Patients with rheumatoid arthritis (RA) represent one of the fragile patient groups that might be susceptible to the critical form of the coronavirus disease − 19 (COVID-19). On the other side, RA patients have been found not to have an increased risk of COVID-19 infection. Moreover, some of the Disease-Modifying Anti-Rheumatic Drugs (DMARDS) commonly used to treat rheumatic diseases like Hydroxychloroquine (HCQ) were proposed as a potential therapy for COVID-19 with a lack of full understanding of their molecular mechanisms. This highlights the need for the discovery of common pathways that may link both diseases at the molecular side. In this research, we used the in silico approach to investigate the transcriptomic profile of RA synovium to identify shared molecular pathways with that of severe acute respiratory syndrome-corona virus-2 (SARS-COV-2) infected lung tissue. Our results showed upregulation of chemotactic factors, including CCL4, CCL8, and CCL11, that all shared CCR5 as their receptor, as a common derangement observed in both diseases; RA and COVID-19. Moreover, our results also highlighted a possible mechanism through which HCQ, which can be used as a monotherapy in mild RA or as one of the triple-DMARDs therapy (tDMARDs; methotrexate, sulphasalazine, and HCQ), might interfere with the COVID-19 infection. This might be achieved through the ability of HCQ to upregulate specific immune cell populations like activated natural killer (NK) cells, which were found to be significantly reduced in COVID-19 infection. In addition to its ability to block CCR5 rich immune cell recruitment that also was upregulated in the SARS-COV-2 infected lungs. This might explain some of the reports that showed beneficial effects.
【초록키워드】 COVID-19, coronavirus disease, therapy, drug, rheumatoid arthritis, COVID-19 infection, cells, Lungs, Research, Patient, Factors, pathway, Mild, HCQ, receptor, molecular, methotrexate, monotherapy, disease, CCR5, Critical, transcriptomic profile, mechanism, rheumatic disease, natural killer, in silico Approach, increased risk, RA synovium, molecular mechanisms, lung tissue, upregulation, treat, CCL11, CCL8, CCL4, potential therapy, Effects, susceptible, highlight, identify, lack, significantly, addition, patient group, reduced, can be used, activated, interfere, upregulated, explain, chemotactic, immune cell population, immune cell recruitment, 【제목키워드】 COVID-19, rheumatoid arthritis, in silico analysis, Chemokine receptor,