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2017 ; 8
(ä): 607
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The Complement System: A Prey of Trypanosoma cruzi
#MMPMID28473804
Lidani KCF
; Bavia L
; Ambrosio AR
; de Messias-Reason IJ
Front Microbiol
2017[]; 8
(ä): 607
PMID28473804
show ga
Trypanosoma cruzi is a protozoan parasite known to cause Chagas disease (CD), a
neglected sickness that affects around 6-8 million people worldwide. Originally,
CD was mainly found in Latin America but more recently, it has been spread to
countries in North America, Asia, and Europe due the international migration from
endemic areas. Thus, at present CD represents an important concern of global
public health. Most of individuals that are infected by T. cruzi may remain in
asymptomatic form all lifelong, but up to 40% of them will develop
cardiomyopathy, digestive mega syndromes, or both. The interaction between the T.
cruzi infective forms and host-related immune factors represents a key point for
a better understanding of the physiopathology of CD. In this context, the
complement, as one of the first line of host defense against infection was shown
to play an important role in recognizing T. cruzi metacyclic trypomastigotes and
in controlling parasite invasion. The complement consists of at least 35 or more
plasma proteins and cell surface receptors/regulators, which can be activated by
three pathways: classical (CP), lectin (LP), and alternative (AP). The CP and LP
are mainly initiated by immune complexes or pathogen-associated molecular
patterns (PAMPs), respectively, whereas AP is spontaneously activated by
hydrolysis of C3. Once activated, several relevant complement functions are
generated which include opsonization and phagocytosis of particles or
microorganisms and cell lysis. An important step during T. cruzi infection is
when intracellular trypomastigotes are release to bloodstream where they may be
target by complement. Nevertheless, the parasite uses a sequence of events in
order to escape from complement-mediated lysis. In fact, several T. cruzi
molecules are known to interfere in the initiation of all three pathways and in
the assembly of C3 convertase, a key step in the activation of complement.
Moreover, T. cruzi promotes secretion of plasma membrane-derived vesicles from
host cells, which prevent the activity of C3 convertase C4b2a and thereby may
hinder complement. In this review, we aim to present an overview on the
strategies used by T. cruzi in order to circumvent the activation of complement
and, consequently, its biological effects.
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