Micronucleus count in nasal epithelial cells from patients with chronic rhinosinusitis and polyps

Drummond, Renata Loss; Rhoden, Cláudia Ramos; Neto, José Faibes Lubianca; Fleck, Alan da Silveira; Padoin, Rita Carolina Pozzer Krumenauer; Amantéa, Sérgio L.

doi:10.1016/j.bjorl.2019.05.004

Cited by 4 publications

(4 citation statements)

References 23 publications

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“…In humans, it is practical to collect buccal and nasal cells, which are also the cells most likely to come in contact with and be infected by the COVID-19 virus [ 215 ]. MN in nasal and buccal cells have been shown to be increased by exposure to airborne genotoxins, malnutrition, infectious diseases and, also, as a result of aging and genetic defects that predispose to chromosomal instability [ [216] , [217] , [218] , [219] , [220] , [221] , [222] ]. Furthermore, cells harboring MN have previously been shown to have increased expression of cGAS and STING in the cytoplasm making it plausible that MN, inflammatory cytokine production and COVID-19 virus progeny may co-exist within nasal and buccal cells [ 91 , 92 ].…”

Section: Implications From Our Hypothesis/esmentioning

confidence: 99%

Inflammatory cytokine storms severity may be fueled by interactions of micronuclei and RNA viruses such as COVID-19 virus SARS-CoV-2. A hypothesis

Kirsch‐Volders

Fenech

2021

Mutation Research/Reviews in Mutation Research

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In this review we bring together evidence that (i) RNA viruses are a cause of chromosomal instability and micronuclei (MN), (ii) those individuals with high levels of lymphocyte MN have a weakened immune response and are more susceptible to RNA virus infection and (iii) both RNA virus infection and MN formation can induce inflammatory cytokine production. Based on these observations we propose a hypothesis that those who harbor elevated frequencies of MN within their cells are more prone to RNA virus infection and are more likely, through combined effects of leakage of self-DNA from MN and RNA from viruses, to escalate pro-inflammatory cytokine production via the cyclic GMP–AMP synthase (cGAS), stimulator of interferon genes (STING) and the Senescence Associated Secretory Phenotype (SASP) mechanisms to an extent that is unresolvable and therefore confers high risk of causing tissue damage by an excessive and overtly toxic immune response. The corollaries from this hypothesis are (i) those with abnormally high MN frequency are more prone to infection by RNA viruses; (ii) the extent of cytokine production and pro-inflammatory response to infection by RNA viruses is enhanced and possibly exceeds threshold levels that may be unresolvable in those with elevated MN levels in affected organs; (iii) reduction of MN frequency by improving nutrition and life-style factors increases resistance to RNA virus infection and moderates inflammatory cytokine production to a level that is immunologically efficacious and survivable.

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Section: Implications From Our Hypothesis/esmentioning

confidence: 99%

Inflammatory cytokine storms severity may be fueled by interactions of micronuclei and RNA viruses such as COVID-19 virus SARS-CoV-2. A hypothesis

Kirsch‐Volders

Fenech

2021

Mutation Research/Reviews in Mutation Research

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“…[ 2 3 ] Most of the viral infections in a cell cause cellular and nuclear damage. [ 4 ] Recurrent insult through infection and inflammation can result eventually in more evident nuclear damage that can be visualized as micronuclear and metanuclear abnormalities.…”

Section: Introductionmentioning

confidence: 99%

Exploratory Study on Micronuclei and Metanuclear Abnormalities in Exfoliated Buccal Cells of COVID-19 Suspected Patients

Vishnu,

Murugan,

Kalidoss

et al. 2023

Journal of Cytology

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Context: SARS-CoV-2 virus causes COVID-19 by infecting nasal and oral cavities primarily by attaching its spike proteins to ACE 2 receptors expressed in epithelial cells. Aim: This study was done to evaluate the micronucleated cell count, metanuclear abnormalities, and genotoxic factor in exfoliated buccal mucosal cell among the COVID-19 suspected patients. Settings and Design: This cross-sectional study was conducted at AIIMS, Mangalagiri, between August and October 2022. Methods: One hundred COVID-19 suspected patients were recruited for this study after obtaining informed and written consent; buccal smear was obtained and stained for papanicolaou test (PAP). The PAP-stained slides were analyzed for micronuclei (MN), pyknotic, karyolytic, and karyorrhexic cell count, respectively. Based on their reverse transcription-polymerase chain reaction (RT-PCR) report, the patients were grouped into COVID-19 positive and negative groups. Statistical Analysis: The genotoxicity factor was calculated using the micronucleated cell count from both the groups using mean and standard deviation. Results: The MN, micronucleated cell, pyknotic, karyolitic, and karyorrhexic cell count in COVID-19 positive patients were 24.12, 15.24, 3.08, 2.88 and 4.40, respectively, than COVID-19 negative patients 5.69, 8.17, 1.08, 1.00 and 2.43, respectively. The genotoxicity factor for SARS-CoV-2 was 2.68 which is a positive genotoxic effect on buccal mucosal cells. Conclusion: SARS-CoV-2 increases the expression of micronucleated cells, pyknotic cells, karyolytic cells, and karyorhexic cells and concludes SARS-CoV-2 is having cytogenotoxic effect on the buccal mucosal cells. This can be used as a reliable marker in identifying the early carcinogenic effects of virus causing COVID-19.

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“…It is well estaliblished that genetic damage is responsible for genomic instability that underlies the development of many chronic degenerative diseases. In infectious diseases, micronuclei have been identified as useful biomarkers of cell damage (5). Micronuclei indicate biological events closely associated with genotoxicity allowing for a better understanding of the etiopathogenesis and consequently, for proposing prevention strategies (6).…”

mentioning

confidence: 99%

Cytogenetic Biomonitoring in Buccal Mucosa Cells of COVID-19 Patients: Preliminary Findings

Pinto

Alpire

Ribeiro

2021

In Vivo

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Background/Aim: COVID-19 may lead to progressive respiratory failure as a consequence of alveolar damage, resulting in death. The aim of this study was to evaluate cytogenetic damage in oral cells of COVID-19 patients by micronucleus assay. Patients and Methods: A total of 11 COVID-19 patients aged 40.7±9.3 years (5 men and 6 women) were included in this study. For the control group, a total of 15 participants not infected with SARS-CoV-2 virus were included. The mean age was 41.6±6.2 years (5 men and 10 women). Results: The results showed statistically significant differences (p<0.05) in micronucleated buccal mucosa cells of COVID-19 patients. In addittion, a statistically significant increase in karyolysis and karrhyorexis (p<0.05) was observed in COVID-19 patients compared to control. Conclusion: SARS-CoV-2 virus can induce mutagenesis and cytotoxicity in oral cells.

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Micronucleus count in nasal epithelial cells from patients with chronic rhinosinusitis and polyps

Cited by 4 publications

References 23 publications

Inflammatory cytokine storms severity may be fueled by interactions of micronuclei and RNA viruses such as COVID-19 virus SARS-CoV-2. A hypothesis

Inflammatory cytokine storms severity may be fueled by interactions of micronuclei and RNA viruses such as COVID-19 virus SARS-CoV-2. A hypothesis

Exploratory Study on Micronuclei and Metanuclear Abnormalities in Exfoliated Buccal Cells of COVID-19 Suspected Patients

Cytogenetic Biomonitoring in Buccal Mucosa Cells of COVID-19 Patients: Preliminary Findings

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