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could contribute by directly inhibiting mast cell release of allergy medi-
ators. 133 This type of molecule may be present in Ascaris because sequence
alignment shows that it has an orthologue product. In addition, reduction
in the basophil responsiveness has been reported recently in mice
chronically infected with filarial nematodes 134 and humans infected with
Ascaris and other helminths. 135 Although the mechanisms are not clear,
the fact is that allergy diagnosis by skin testing is impaired in parasited
populations in the tropics. Since the immunosuppression may also
diminish allergy symptoms, this epidemiologic finding may be not visible
at the individual patient e physician level. However, if sensitization to
allergens is evaluated in these communities using skin tests, false negative
results will be common, which may lead to the opinion that not only
allergy symptoms but also allergen sensitization are infrequent in par-
asited populations. Whether this is what actually occurs is a matter of
current investigation in our birth cohort. 45
AS CARIASIS AND ASTHMA SEVERI TY
There are few studies evaluating the role of ascariasis on the severity of
asthma. This may be because of the inherent general difficulties in the
investigation of risk factors for asthma severity, but also because the
studies should be done in places where most of the population does not
receive the appropriate asthma treatment. One indirect analysis of the
problem is to observe the effect of anthelmintic treatment on clinical
symptoms. In one study the treatment ameliorated the frequency asth-
matic crisis or other markers of severity, suggesting that ascariasis
increases asthma severity in endemic zones. 136 In a more direct way,
Hunninhake et al. studied the problem in a cross-sectional survey in
asthmatic children from Costa Rica 69 and found that sensitization to
Ascaris was associated with increased severity and morbidity of asthma.
Although in this study the role of co-sensitization with mites, one of the
main causes of asthma, was not totally excluded, the side effects of the IgE
response to Ascaris cannot be ruled out. As has been analyzed in this
chapter, most of the evidence that supports an increase of the Th2
inflammatory response in the lungs induced by ascariasis is related to the
immune responses to the nematode.
The direct effect of pro-inflammatory cytokines on the airways is
another possibility when analyzing the relationship between ascariasis
and asthma severity. This is especially problematic because it is expected
that such a mechanism may occur during the most severe infec-
tions by Ascaris , which are supposed to be the majority inducers of
immunoregulation. However, it should be mentioned that cytokines such
as TNF-alpha, IL-13, and IL-17, which are central mediators of allergic
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