Molecular Detection of Chlamydia Pneumoniae, Haemophilus Influenza, and Streptococcus Pneumoniae and Expression of Mir-146, Mir-16, and Mir-221 in Patients With Chronic Obstructive Pulmonary Diseases Publisher



N Moattarhusseini NEDA ; A Mohamadnia ABDOLREZA ; F Hosseini FARZANEH ; N Bahrami NAGHMEH
Source: Biomedical and Biotechnology Research Journal Published:2024

Abstract

Background: Chronic obstructive pulmonary disease (COPD) is a debilitating respiratory condition characterized by persistent airflow limitation and chronic inflammation. Microbial infections and dysregulated microribonucleic acid (miRNA) expression have been implicated in COPD pathogenesis. This study aimed to investigate the molecular detection of three respiratory pathogens, Chlamydia pneumoniae, Haemophilus influenzae, and Streptococcus pneumoniae, in the respiratory secretions of COPD patients. In addition, it evaluated the expression levels of miR-146, miR-16, and miR-221 in the peripheral blood of COPD patients. Methods: Peripheral blood and respiratory secretions were collected from 40 healthy individuals and 40 COPD patients. The messenger ribonucleic acid expression levels of miR-146, miR-16, and miR-221 were determined using real-time polymerase chain reaction. Statistical analyses, including t-test, binomial test, and Pearson correlation, were performed. Results: H. influenzae, S. pneumoniae, and C. pneumoniae were detected in the sputum of 12.5%, 17.5%, and 7.5% of COPD patients, respectively. The expression of miR-146, miR-221, and miR-16 was observed in 65%, 15%, and 85% of COPD patients, respectively, compared to 13%, 80%, and 15% of healthy subjects. While miR-221 was downregulated in COPD patients, miR-16 and miR-146 were upregulated. No significant differences were found in the expression of these miRNAs between infected and noninfected COPD patients. Conclusion: The molecular detection of respiratory pathogens and the expression profiles of miR-146, miR-16, and miR-221 in COPD patients may have potential diagnostic value. Further research is needed to elucidate the role of these markers in COPD pathogenesis. © 2024 Elsevier B.V., All rights reserved.