<i>Mucor circinelloides</i> induces platelet aggregation through integrin αIIbβ3 and FcγRIIA

Ghuman, Harlene; Shepherd-Roberts, Alicia; Watson, SP; Zuidscherwoude, Malou; Watson, Steve P.; Voelz, Kerstin

doi:10.1080/09537104.2017.1420152

Cited by 16 publications

(7 citation statements)

References 32 publications

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“…Fungi and bacteria can interact with platelets and induce platelet activation and aggregation (86, 87, 89). Although many bacteria activate platelets in a GPIIb/IIIa- or FcγRIIA-dependent manner and involve plasma proteins such as IgG, complement proteins and fibrinogen, other bacteria directly bind and activate platelet receptors such as GPVI and TLRs, increasing platelet activation and PLA formation (46, 87, 106).…”

Section: Platelets In Sepsismentioning

confidence: 99%

Platelets in Sepsis: An Update on Experimental Models and Clinical Data

et al. 2019

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Beyond their important role in hemostasis, platelets play a crucial role in inflammatory diseases. This becomes apparent during sepsis, where platelet count and activation correlate with disease outcome and survival. Sepsis is caused by a dysregulated host response to infection, leading to organ dysfunction, permanent disabilities, or death. During sepsis, tissue injury results from the concomitant uncontrolled activation of the complement, coagulation, and inflammatory systems as well as platelet dysfunction. The balance between the systemic inflammatory response syndrome (SIRS) and the compensatory anti-inflammatory response (CARS) regulates sepsis outcome. Persistent thrombocytopenia is considered as an independent risk factor of mortality in sepsis, although it is still unclear whether the drop in platelet count is the cause or the consequence of sepsis severity. The role of platelets in sepsis development and progression was addressed in different experimental in vivo models, particularly in mice, that represent various aspects of human sepsis. The immunomodulatory function of platelets depends on the experimental model, time, and type of infection. Understanding the molecular mechanism of platelet regulation in inflammation could bring us one step closer to understand this important aspect of primary hemostasis which drives thrombotic as well as bleeding complications in patients with sterile and infectious inflammation. In this review, we summarize the current understanding of the contribution of platelets to sepsis severity and outcome. We highlight the differences between platelet receptors in mice and humans and discuss the potential and limitations of animal models to study platelet-related functions in sepsis.

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Section: Platelets In Sepsismentioning

confidence: 99%

Platelets in Sepsis: An Update on Experimental Models and Clinical Data

et al. 2019

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“…Although traditionally described as playing a key role in maintaining haemostasis, thrombosis and inflammation, platelets have more recently been recognised as key players of the innate immune response to infection [132]. Whilst nonphagocytic, platelets have been shown to interact with and be activated by bacteria, viruses and fungi, leading to the release of various platelet antimicrobial peptides [133][134][135][136][137]. Thrombocytopenia is a known risk factor for invasive fungal infections, including candidiasis [136].…”

Section: Candidemiamentioning

confidence: 99%

Immune Sensing of Candida albicans

Bojang

Ghuman

Kumwenda

et al. 2021

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Candida albicans infections range from superficial to systemic and are one of the leading causes of fungus-associated nosocomial infections. The innate immune responses during these various infection types differ, suggesting that the host environment plays a key role in modulating the host–pathogen interaction. In addition, C. albicans is able to remodel its cell wall in response to environmental conditions to evade host clearance mechanisms and establish infection in niches, such as the oral and vaginal mucosa. Phagocytes play a key role in clearing C. albicans, which is primarily mediated by Pathogen Associated Molecular Pattern (PAMP)–Pattern Recognition Receptor (PRR) interactions. PRRs such as Dectin-1, DC-SIGN, and TLR2 and TLR4 interact with PAMPs such as β-glucans, N-mannan and O-mannan, respectively, to trigger the activation of innate immune cells. Innate immune cells exhibit distinct yet overlapping repertoires of PAMPs, resulting in the preferential recognition of particular Candida morphotypes by them. The role of phagocytes in the context of individual infection types also differs, with neutrophils playing a prominent role in kidney infections, and dendritic cells playing a prominent role in skin infections. In this review, we provide an overview of the key receptors involved in the detection of C. albicans and discuss the differential innate immune responses to C. albicans seen in different infection types such as vulvovaginal candidiasis (VVC) and oral candidiasis.

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“…Previous literature has indicated that GP IIb/IIIa recognized the fungus Mucor circinelloides and a variety of viruses, such as dengue virus and hantavirus, leading to platelet activation and aggregation ( Ghuman et al., 2019 ; Gautam et al., 2020 ). However, studies on GP IIb/IIIa-mediated interactions between C. albicans and platelets are limited.…”

Section: Discussionmentioning

confidence: 99%

GP IIb/IIIa-Mediated Platelet Activation and Its Modulation of the Immune Response of Monocytes Against Candida albicans

Zheng

Duan

Tang

et al. 2021

Front. Cell. Infect. Microbiol.

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Candida albicans is the most common fungal pathogen in humans, causing invasive disease and even potentially life-threatening systemic infections when tissue homeostasis is disrupted. Previous studies have identified an essential role of platelets in infection and immunity, especially when they are activated. However, it is still unclear whether platelets can be activated by C. albicans, and even less is known about the role of platelets in C. albicans infection. Herein, we showed that C. albicans induced platelet activation in vitro. C. albicans elevated the levels of AKT Ser473 phosphorylation, and inhibition of the PI3K-AKT signaling pathway reversed C. albicans-induced platelet activation. Surprisingly, C. albicans-induced platelet activation occurred in an integrin glycoprotein (GP) IIb/IIIa-dependent manner but was independent of the pattern recognition receptors toll-like receptor (TLR) 2 and TLR4. Interestingly, platelets enhanced the phagocytosis of human monocytes challenged with C. albicans and upregulated the expression of inflammatory cytokines, which were dependent on platelet activation mediated by GP IIb/IIIa. The present work provides new insights into the role of activated platelets in the defense against C. albicans, highlighting the importance of GP IIb/IIIa in the recognition of C. albicans.

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Mucor circinelloides induces platelet aggregation through integrin αIIbβ3 and FcγRIIA

Cited by 16 publications

References 32 publications

Platelets in Sepsis: An Update on Experimental Models and Clinical Data

Platelets in Sepsis: An Update on Experimental Models and Clinical Data

Immune Sensing of Candida albicans

GP IIb/IIIa-Mediated Platelet Activation and Its Modulation of the Immune Response of Monocytes Against Candida albicans

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