key: cord-1017206-59xtqx4f
authors: Theoharides, Theoharis C.
title: Potential Association of Mast Cells with COVID-19
date: 2020-11-06
journal: Ann Allergy Asthma Immunol
DOI: 10.1016/j.anai.2020.11.003
sha: 5cd92797ef9257508164213be8d0a0d69a4f9548
doc_id: 1017206
cord_uid: 59xtqx4f

nan

The recent Coronovirus [severe acute respiratory syndrome (SARS)-CoV-2] is 1 associated with high morbidity and mortality mostly in adults, due to systemic symptoms, 2 especially pulmonary sequalae, known as COVID-19. 3 Interestingly, children appear to have milder symptoms than adults associated with 4 COVID-19. Moreover, the incidence of allergy and/or asthma in children infected with COVID-5 19 appears to be lower than the general population giving the impression that these atopic 6 diseases may be protective. 1 Such a conclusion is premature because the increased lung 7 eosinophils found in these diseases may had some protective effect especially since reduced 8 numbers of eosinophils were reported in COVID-19. 1 Moreover, medications used for the 9 treatment of these atopic diseases (e.g. antihistamines, corticosteroids) my had offered some 10 protection rather than the atopic diseases, themselves. Nevertheless, there have been recent 11 reports of childhood Multisystem Inflammatory Syndrome (MIS-C) with symptoms resembling 12 toxic shock or Kawasaki syndrome 2 suggesting that children may still experience symptoms 13 related to inflammation. 14 The pulmonary pathology associated with COVID-19 appears to result from release of 15 multiple pro-inflammatory cytokines, especially IL-6, that can damage the lungs. 3 A key source 16 of such cytokines and chemokines is the mast cells, which are ubiquitous in the body, especially 17 the lungs, and are critical for allergic and pulmonary diseases. 3 In fact, activated mast cells were Mast cells are typically activated by allergic triggers, but can also be triggered by 23 pathogen-associated molecular patterns (PAMPS) via toll-like receptors (TLR). In addition, mast 24 cells also express the renin-angiotensin system, the ectoprotease Angiotensin Converting 25 Enzyme 2 (ACE2) required for SARS-CoV-2 binding, and serine proteases, including TMPRSS2 26 required for priming of the corona spike protein. 3 Such triggers could lead to secretion of 27 multiple pro-inflammatory mediators selectively, without release of histamine or tryptase, as we 28 had previously reported in J Immunol for release of IL-6 in response to IL-1β from cultured 29 human mast cells (Fig. 1 ). 3 Moreover, we recently reported in PNAS that human mast cells can 

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This work was supported by anonymous donations.J o u r n a l P r e -p r o o f