGFR) protein. Similar results were observed accompanying STAT5 and phosphorylated STAT5 (pSTAT5) protein in both short-term and complete exposures, nevertheless the 0.4 µM dose had the highest verbalization at 24 h. EGFR/STAT5 inducible genes were also upregulated in Cd-medicated cells in just 24 h. These dossier demonstrate that epithelial cells can overcome Cd-intervened toxicity by activating the EGFR/STAT5 road to induce cell continuation and proliferation, chief to EMT.

Author(s) Details:

Aikaterini Stavrou,
Department of Medicine, Division of Environmental Medicine, New York University Grossman School of Medicine, New York, NY 10010, USA.

Angelica Ortiz,
Department of Medicine, Division of Environmental Medicine, New York University Grossman School of Medicine, New York, NY 10010, USA.

Max Costa,
Department of Medicine, Division of Environmental Medicine, New York University Grossman School of Medicine, New York, NY 10010, USA.

Please see the link here: https://stm.bookpi.org/CIDHR-V7/article/view/12042