632 Theme Issue Article
Platelet immunology in fungal infections
Infections and the role of plasma
Cornelia Speth; Günter Rambach; Cornelia Lass-Flörl
proteins and platelets
Division of Hygiene and Medical Microbiology, Innsbruck Medical University, Innsbruck, Austria
Summary
Up to date, perception of platelets has changed from key players in co-
agulation to multitaskers within the immune network, connecting its
most diverse elements and crucially shaping their interplay with in-
vading pathogens such as fungi. In addition, antimicrobial effector
molecules and mechanisms in platelets enable a direct inhibitory ef-
fect on fungi, thus completing their immune capacity. To precisely as-
sess the impact of platelets on the course of invasive fungal infections
is complicated by some critical parameters. First, there is a fragile bal-
ance between protective antimicrobial effects and detrimental reac-
tions that aggravate the fungal pathogenesis. Second, some platelet
Correspondence to:
Dr. Günter Rambach
Division of Hygiene and Medical Microbiology, Innsbruck Medical University
Schöpfstr. 41, 6020 Innsbruck, Austria
Tel.: +43 512 9003 70705, Fax: +43 512 9003 73700
E-mail: guenter.rambach@i-med.ac.at
Introduction
Platelets are small anucleate cell fragments derived from megaka-
ryocytes in the bone marrow. With a concentration of 150–400 x
108 per litre, they make up the most abundant solid component of
human blood. This abundance implies that each pathogen is con-
fronted with a superior number of platelets on entering the blood
stream. The key role of platelets in haemostasis and wound healing
often distracts attention from their participation in a number of
other processes, like tumour growth, atherosclerosis, inflamma-
tory reactions, pathogen attack and modulation of innate and
adaptive immunity (1).
Upon stimulation, platelets release a variety of biologically ac-
tive molecules from their storage granules. More than 300 different
proteins can be secreted after activation (2), including soluble and
membrane-bound components (more detailed in [1, 3, 4]). The
α-granules contain a multitude of effector molecules like growth
and mitogenic factors, proteases, clotting and fibrinolytic factors,
cytokines and chemokines, antimicrobial peptides, whereas sero-
tonin, ADP and calcium are the main components in dense bodies
(3).
Invading pathogens entering the blood stream are faced with
the immunocompetence of platelets, which comprises direct anti-
microbial effects as well as interactions with cells of the innate and
adaptive immune system. Platelets sense microorganisms by vari-
ous receptors, including toll-like receptors (TLRs) (5–8); the sub-
sequent direct antimicrobial attack of activated platelets can occur
by secretion of platelet microbicidal peptides (PMPs, thromboci-
dins and kinocidins), or generation of reactive oxygen species
Thrombosis and Haemostasis 112.4/2014
effects are exerted indirectly by other immune mediators and are thus
difficult to quantify. Third, drugs such as antimycotics, antibiotics, or
cytostatics, are commonly administered to the patients and might
modulate the interplay between platelets and fungi. Our article high-
lights selected aspects of the complex interactions between platelets
and fungi and the relevance of these processes for the pathogenesis of
fungal infections.
Keywords
Platelets, fungi, invasive infection, innate immunity
Downloaded by: UC Santa Barbara. Copyrighted material.
Received: January 24, 2014
Accepted after major revision: May 30, 2014
Epub ahead of print: July 3, 2014
http://dx.doi.org/10.1160/TH14-01-0074
Thromb Haemost 2014; 112: 632–639
(ROS) (1, 4, 9, 10). Furthermore, phagocytosis of particles and pa-
thogens is discussed for platelets ([11]; further references in [4]).
The immune functions of stimulated platelets are completed by
an intense crosstalk with other immune cells by secreted (e.g. cyto-
kines, chemokines) and membrane-bound molecules (e.g. CD154
that binds to CD40 on endothelial cells, neutrophils, monocytes,
DCs, B cells and T cells) (1, 4, 12–17). This crosstalk includes at-
traction and activation of neutrophils and monocytes, stimulation
of monocytes differentiation to macrophages and dendritic cells
(DCs), induction of DC maturation and triggering the secretion of
proinflammatory cytokines from macrophages. Platelets also build
bridges to adaptive immunity by direct and indirect interplay with
B cells (inducing proliferation, differentiation, memory cell gener-
ation) and T cells (differentiation, activation, cytokine produc-
tion). More detailed facts about platelets in immune and inflam-
matory processes are given in (1, 3, 4, 12, 18–22). In the following,
we describe how platelets apply these antimicrobial functions to
the situation of invasive fungal infections. The different beneficial
and detrimental consequences of platelet-associated reactions are
highlighted as well as the influence of some additional players,
such as the complement system and drugs (antimycotics, anti-
biotics, cytostatics).
Invasive fungal infections
Invasive fungal infections (IFIs) represent a major threat, particu-
larly to immunocompromised patients. Haematological and trans-
plant patients are primarily affected, but also individuals admitted
© Schattauer 2014

to intensive care units (ICU) are at risk, due to complex surgical
procedures, invasive medical devices, and prescription of long-
term, broad-spectrum antibiotics. Both yeasts and moulds signifi-
cantly contribute to morbidity and mortality of affected patients
and provoke longer hospital stays and increased health care costs.
Aspergillus, Candida, and Cryptococcus are the most prevalent cau-
sative species with varying distribution regarding geography, hos-
pital units and underlying patient condition. The mucormycetes
(formerly called zygomycetes) represent a further mould group
with ascending incidence (23, 24).
The poor clinical outcome despite all recent advances in diag-
nosis and antifungal therapy draws the attention to the elucidation
of IFI immunology. In the following, the knowledge about the rel-
evance of platelets as immune cells is summarized for different
fungal pathogens.
Interplay between platelets and fungi:
at different sites and with different fungal
molecules
Platelets are believed to interact with invading fungi at different
stages of the infection and also at different sites of the body.
In most invasive mould infections, the pathogens enter the
body as spores via the respiratory tract. In the lung, the fungi may
come for the first time in contact with platelets, since bleeding and
haemoptysis are rather common symptoms of IFI (25–27). In
further course of infection, the moulds can penetrate the endothe-
lial lining of the blood vessels of the lung; hyphal fragments might
break away and circulate in the bloodstream (28), giving rise to
further dissemination or even fungal sepsis.
Transmission of fungal pathogens can also start independently
from the lung. Candida, that causes the majority of IFI and fungal
sepsis, mostly starts the infection endogenously from colonisation
of gastrointestinal, oral or vaginal mucosa; otherwise disturbed
physical integrity of the skin barrier (e.g. by intravascular access
A B
Figure 1: Thrombocytes interact with fungal hyphae and conidia. Platelet-rich plasma was incubated with hyphae (A) or conidia (B) of A. fumigatus;
interaction was visualised with a field-emission scanning electron microscope (photos by K. Pfaller).
© Schattauer 2014
Speth et al. Platelet immunology in fungal infections 633
devices, wounds, surgery) allows infection and dissemination of
the pathogen into the systemic circulation (29, 30).
Infections and the role of plasma
Regardless of the precise way of infection, the bloodstream rep-
resents the main site of contact and mutual affectation between
proteins and platelets
fungi and platelets. Sequestration of IFI in various organs affords
another opportunity of interaction between fungi and platelets,
when bleeding into the affected organs occurs (31).
The overall image of platelet-fungus interaction not only in-
cludes different body sites where the contact can occur, but also
different fungal elements and products. Platelets can interact with
the fungal cell surface, with circulating cell wall fragments, as well
as with metabolites and other secreted fungal compounds (32–34).
Platelets recognise the surface of yeast or hyphal cells, and (e.g.
in the lung) of spores. Examples for this direct interaction are
given in ▶ Figure 1, showing the binding of platelets to fungal
hyphae (panel A) and to conidia (panel B). Furthermore, fungal
cell wall components such as 1,3-β-glucan or galactomannan are
released into the environment during growth or tissue invasion
(35, 36). Circulating in the blood stream, they might bind to as yet
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unknown receptors on the platelets and thus affect their activation
status; putative receptor candidates might be TLRs (37) or pro-
tease-activated receptors (PARs). In addition, each fungal species
secretes, dependent on the growth conditions, various compounds
(32–34) that might interact with platelets (4). Proteases are of
special interest within this fungal secretome, since platelets express
protease-activated receptors (PAR), which react on proteolytic
cleavage with induction of a signalling cascade. Mycotoxins, sec-
ondary fungal metabolites, are also known to change the biological
activity of platelets (4, 38).
Antifungal platelet activities and modulating
factors
The contact with fungal molecules, either surface-bound or se-
creted, can stimulate the platelets to exert a variety of antifungal
Thrombosis and Haemostasis 112.4/2014
 634 Speth et al. Platelet immunology in fungal infections
activities (▶ Figure 2). A direct fungistatic or fungicidal effect
might be mediated by the release of PMPs, but other molecules in
Infections and the role of plasma
the granules such as serotonin (39) may have a similar impact. Pla-
telets also act synergistically with antimycotic drugs, making the
proteins and platelets
fungi more vulnerable for their action. Other mediators contribu-
ting to the antifungal activity of platelets include the complement
system and phagocytes. The complement cascade is triggered by
activated platelets and can result in opsonisation of the pathogens,
thus facilitating their phagocytic clearance (see below). Platelets
further support the elimination of invading pathogens by chemot-
actically attracting, directly or via complement products, the
phagocytes and by activating them. A more detailed discussion is
given below for the different fungi.
The putative consequences of the platelet – fungus interaction
for the affected patient are multifaceted (▶ Figure 3). The benefi-
cial outcome might be a decrease of fungal load due to the anti-
microbial activity of the platelets as well as the support of adaptive
and innate immunity. This effect might significantly help to reduce
morbidity and mortality in infected patients. However, side effects
might accompany this big advantage of platelet activity. Tissue
damage might be induced if the triggered inflammatory reaction is
exaggerated or when the stimulated platelets aggregate and form
thrombi in the course of the fungal infection. Since activated pla-
telets are cleared from the blood stream, platelet loss and throm-
bocytopenia might be further harmful consequences of their anti-
microbial activity. Analogous to the situation in viral infections, it
can even be hypothesised that platelets might endocytose spores or
small hyphal fragments and transport them throughout the body.
This protection of the pathogen from immune attack might con-
tribute to dissemination ([40, 41]; reviewed in [4]).
Thrombosis and Haemostasis 112.4/2014
Not only the divergence of positive outcome and negative side-
effects makes it difficult to weigh the putative relevance of platelet
activity for the patient, but also the spectrum of factors that modu-
late the interplay between platelets and fungi (▶ Figure 4). Acti-
vated platelets themselves are also opsonised by complement and
thus a target for phagocytic elimination. This feedback mechanism
protects the body, but also limits the time span for the antifungal
activity of platelets. Fungi have also evolved mechanisms to restrict
platelets attack: metabolites inhibit the activation process of pla-
telets, and fungal surface molecules can help to evade this cell type.
In addition, drugs that are frequently prescribed to patients with
risk for IFIs further modify the extent of platelet activity. Some
antibiotics contribute to platelet elimination by triggering drug-in-
duced immune thrombocytopenia (DIT), and cytostatic drugs
generally impair production and maturation of platelets in the
bone marrow. These effects are discussed below in detail.
Platelets and Aspergillus
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Aspergillus is a ubiquitous mould in the environment; after inha-
lation the small conidia can germinate in the lungs of immunosup-
pressed individuals. A. fumigatus is the predominant human pa-
thogenic species to induce invasive aspergillosis (IA), an infection
which presents as a disease with high lethality and elevated treat-
ment costs. The rate of IA has steadily risen within the last decades
due to medical progress and thus higher numbers of immunocom-
promised patients (42, 43).
Platelets attach to Aspergillus fumigatus conidia and hyphae,
and this interaction is associated with a strong activation of the
Figure 2: Direct and
indirect antifungal
activities that might
be exerted by the pla-
telets. AM: antimycotics;
PMPs: platelet microbici-
dal peptides.
© Schattauer 2014

Figure 3: Putative
beneficial (green) and
detrimental (yellow)
consequences of the
interplay between pla-
telets and fungi.
platelets, as seen by increased exposure of CD62P (marker for
α-granule release) and CD63 (marker for dense granule release)
and by secretion of pro-inflammatory molecules (44, 45). Laser
microscopy visualised this activation, showing that the platelets
aggregated around the Aspergillus conidia and covered their sur-
face (46) (see also ▶ Figure 1). Platelet activation in IA might also
be triggered by soluble fungal compounds. During growth, Asper-
gillus fumigatus secretes factors, e.g. proteases and mycotoxins,
which induce granule release, aggregation, and membrane conver-
sion (47).
Aspergillus-driven platelet activation results in fungal damage,
as visible by loss of wall integrity and decreased viability (44, 46).
The relevance of this effect for infected patients can be proven stat-
istically: a low baseline platelet count is a highly significant predic-
tor for bad IA outcome and allows the stratification of patients into
risk categories (48).
However, as mentioned above, fungus-induced platelet acti-
vation might also harbour negative effects with excessive inflam-
mation and thrombosis. A strong hint comes from a comparative
study between two A. terreus isolates; the isolate that triggered pla-
telet activation more efficiently, induced faster death of infected
animals (49).
Platelets and Candida
The yeast Candida (C.) spp is a frequent part of the oral, vaginal,
and gastrointestinal flora and most Candida infections are endo-
genous. Perturbation of skin or mucosa integrity (intravascular ac-
cess devices, wounds), disturbed host defence and antibiotic treat-
ment are main risk factors for infection and dissemination. C. albi-
cans accounts for about half of invasive candidiasis cases, but the
non-albicans species (C. glabrata, parapsilosis, krusei and tropica-
lis) increase in frequency (23, 50).
© Schattauer 2014
Speth et al. Platelet immunology in fungal infections 635
Infections and the role of plasma
proteins and platelets
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Former studies proved attachment of C. albicans yeast cells and
germ tubes to aggregated platelets, whereas other species (C. tropi-
calis, parapsilosis, krusei) adhered to a much lesser extent (51, 52).
The adherence was confirmed in vivo: blood samples from Candi-
da-infected mice revealed that virtually all yeast cells were bound
to platelets (53). Interestingly, no difference between albicans and
the non-albicans species was detected in these animal experiments.
The consequences of Candida – platelet interaction are re-
ported somewhat contradictory. Willcox et al. demonstrated that
platelets react on the contact with Candida cells with activation
and aggregation (54). Confirmation comes from studies in pa-
tients with C. albicans sepsis, where increased levels of micropar-
ticles derived from activated platelets were detected in the blood
(55). In contrast, Carvalho-Neiva et al. showed that C. albicans
cells were unable to aggregate platelets; instead, preincubation of
platelets with the yeast even inhibited subsequent stimulation by
collagen or ADP (56). Similarly, Bertling et al. found that C. albi-
cans cells inhibit platelet aggregation and fibrinogen binding (38).
Secreted compounds might have additional effects on the platelets,
although these results are contradictory, too. While Bertling et al.
demonstrated that gliotoxin, a metabolite secreted by C. albicans,
inhibits fibrinogen binding of platelets and aggregation (38), Car-
valho reported that culture supernatants from C. albicans had no
inhibitory effect on platelet aggregation (56). Own experiments
even indicated an activation of platelets by gliotoxin (47).
The Candida-induced modification of platelets retroactively af-
fects the viability of the yeast cells. Platelet-rich plasma has anti-
microbial effectiveness against Candida and inhibits its growth
(54, 57). Detailed analyses allowed the identification of three anti-
microbial peptides secreted by platelets and harbouring anticandi-
dal activity: the chemokine RANTES, platelet factor-4 (PF-4) and
thrombocidin-1 (TC-1) (58, 59).
Thrombosis and Haemostasis 112.4/2014
 636 Speth et al. Platelet immunology in fungal infections
Platelets and other fungi
Infections and the role of plasma
Mucormycetes
Mucormycosis is caused by the ubiquitous filamentous mucormy-
proteins and platelets
cetes, formerly called zygomycetes; it has emerged as a common
mycosis in patients with immunosuppression, iron overload, or
diabetes mellitus (60). The high tendency of angioinvasion implies
that contact with platelets occurs particularly frequent.
Platelets adhere to hyphae and spores of different mucormy-
cetes species, such as Rhizomucor, Mucor, Lichtheimia and Rhizo-
pus. This adherence runs parallel to exposure of the activation
marker CD62P on the platelet surface (61). Platelet adhesion and
activation result in hyphal damage and suppression of spore ger-
mination, indicating a critical role of this cell type also in mucor-
mycosis (61). However, the frequently reported thromboses (62)
indicate the detrimental side effects for the beneficial platelet-de-
rived antimicrobial capacity.
Cryptococcus
The encapsulated yeast Cryptococcus induces severe infections
mainly in HIV-infected individuals. The lung is most commonly
affected, but meningitis is also a frequent manifestation. Dissemi-
nation from lung to brain implies contact with platelets and a pu-
tative role of these cell fragments in the outcome of infection.
Similar to the results with Candida, Carvalho-Neiva et al. found
Cryptococcus to inhibit platelet activation (56). More detailed ana-
lyses revealed differences in the platelet interaction between capsu-
lar and non-encapsulated cryptococcal strains. Platelets exclusively
attached to non-encapsulated isolates, which were also the only
ones to be susceptible to antifungal activity of the platelet micro-
bicidal peptide tPMP (63). Further platelet-derived proteins that
Thrombosis and Haemostasis 112.4/2014
act fungicidal against Cryptococcus are thrombocidins, RANTES,
PF-4 and the fibrinopeptins (9, 59).
Single reports also imply that platelets might play a role in other
fungal infections, e.g. by Fusarium, Pneumocystis or Scedosporium,
however, analyses for these pathogens are yet too fragmentary.
Additional players in the interplay platelets –
fungi
A variety of additional factors influence and modify the interplay
between platelets and fungi, including cellular (e.g. neutrophils,
monocytes/macrophages) and non-cellular (e.g. complement,
antimycotics, antibiotics, cytostatics) ones. These factors can have
dual effects: on one hand they can enhance the antimicrobial activ-
ity of platelets or contribute to their antifungal effect; on the other
side they might interfere with the platelet-associated immune
functions (see ▶ Figure 3 and ▶ Figure 4). Due to limited space
only some selected players are discussed here.
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Complement
The complement system is a potent element of the soluble innate
immunity. Being activated by three different pathways, the com-
plement cascade can fulfil various functions (reviewed in [64–66]):
(i) complement proteins can form pores in the membrane of pa-
thogens or cells with subsequent lysis; (ii) complement factors op-
sonise pathogens or cells to target them for phagocytic clearance;
(iii) complement-derived anaphylatoxins (C3a, C5a) attract
phagocytes to the site of infection; (iv) complement activates
lymphocytes, thus guaranteeing effective adaptive immunity.
Figure 4: Factors inter-
fering with platelet-
associated antifungal
functionality. AB: anti-
biotics, CS: cytostatics,
DIT: drug-induced im-
mune thrombocytopenia.
© Schattauer 2014

In the course of IFI, complement can be hypothesized to modu-
late the platelet-fungus interaction in several respects, which are
described in the following. Platelets that have been activated by
fungi might initiate the complement cascade and thus become a
target for complement-induced lysis or phagocytic clearance. Indi-
cations for that come from reports that platelets can trigger the
complement cascade by different mechanisms. CD62P on the sur-
face of activated platelets can start the alternative complement
pathway (67), and the classical pathway might be induced by bind-
ing of its starter molecule C1q to receptors on platelets (68). Fur-
thermore, chondroitin sulphate that is released from platelet gran-
ules can subsequently bind to the surface of activated platelets and
interact with complement proteins (69, 70). Complement acti-
vation can trigger lysis, but also opsonisation of the platelet sur-
face. As a consequence, phagocytes bearing corresponding recep-
tors (e.g. CR3) can bind and eliminate the opsonised platelets. A
complement-dependent loss of activated platelets by lysis or pha-
gocytic clearance was shown for diseases such as immune throm-
bocytopenic purpura (ITP), where complement deposition on pla-
telets correlates with the degree of thrombocytopenia (71).
Alternatively, fungus-induced platelet activation and subse-
quent opsonisation might support formation of thrombosis, a hall-
mark of IFI pathogenesis. A correlation of complement deposition
on platelets with appearance of arterial thrombosis was demon-
strated for patients with systemic lupus erythematodes (72, 73).
Some putative mechanisms how complement participates in
thrombus formation are described in literature. First, endothelial
cells might interact directly with opsonised platelets, since they ex-
press the complement receptors CR1 (CD35) and CD4
(CD11c/CD18) (74). Second, C5a up-regulates the expression of
ICAM-1 on endothelial cells, thus enhancing their stickiness for
platelets and phagocytes that express the counter-receptor comple-
ment receptor 3 (CR3) (75). C5a also upregulates tissue factor ex-
pression on endothelial cells, a membrane protein that serves as
cofactor for blood coagulation and thrombus formation (76, 77).
Third, complement activation on platelets results in formation of
C5b-9, which stimulates procoagulant activity (78). Fourth, pla-
telets expressing complement receptors (4) can bind to opsonised
platelets, thus further increasing the formation of thrombi (79). It
is intriguing to speculate that these mechanisms also contribute to
thrombosis in IFI patients.
Antimycotic drugs
Antimycotic drugs in therapy and prophylaxis can also influence
the interplay between platelets and fungi.
Fluconazole treatment significantly diminishes Candida adher-
ence to platelets; the presence of PMPs further enhances this effect
(80). Consequently, dissemination of the yeast and its binding to
the endothelium via aggregated platelets might be reduced. On the
other hand, this process might interfere with platelets’ anti-candi-
dal function (trapping of Candida cells, presenting them to phago-
cytes, release of antimicrobial peptides). A rabbit model of Candi-
da-induced endocarditis evaluated these two aspects and revealed
that fluconazole and PMPs collaborate to support fungal clearance
© Schattauer 2014
Speth et al. Platelet immunology in fungal infections 637
in the infected animals (81). In vitro studies confirmed this posi-
tive effect, showing increased fluconazole efficacy when Candida
Infections and the role of plasma
isolates are susceptible to PMPs (81).
Besides fluconazole, other antimycotic drugs have also been
proteins and platelets
shown to interact with platelets, supporting their action and being
supported by them in the antifungal effect. The combination of
platelets and anidulafungin significantly reduced the germination
rate of A. fumigatus conidia and hyphal elongation (82). Fur-
thermore, platelets and amphotericin B or posaconazole had a
more prominent effect on A. fumigatus germination than the
antimycotic or the platelets alone (83). A similar effect could be
demonstrated for some Aspergillus species other than A. fumigatus
(84). Platelet-derived serotonin was also able to enhance the am-
photericin activity against A. fumigatus (85).
Own unpublished results highlight another aspect of the inter-
play between antimycotic drugs and platelets. “Drugs can not only
increase the susceptibility of the fungus for the antimicrobial ac-
tion of the platelets and vice versa, but also induce platelet acti-
vation and thus support their antifungal activity, as shown for the
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echinocandins caspofungin and anidulafungin (Speth et al., manu-
script in preparation).
Other drugs (cytostatics, antibiotics)
Most immunosuppressed patients at risk of fungal infections also
receive other drugs, particularly antibiotics and cytostatics; at least
some of them may modify the relation between platelets and fungi.
For that reason, some selected aspects are discussed in the follow-
ing.
Various antibiotics and cytostatics can induce platelet loss with
consequent risk of bleeding, but also a loss of platelet-associated
antifungal activity. A DIT can result either from decreased platelet
production by inhibition of haematopoiesis in the bone marrow or
from increased platelet destruction by an immune-mediated
mechanism. Linezolid, an oxazolidinone antibiotic that inhibits
the bacterial protein synthesis, suppresses the bone marrow with
subsequent thrombocytopenia (86). The same myelosuppressive
effect is induced by chemotherapeutic drugs used for patients with
malignancies (87). In contrast, the beta-lactam antibiotic penicillin
induces DIT by increasing platelet destruction: although not im-
munogenic itself, penicillin can form a linkage with platelet pro-
teins and thus induce the formation of antibodies that recognize
the platelet protein and trigger platelet removal in the spleen and
the liver by cells of the mononuclear phagocyte system (88).
Not only the number, but also the functions of platelets may be
affected by drugs. For example, beta-lactam antibiotics were
shown to exert inhibitory effects on platelet activation (89, 90).
Summary and outlook
Understanding the interaction of platelets with disseminating fun-
gal pathogens might provide important insights in the pathogen-
esis of IFIs. Pivotal aspects, like attraction of immune cells, com-
plement activation, and release of microbicidal proteins, have al-
Thrombosis and Haemostasis 112.4/2014
 638 Speth et al. Platelet immunology in fungal infections
ready been clarified and will surely be complemented in the near
future. A central principle is the bivalence of the outcome of pla-
Infections and the role of plasma
telet-associated reactions: beneficial antifungal effects with de-
crease of disease burden are faced with harmful consequences
proteins and platelets
such as excessive inflammation, thrombosis and thrombocytope-
nia. Additional valuable insights in the role of platelets in IFIs
might, in the far future, provide the prerequisites for the develop-
ment of novel platelet-based adjunctive therapies.
Acknowledgements
This work was supported by the Austrian National Bank (Project
15352) and by the Austrian Science Fund (FWF Project
P26117-B20). We are very grateful to A.Univ.Prof. Kristian Pfaller
for Electron Microscopy.
Conflicts of interest
None declared.
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