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Review
. 2023 Mar 16:10:1135695.
doi: 10.3389/fmed.2023.1135695. eCollection 2023.

Serum amyloid A-A potential therapeutic target for hyper-inflammatory syndrome associated with COVID-19

Affiliations
Review

Serum amyloid A-A potential therapeutic target for hyper-inflammatory syndrome associated with COVID-19

Eman M Almusalami et al. Front Med (Lausanne). .

Abstract

Serum amyloid-A (SAA) is associated with inflammatory disorders such as rheumatoid arthritis, Familial Mediterranean Fever, sarcoidosis, and vasculitis. There is accumulating evidence that SAA is a reliable biomarker for these autoinflammatory and rheumatic diseases and may contribute to their pathophysiology. Hyperinflammatory syndrome associated with COVID-19 is a complex interaction between infection and autoimmunity and elevation of SAA is strongly correlated with severity of the inflammation. In this review we highlight the involvement of SAA in these different inflammatory conditions, consider its potential role and discuss whether it could be a potential target for treatment of the hyperinflammatory state of COVID-19 with many potential advantages and fewer adverse effects. Additional studies linking SAA to the pathophysiology of COVID-19 hyper-inflammation and autoimmunity are needed to establish the causal relationship and the therapeutic potential of inhibitors of SAA activity.

Keywords: COVID-19; arthritides; cytokines; hyperinflammation; inflammation; serum amyloid A; target.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Flow chart demonstrating the literature review and the study selection process.
Figure 2
Figure 2
The cytokines and chemokines induced by SAA. Elevated levels of IL-6, IL-1β, and TNF-α stimulate the liver to produce SAA which in turn induces the production of different cytokines and chemokines from different cells.

References

    1. Ein D, Kimura S, Terry WD, Magnotta J, Glenner GG. Amino acid sequence of an amyloid fibril protein of unknown origin. J Biol Chem. (1972) 247:5653–5. doi: 10.1016/S0021-9258(20)81154-5, PMID: - DOI - PubMed
    1. Levin M, Franklin EC, Frangione B, Pras M. The amino acid sequence of a major nonimmunoglobulin component of some amyloid fibrils. J Clin Invest. (1972) 51:2773–6. doi: 10.1172/JCI107098, PMID: - DOI - PMC - PubMed
    1. Linke RP, Sipe JD, Pollock PS, Ignaczak TF, Glenner GG. Isolation of a low-molecular-weight serum component antigenically related to an amyloid fibril protein of unknown origin. Proc Natl Acad Sci. (1975) 72:1473–6. doi: 10.1073/pnas.72.4.1473, PMID: - DOI - PMC - PubMed
    1. Sack GH. Serum amyloid A–a review. Mol Med. (2018) 24:46–27. doi: 10.1186/s10020-018-0047-0, PMID: - DOI - PMC - PubMed
    1. Migita K, Izumi Y, Jiuchi Y, Kozuru H, Kawahara C, Nakamura M, et al. . Serum amyloid a induces NLRP-3-mediated IL-1β secretion in neutrophils. PLoS One. (2014) 9:e96703. doi: 10.1371/journal.pone.0096703, PMID: - DOI - PMC - PubMed

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