Severe SARS-CoV-2 infected patients are associated with up-regulation of CCL3 and down-regulation of CCL2

International Journal of Molecular and Clinical Microbiology

مقالات آماده انتشار، پذیرفته شده، انتشار آنلاین از تاریخ 19 دی 1403

نوع مقاله: Research Article

شناسه دیجیتال (DOI): 10.22034/ijmcm.2025.2009100.1312

نویسندگان

Asieh Asadpour-Behzadi¹؛ Ashraf Kariminik^{* 2}؛ Babak Kheirkhah³

¹Department of Microbiology, Kerman Branch, Islamic Azad University, Kerman, Iran

²Department of Microbiology, Kerman Branch, Islamic Azad University, Kerman, Iran, Food and Agricultural Safety Research Center, Kerman Branch, Islamic Azad University, Kerman, Iran

³Department of Veterinary Medicine, Baft Branch, Islamic Azad University, Baft, Iran.

چکیده

Background and Aim: The diverse range of clinical manifestations of SARS-CoV-2 infection indicates that individual immune responses to the virus are pivotal in shaping the subsequent clinical trajectory post-initial exposure. Research in immunology has primarily concentrated on individuals with moderate to severe illness, revealing heightened inflammation in tissues and resultant organ impairment. Chemokines play key roles in the regulation of immune responses against viral infections.

Materials and Methods: The current study was aimed to evaluate the CC ligand 2 (CCL2) and CCL3 in the SARS-CoV-2 infected patients with severe inflammation. The patients tested positive for SARS-CoV-2 RNA through Real-Time PCR analysis of the nasopharyngeal sample obtained at the onset of hospitalization and prior to any therapeutic interventions. Serum levels of CCL2 and CCL3 were evaluated in 69 Iranian SARS-CoV-2 infected patients with severe inflammation and 65 healthy subjects using ELISA technique.

Results: The results showed that serum levels of CCL2 and CCL3 were significantly decreased and increased, respectively in the Iranian SARS-CoV-2 infected patients with severe inflammation when compared to healthy controls.

Conclusion: Based on the results, it may be concluded that CCL3, but not CCL2, significantly participates in the induction of severe inflammation during severe coronavirus disease 2019 (COVID-19).

کلیدواژه‌ها

Covid 19؛ Chemokine؛ Immune system؛ Immunity؛ Human