Kawasaki Disease Following Severe Sunburn Injury

Okada, Seigo; Hashimoto, Shintaro; Miyake, Akiko; Okada, Yusuke; Hirano, Reiji; Fukunaga, Shinnosuke; Ishikawa, Yuichi

doi:10.3389/fped.2020.00006

Cited by 7 publications

(14 citation statements)

References 19 publications

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“…Damaged self-DNA, due to viral infections or other triggers, is another major activator of the STING pathway. The report of a 17-month-old Japanese female who was hospitalized for KD following severe sunburn all over her body, with high levels of the DAMP HMGB1, and infection ruled out as a cause, also supports the hypothesis that STING activation contributes to KD [32] in young patients with at risk TMEM173 variants.…”

Section: Introductionsupporting

confidence: 56%

Kawasaki-like diseases and thrombotic coagulopathy in COVID-19: delayed over-activation of the STING pathway?

Berthelot

Drouet

Lioté

2020

Emerging Microbes & Infections

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We previously made the hypothesis that STING contributes to COVID-19. The present review detail new arguments for over-activation of STING pathways in COVID-19, following the description of hyper-coagulability and Kawasaki-like diseases in children. Indeed, Kawasaki disease is induced by overreaction of innate cells following exposition to various viruses, including herpes viruses which trigger STING. It predisposes to diffuse vasculitis and aneurysms, whereas STING is over-expressed in arterial aneurisms. The redness at the inoculation site of bacillus Calmette-Guérin, a specific feature of Kawasaki disease, is reproduced by activation of the STING pathway, which is inhibited upstream by aspirin, intravenous immunoglobulins, and Vitamin-D. SARS-CoV2 binding to ACE2 can lead to excessive angiotensin II signaling, which activates the STING pathway in mice. Over-activation of the STING-pathway promotes hyper-coagulability through release of interferon-β and tissue factor by monocytes-macrophages. Aspirin and dipyridamole, besides their anti-platelet activity, also reduce tissue factor procoagulant activity, and aspirin inhibits the STING pathway upstream of STING. Aspirin and dipyridamole may be used, in combination with drugs blocking downstream the activation of the STING pathway, like inhibitors of IL-6R and JAK/STAT pathways. The risk of bleeding should be low as bleeding has not been reported in severe COVID-19 patients. Triggering of the STING pathway by alien or self cytosolic DNA, can activate (from right to left): IRF-3 (partly inhibited by IVIgs after linking of FcγRIIa [38]), NK-κB, and the inflammasome NLRP3 [9]. This might occur even more frequently in COVID-19 patients with simultaneous enhancement of STING synthesis following excess of angiotensin II on cell membrane, secondary to the ACE1/2 imbalance (more pronounced in males), induced by the binding of SARS-CoV2 to ACE2 [42-45].

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Section: Introductionsupporting

confidence: 56%

Kawasaki-like diseases and thrombotic coagulopathy in COVID-19: delayed over-activation of the STING pathway?

Berthelot

Drouet

Lioté

2020

Emerging Microbes & Infections

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“…For instance, patients with KD associated with burn and severe sunburn injuries have been reported in Canada, Japan and China. [46][47][48][49] In these patients, KD occurred on days 2-5 of the burn or sunburn injury, and seven of the 10 patients showed negative results in their wound cultures. All patients responded to intravenous immunoglobulin administration, and one patient had coronary artery dilatation.…”

Section: Involvement Of Microbes Pamps and Damps In Kdmentioning

confidence: 99%

“…All patients responded to intravenous immunoglobulin administration, and one patient had coronary artery dilatation. [46][47][48][49] Damage-associated molecular patterns including small molecules and bioactive lipids that leak from damaged cells are significantly elevated immediately after a burn injury. Because necrosis is a predominant type of cell death in burns, these molecules contribute to the activation of many monocytes/macrophages, which is a characteristic pathological finding in patients with burns.…”

Section: Involvement Of Microbes Pamps and Damps In Kdmentioning

confidence: 99%

“…50 An infant with KD, following severe sunburns, showed high serum levels of highmobility group box protein 1 (HMGB1), one of the DAMPs identified during the acute phase of KD. 47 However, additional host and microbial factors may also be involved in the induction of KD, as burns and severe sunburn injuries are rarely associated with KD.…”

Section: Involvement Of Microbes Pamps and Damps In Kdmentioning

confidence: 99%

“…There have been reports of nonmicrobial triggers as well. For instance, patients with KD associated with burn and severe sunburn injuries have been reported in Canada, Japan and China 46–49 . In these patients, KD occurred on days 2–5 of the burn or sunburn injury, and seven of the 10 patients showed negative results in their wound cultures.…”

Section: Involvement Of Microbes Pamps and Damps In Kdmentioning

confidence: 99%

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The up‐to‐date pathophysiology of Kawasaki disease

2021

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Kawasaki disease (KD) is an acute systemic vasculitis of an unknown aetiology. A small proportion of children exposed to severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) or infected by Yersinia reproducibly develop principal symptoms of KD in various ethnic areas, but not in all studies. These microbes provoke a rapid cell‐damaging process, called ‘pyroptosis’, which is characterised by a subsequent release of proinflammatory cellular components from damaged endothelial and innate immune cells. In agreement with these molecular events, patients with KD show elevated levels of damage‐associated molecular patterns derived from cell death. In addition, an overwhelming amount of oxidative stress‐associated molecules, including oxidised phospholipids or low‐density lipoproteins, are generated as by‐products of inflammation during the acute phase of the disease. These molecules induce abnormalities in the acquired immune system and activate innate immune and vascular cells to produce a range of proinflammatory molecules such as cytokines, chemokines, proteases and reactive oxygen species. These responses further recruit immune cells to the arterial wall, wherein inflammation and oxidative stress closely interact and mutually amplify each other. The inflammasome, a key component of the innate immune system, plays an essential role in the development of vasculitis in KD. Thus, innate immune memory, or ‘trained immunity’, may promote vasculitis in KD. Hence, this review will be helpful in understanding the pathophysiologic pathways leading to the development of principal KD symptoms and coronary artery lesions in patients with KD, as well as in subsets of patients with SARS‐CoV‐2 and Yersinia infections.

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In vivo urinary compatibility of Mg-Sr-Ag alloy in swine model

Tie

Hort

Chen

et al. 2022

Bioactive Materials

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A biodegradable metallic ureteral stent with suitable mechanical properties and antibacterial activity remains a challenge. Here we reveal the scientific significance of a biodegradable Mg-Sr-Ag alloy with a favorable combination of balanced mechanical properties, adjustable indwelling time in urinary tract and evident antibacterial activity via in vivo experiments in a swine model. Attributed to the rheo-solidification process, equiaxial microstructure and significantly refined grains (average grain size: 27.1 μm) were achieved. Mg 17 Sr 2 and Mg 4 Ag were found as the primary precipitates in the matrix, due to which the alloy obtained ca. 111% increase in ultimate tensile strength in comparison to pure magnesium. Both the in vitro and in vivo results demonstrated the satisfactory biocompatibility of the alloy. Histological evaluation and bioindicators analysis suggested that there was no tissue damage, inflammation and lesions in the urinary system caused by the degradation process. The stent also improved the post-operative bladder functions viewed from the urodynamic results. Our findings highlight the potential of this alloy as antibacterial biodegradable urinary implant material.

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Kawasaki Disease Following Severe Sunburn Injury

Cited by 7 publications

References 19 publications

Kawasaki-like diseases and thrombotic coagulopathy in COVID-19: delayed over-activation of the STING pathway?

Kawasaki-like diseases and thrombotic coagulopathy in COVID-19: delayed over-activation of the STING pathway?

The up‐to‐date pathophysiology of Kawasaki disease

In vivo urinary compatibility of Mg-Sr-Ag alloy in swine model

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