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Review
. 2022 Oct 14;23(20):12260.
doi: 10.3390/ijms232012260.

Inflammation Causes Exacerbation of COVID-19: How about Skin Inflammation?

Mayumi Komine  1 , Tuba Mussarat Ansary  1 , Md Razib Hossain  1 , Koji Kamiya  1 , Mamitaro Ohtsuki  1
Affiliations
Review

Inflammation Causes Exacerbation of COVID-19: How about Skin Inflammation?

Mayumi Komine et al. Int J Mol Sci. .

Abstract

COVID-19 is a recently emerged viral infection worldwide. SARS-CoV-2, the causative virus, is believed to have emerged from bat coronaviruses, probably through host conversion. The bat coronavirus which has the highest gene homology to SARS-CoV-2 specifically infects deep forest bats in China whose habitat extends through the Middle East to Southern Europe. Host conversion might have occurred due to the deforestation by humans exposing wild bats to the environment they had never encountered before. SARS-CoV-2 infects cells through two mechanisms: through its receptor ACE2 with the help of enzyme TMPRSS and through membrane fusion with the help of elastases in the inflammatory condition. Obesity, hypertension, diabetes mellitus, and pulmonary diseases cause poor prognosis of COVID-19. Aging is another factor promoting poor prognosis. These diseases and aging cause low-level and persistent inflammation in humans, which can promote poor prognosis of COVID-19. Psoriasis and atopic dermatitis are the major inflammatory skin diseases. These inflammatory skin conditions, however, do not seem to cause poor prognosis for COVID-19 based on the epidemiological data accumulated so far. These mechanisms need to be elucidated.

Keywords: COVID-19; SARS-CoV-2; atopic dermatitis; inflammation; psoriasis; skin.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Three stages of COVID-19 infection. Modified from reference [8].
Figure 2
Figure 2
The infection pathway of SARS-CoV-2 differs depending on the inflammation status. Without inflammation, SARS-CoV-2 utilizes TMPRSS2 to enter cells with the ACE2 receptor through endocytosis, while with inflammation, SARS-CoV-2 utilizes environmental elastases to enter cells through membrane fusion, with rapid replication of themselves. Modified from reference [13].
Figure 3
Figure 3
SARS-CoV-2 and SARS-CoV utilize ACE2 as their receptor with no inflammation, while they utilize abundant environmental elastases with inflammatory condition to enter cells.
Figure 4
Figure 4
The scheme of the JAK–STAT pathway. When a cytokine binds to its receptor, the receptor makes a receptor complex, which phosphorylates JAK, and JAK phosphorylates itself and STATs. Phosphorylated STATs make homo- or heterodimers and translocate in the nucleus, where they exert their function as nuclear proteins. Modified from reference [71].
Figure 5
Figure 5
Several cytokine receptors utilize the JAK–STAT pathway to transduce their signals to the nucleus. Different cytokine receptors utilize different combinations of JAK family members and phosphorylate different STAT family members. Modified from reference [71].
See this image and copyright information in PMC

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