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. 2022 Feb 15;13:813358. doi: 10.3389/fmicb.2022.813358

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Copyright © 2022 Mehta, Rolta, Mehta, Kaushik, Choi and Kaushik.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Pictorial representation of pathological events that occurred during COVID-19 and the efficacy of corticosteroid to control COVID-19 infection. SARS-CoV-2 gets inside the host via the pulmonary route, penetrates the alveoli, and interacts with alveolar macrophages (AMs) and pneumocytes (P). Infectious AMs release cytokines/chemokines that recruit and trigger other immune cells such as T cells (T) to produce cytokines, causing “cytokine storm,” and monocytes (M) along with neutrophils (N) move from the blood to the infection site. The lungs in COVID-19 cases in severe condition at late stage lead to acute respiratory distress syndrome (ARDS) and pulmonary fibrosis. Corticosteroids help in inhibiting inflammation caused by cytokine storms and prevent several problems associated with severe COVID-19 including pneumonia, edema, ARDS, and fibrosis. Adapted and modified from Gopalaswamy and Subbian (2021) with permission.