(Eh) y metanólico (Em) de Pera distichophylla sobre un aislado de ...

Helminth infection can bias the human immune response
towards a Th2 type over a Th1 and a Th17
response (Walsh et al., 2009), thus impairing the
host’s ability to control concurrent intracellular microparasite
infections (Ezenwa et al., 2010), such
as T. cruzi, and potentially modify disease dynamics.
Hence, helminths are likely to make hosts more
resistant to pathogens in which protection is mediated
by the Th2-like response and more susceptible
to pathogens in which protection is mediated by the
Th1-like response.
In the last five years, several interesting review
articles dealing with the immunomodulation of
helminths in their hosts and its consequences on coinfections
with intracellular protozoans have been
published (van Riet et al., 2007; Graham, 2008;
Pullan and Brooker, 2008; Helmby, 2009; Moreau
and Chauvin, 2010; Supali et al., 2010; Ezenwa
and Jolles, 2011, among others), coinciding on
the ability of helminths to alter host immune
responses. This ability could be of detriment to the
host if it negatively interferes in protective immune
responses against other infections or may have a
beneficial role in controlling autoimmune or other
excessive inflammatory responses provoked by
other pathogens.
Considering intracellular protozoan parasites,
the effects of helminth co-infection have been
studied mainly in malaria and secondarily in
leishmaniosis and toxoplasmosis. There are two
main aspects to elucidate as a consequence of the
interaction. First, if the susceptibility to acquire
the protozoan infection is higher or lower in
wormy hosts, and if these hosts present better or
worse clinical signs compared with those free of
helminths.
Malaria and helminths
Although interest in the subject of the interaction
between worms and malaria has recently increased,
there are still no large-scale studies in humans
dealing with the real consequences of this interaction,
i. e. to determine whether worms increase
or decrease incidence and whether they protect or
not from different presentations of severe malaria.
An early study performed more than 30 years
ago described that anthelminthic treatment of
severe ascariasis in a high-transmission area was
followed by an increase in symptomatic malaria
Rev. Ibero-Latinoam. Parasitol. (2012); 71 (1): 5-13
CHAGAS DISEASE IN A WORMY WORLD
(Murray et al., 1978). However, several decades
later, the notion that infection with helminths
increases the susceptibility to malaria infection was
backed (Hartgers and Yazdanbakhsh, 2006).
Concerning the course of the disease, deworming
malaria patients would be like ‘robbing Peter
to pay Paul’ since evidence suggests that helminth
co-infection leads to higher plasmodium loads being
less harmful, as helminth infection protects from
acute renal failure and cerebral malaria (Specht and
Hoerauf, 2007). In a murine model, Schistosoma
mansoni infection reduced the incidence of cerebral
malaria (Waknine-Grinberg et al., 2010). Recently,
a survey carried out in Nigeria provided evidence
that asymptomatic falciparum malaria and intestinal
helminth infections do co-exist without clinical
symptoms (Ojurongbe et al., 2011).
However, in filarial/malaria co-infection, the
presence of filarial infection may lead to a profound
inability to mount an effective response to provide
protection against severe malaria and also dampens
the success of malaria vaccination schemes in
filaria-endemic regions of the world (Metenou et
al., 2011).
These analyses of helminth and malaria coinfections
seem controversial depending on the
helminth species involved, the intensity of duration
of worm infection, and the age of the individual
under study. Nevertheless, helminths may be
a missing link in the understanding not only a
number of facts about malaria but also the failures
of certain anti-malaria vaccine strategies (Nacher,
2001; Noland et al., 2010).
Leishmaniosis and helminths
Just as in CD, a Th1-type immune response
is crucial in the control of leishmania infection.
However, excessive inflammation caused by Th1
cytokine release has also been implicated in the
pathogenesis of cutaneous leishmaniosis.
Two first studies examining the interplay
between schistosomiasis and Leishmania major
(Yoshida et al., 1999; La Flamme et al., 2002)
showed not only a delay in lesion resolution but
also in its development (La Flamme et al., 2002)
in mice. Later, the co-infection between a filarial
nematode and also L. major in mice was studied
(Lamb et al., 2005) and the results obtained were
similar to those previously observed (La Flamme
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