Coronary Vasculitis Induced in Mice by Cell Wall Mannoprotein Fractions of Clinically Isolated &lt;i&gt;Candida&lt;/i&gt; Species

Tanaka, Hiroaki; Yanai, Chiho; Miura, Noriko N.; Ishibashi, Keiichiro; Yamanaka, Daisuke; Ohnìshì, H.; Ohno, Naohito; Adachi, Yoshiyuki

doi:10.3314/mmj.20-00008

Cited by 5 publications

(4 citation statements)

References 76 publications

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“…Following this, Candida sp. derived substances were demonstrated to induce coronary vasculitis in experimental mice models ( 64 , 65 ). This implies that the putative causative agent, possibly a fungal toxin, is transported across by strong air currents that develop in upper troposphere, supporting the theory that KD may be caused by an ubiquitous air-borne infectious organism.…”

Section: Airborne Agentsmentioning

confidence: 99%

Kawasaki disease and the environment: an enigmatic interplay

Aggarwal,

Pilania,

Sharma

et al. 2023

Front. Immunol.

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Kawasaki disease (KD) is a common systemic vasculitis of childhood. Although it has been almost 6 decades since Dr. Tomisaku Kawasaki reported the first case series of KD, the underlying cause remains a mystery. KD is a self-limiting disease. However, a dreaded complication is development of coronary artery abnormalities (CAAs). KD is the most common cause of acquired heart disease in children in the developed world and is being increasingly reported from developing countries too. Over the years, significant observations have been made about epidemiology of KD. It usually affects children below 5, has male preponderance and has significantly higher incidence in North East Asian countries. While several hypotheses have been proffered for etiology of KD, none have been conclusive. These include associations of KD epidemics in Japan and the United Stated with changes in tropospheric wind patterns suggesting wind-borne agents, global studies showing peaks of incidence related to season, and increased rates in populations with a higher socioeconomic profile related to hygiene hypothesis and vaccination. Furthermore, the self-limiting, febrile nature of KD suggests an infectious etiology, more so with sudden decline noted in cases in Japan with onset of COVID-19 mitigation measures. Finally, single nucleotide polymorphisms have been identified as possible risk alleles in patients with KD and their significance in the pathogenesis of this disease are also being defined. The purpose of this review is to elucidate the puzzling associations of KD with different environmental factors. Looking at patterns associated with KD may help us better predict and understand this disease.

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Section: Airborne Agentsmentioning

confidence: 99%

Kawasaki disease and the environment: an enigmatic interplay

Aggarwal,

Pilania,

Sharma

et al. 2023

Front. Immunol.

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“…Dectin-2 (CLEC6A) is a CLR that mainly exists in dendritic cells, macrophages, and neutrophils. Dectin-2 has been proven to recognize α-Mannan in the fungal cell walls (Figure 3) [59,60]. After α-mannan is recognized by Dectin-2, it can also send signals through CARD9, causing the activation of NF-κB, and inducing the production of inflammatory cytokines [61].…”

Section: Dectin-2mentioning

confidence: 99%

The interaction of Candida albicans with C-type lectin receptors

2023

PPM

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Candida albicans (C. albicans) is a ubiquitous commensal in the mammalian flora and the most prevalent fungal pathogen of humans. As an opportunistic fungus, C. albicans can cause mucosal and invasive infections. Invasive candidiasis infected by C. albicans is a leading cause of perioperative death in immunocompromised and immunodeficient patients. The morphological change from the yeast to the mycelium plays a key role in the pathogenesis of C. albicans. C-type lectin receptors (CLRs), including Dectin-1, Dectin-2, Dectin-3, Mincle, and dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin, are among the pattern recognition receptors expressed by innate immune cells that can recognize C. albicans. The emergence of drug-resistant C. albicans put pressure on the healthcare system, whereby CLRs have also attracted extensive attention from physicians. Thus, in this article, we discuss the interaction between CLRs and C. albicans and the treatment prospects of CLRs on anti-C. albicans.

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“…The CAWS complex was prepared as described elsewhere 21,22,40,41 . Briefly, C. albicans ATCC 18804 ® was cultured in C-limiting medium 42 for 48h.…”

Section: Introductionmentioning

confidence: 99%

“…A wide variety of innate and adaptive immune cells, including monocytes, macrophages, neutrophils, and Tlymphocytes, infiltrate the coronary artery wall in KD, which is linked to the condition 3,[17][18][19][20][21][22] . These cells produce a large quantity of inflammatory cytokines such as Interleukin 1 (IL1), tumor necrosis factor a (TNF), and Interleukin 17 (IL17) that can directly disturb the vascular homeostasis [23][24][25] and lead to vascular dysfunction as described elsewhere [23][24][25][26] .…”

Section: Introductionmentioning

confidence: 99%

Progression of vascular function and blood pressure in a mouse model of Kawasaki disease

DelVechio

Alves

Saiyi

et al. 2022

Preprint

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Background: Kawasaki disease (KD) is a systemic vasculitis of childhood characterized by vascular damage in the acute stage, which can persist into the late stage. Aneurysms, myocardial infarction, and death are long-standing complications associated with KD. The vascular mechanisms in the cardiovascular risk of KD are not fully studied. Herein, we investigated the vascular function and blood pressure regulation in a murine model of KD. Material and methods: We used the Candida albicans water soluble (CAWS) fraction model. Mice were injected with 4 mg CAWS for five consecutive days and separated into 3 groups. Control (Ctrl): water injected for 5 days; CAWS 7 days (C7): CAWS injected for 5 days plus 2 additional days of wait; CAWS 28 days (C28): CAWS injected for 5 days plus 23 additional days of wait. Blood pressure was analyzed via radiotelemetry. In the end, the heart and arteries were harvested for vasculitis characterization and vascular function in a wire myograph. Rat Aortic Vascular Smooth Muscle cells (RASMC) were used to dissect the molecular mechanisms in vitro. Main findings: C7 presented elevated inflammatory markers in the coronary area (CA) and abdominal aortae (AA), whereas C28 showed severe vasculitis in CA and AA. No difference was found in blood pressure and heart rate. Vascular dysfunction characterized by higher contractility to norepinephrine (NA) in C7 and C28 was abolished by blocking nitric oxide (NO) production, reactive oxygen species (ROS), and cyclooxygenase (COX)-derived products. RASMC treated with CAWS (10ug/mL) presented an increase in COX2 expression, which was prevented by pre-treating the cells with TAK-242 [Toll like receptor 4 (TLR4) antagonist, 3x10-5M]. Conclusion: Our data indicate that the murine model of KD is associated with vascular dysfunction likely dependent on COX-derived products, oxidant properties, and NO bioavailability. Furthermore, VSMC may present an important role in the genesis of vascular dysfunction and vasculitis via the TLR4 pathway. Finally, the CAWS model seems not to be appropriate to study KD-associated shock. More studies are necessary to understand whether vascular dysfunction and COXs are triggers for vasculitis.

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Coronary Vasculitis Induced in Mice by Cell Wall Mannoprotein Fractions of Clinically Isolated <i>Candida</i> Species

Cited by 5 publications

References 76 publications

Kawasaki disease and the environment: an enigmatic interplay

Kawasaki disease and the environment: an enigmatic interplay

The interaction of Candida albicans with C-type lectin receptors

Progression of vascular function and blood pressure in a mouse model of Kawasaki disease

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