![]() ![]() The diagnosis was confirmed by real-time reverse-transcriptase polymerase-chain reaction (RT-PCR) assay for nasal and pharyngeal swab specimens. Therefore, this study focuses on the profile of IL-1β and IL-10, as well as the ratio of the two cytokines, in the severity of COVID-19 over time.ĬOVID-19 was diagnosed in patients hospitalized in the isolation ward of Dr Soetomo General Hospital. We believe that through the comparison of both IL-1β and IL-10, it may be possible to detect early aggravation of COVID-19 severity, which will facilitate appropriate and individualized management strategies in patients with this disease. According to the established facts and theories, both cytokines are known to potently cause tissue damage. Both cytokines were reportedly increased in patients with severe COVID-19 however, there are currently no studies comparing the effect and influence of both cytokines together. The simultaneous increase in the concentrations of pro-inflammatory and anti-inflammatory cytokines is evidenced by two cytokines, IL-1β and IL-10. 12 There is increasing research on IL-10 as a potential biomarker for COVID-19 severity, and high expression of IL-10 may predict a worse prognosis in patients with COVID-19. IL-10 is identified as an inhibitory factor of Th1 secreted by Th2 cells. IL-10 has strong anti-inflammatory and immunosuppressive activity on myeloid cell function, which forms the basis of its involvement in acute and chronic inflammatory diseases. 6, 11 Interleukin 10 (IL-10) is a cytokine with a powerful anti-inflammatory function, and plays a key role in restricting the host’s immune response against pathogens, thereby avoiding damage to the host and maintaining normal tissue homeostasis. IL-6 regulates the acute phase response and is involved in acute inflammation, which ultimately leads to tissue damage. 9, 10 Furthermore, IL-1β is a gatekeeper of inflammation owing to its ability to regulate several cascades through other inflammation-associated molecules, such as interleukin-6 (IL-6). The index between the effective and toxic functions of IL-1 is understood to be very narrow, therefore regulation of IL-1 in the human body is tightly controlled. IL-1β is an important, robust pro-inflammatory cytokine involved in the body’s immune response against infection and injury. Interleukin-1β (IL-1β) is a member of the interleukin 1 family of cytokines that are instrumental in inflammatory responses. In cytokine storm, the levels of several cytokines such as IL-1β, IL-10, and TNF-α are increased, which correlate with disease severity. This condition causes damage to the alveolar epithelium and the epithelium-endothelium barrier, and consequently ARDS occurs, which is identified by tissue hypoxia and hypoxemia. 7 CXCL10 is a chemokine that is able to recruit more monocytes, macrophages, and neutrophils to the infection site, resulting in the production of more pro-inflammatory cytokines at the site, culminating in the occurrence of a cytokine storm. ![]() Infiltrating immune cells secrete pro-inflammatory cytokines (IFNα, IFNγ, IL-1β, IL-6, IL-12, IL-18, IL-33, TNFα, and TGFβ) which the onset and the maintenance feed-back loop will cause the maintenance of chemokines secretion. ![]() Through a multistep process involving adherence and migration across the endothelium, followed by trafficking through the interstitium, the immune cells reach the site of the infection. Consequently, resident lung cells begin to secrete chemokines (CXCL10, CXCL8, CXCL9, CCL2, CC元, CCL5) and this is accompanied by the recruitment of immune cells expressing the specific chemokine receptors. Cell stress then occurs, stimulating pyroptosis, which produces several damage-associated-molecular patterns. 6 SARS-CoV-2 enters lung cells by binding to the ACE-2 receptor and undergoes intracellular viral replication. 5 The occurrence of ARDS in patients with COVID-19 is predicted to be caused by an excessive immune response that culminates in cytokine-release syndrome (CRS), commonly known as “cytokine storm.” Cytokine storm, as the consequence of ARDS, results from the combined effects of many immune-active molecules including interferons, interleukins, chemokines, colony-stimulating factors, and TNF-alpha. 4 COVID-19 pneumonia generally causes acute respiratory distress syndrome (ARDS), which is the most common reason for mortality. 1–3 Mortality in patients with COVID-19 is predominantly due to respiratory failure arising from severe pneumonia. Human-to-human transmission is the confirmed etiology of this disease. Although COVID-19 is associated with several systemic symptoms, the dominant symptom is respiratory inconvenience. Coronavirus 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was first reported at the end of 2019 and rapidly became a global pandemic. ![]()
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