From COVID-19 to Sarcoidosis: How Similar Are These Two Diseases?

Abstract

Coronavirus disease 2019 (COVID-19), which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), leads to the dysregulation of the immune system, exacerbates inflammatory responses, and even causes multiple organ dysfunction syndrome in patients with severe disease. Sarcoidosis is an idiopathic granulomatous multisystem disease characterized by dense epithelioid non-necrotizing lesions with varying degrees of lymphocytic inflammation. These two diseases have similar clinical manifestations and may also influence each other and affect their clinical courses. In this study, we analyzed some possible connections between sarcoidosis and COVID-19, including the role of the renin–angiotensin system in the respiratory system, immune response, and cell death pathways, to understand the underlying mechanisms of SARS-CoV-2 infection, predisposing patients to severe forms of COVID-19. This review will provide a new prospect for the treatment of COVID-19 and an opportunity to explore the pathogenesis and development of sarcoidosis.

Circulating Regulatory T Cell Subsets in Patients with Sarcoidosis

“…It has been reported that alveolar macrophages from sarcoidosis patients secreted large amounts of CXCR3 ligands, including CXCL9, CXCL10, and CXCL11, that could play crucial roles in the accumulation of Tregs in the site of inflammation [ 65 , 66 ]. Similarly, the serum levels of CXCR3 ligands were also dramatically increased in sarcoidosis patients [ 67 , 68 , 69 ]. Furthermore, d’Alessandro et al noted an increased expression in Tregs of tissue-homing cell surface molecule CD103 that stimulated cell migration to inflamed mucosal tissues [ 70 ].…”

Sarcoidosis following COVID infection: A case series

“…First, the classical renin‐angiotensin system (RAS) (consisting of angiotensin converting enzyme (ACE), angiotensin II, and angiotensin II type 1 receptor (aT1R)) is negatively regulated by ACE2. SARS‐CoV has been shown to reduce pulmonary expression of ACE2 12 with the consequent hyperactivity of the RAS system postulated to contribute to the inflammatory response and cytokine storm seen in COVID‐19 lung disease 11 . Sarcoidosis is also associated with elevated circulating ACE levels 13 .…”

“…Similarities in immune features of sarcoidosis and SARS‐CoV‐2 may potentially be indicative of a common pathophysiology that could explain their co‐existence. For example, the ‘cytokine storm’ seen in severe COVID‐19 pulmonary disease is characterized by elevated serum levels of a host of inflammatory cytokines, many of which are also upregulated in sarcoid lungs 11 . However, the majority of post‐COVID‐19 sarcoid‐like reactions reported have occurred in patients with mild disease.…”

Sarcoidosis and autoimmunity: In the depth of a complex relationship

“…Zhao et al ( 46 ) identified several common clinical and immunological features between sarcoidosis and COVID-19.…”

“…Moreover, an impaired function of Treg cells is also probably shared by both diseases, with a consequent role in amplifying immunoinflammatory response. COVID-19 and sarcoidosis share cytokine-releasing patterns: high levels of IL-6, IL-10, TNF-α, and IFN-γ are common in both diseases ( 46 ).…”