Jaarboek no. 87. 2008/2009 - Koninklijke Maatschappij voor ...

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130 Diligentia frequent in children with older siblings and those from large families. He suggested that frequent exchange of childhood infections among siblings in large and less affluent families was responsible for the lower incidence of allergic disorders. Following interest in the hygiene hypothesis numerous studies have examined the relationship between infections and allergic disorders using approximations to measure infections. Several associations between viral, bacterial and parasitic infections and allergies have been shown with indirect measurements of infections. Antibodies to hepatitis A, to Toxoplasma gondii or H. Pylori, as well as cellular responses to mycobacterial antigens were shown to be inversely associated with prevalence of asthma or skin prick test positivity. The only studies that have related the actual presence of infections to allergic disorders are those measuring viral or parasitic infections in the cohorts studied. Whereas respiratory viral infections have been shown to be associated with exacerbation of asthma, parasitic helminth infections have often been shown to be negatively associated with allergic disorders. However, the latter relationship is complex as a number of studies have indicated that helminth infections do increase the risk of allergic sensitization, atopy and symptoms. In most studies where an exacerbation is seen, the helminth infection loads were light or humans were not the definitive host. The current thinking is that the protective effects of helminth infections on allergic disorders would only be seen if helminth infections are chronic in nature and intense. Interestingly, short-term application of anti-helminth drugs (12 months) in Ecuador did not change the prevalence or atopy nor of clinical signs of allergy (wheeze) in comparison to the untreated group. However, long-term anti-helminth treatment in Venezuelan (> 22 months) or Gabonese (> 30 months) children resulted in increased skin prick test reactivity to house dust mite, supporting a direct effect of helminth infections on allergic atopy. The cellular immunological explanations of the Hygiene Hypothesis In Western countries where the increase in allergic disorders had been observed, the hypothesis was put forward that allergic responses might result from a faulty maturation and polarizaiton of the immune system. It was presumed that the decrease in exposure to bacterial and viral infections might lead to a slower development of Th1 adaptive responses, allowing pro allergic Th2 responses to develop unhindered. Birth cohort studies in affluent countries seem to support the notion that a slow developing Th1 response could indeed be responsible for increased susceptibility to allergic disorders. The distorted balance between Th1 and Th2 becomes interesting when considering developing countries and in particular the rural areas in these countries, where infections leading to Th2 type responses are highly prevalent. The parasitic helminths are the strongest natural stimuli for the development of Th2 responses, characterized by IL-4,IL-5 and IL-13 secretion from T cells and resultant increased IgE antibodies and eosinophils in peripheral blood. Importantly, these infections being present during pregnancy of an infected mother, can affect the immune response of the foetus. Increased Th2 responses have been measured in neonates born to mothers with parasitic helminths. The question how a Th2-inducing infection might be associated with decreased risk of atopy has been addressed in some studies, but as yet there is no definitive proof. The possible mechanisms that may explain why helminth infections that lead to a strong Th2 do not lead to the development of allergies and even seem to play a protective role, may be as follows: 1. the functional capacity of the IgE generated to an allergen during helminth infections might be different, in such a way that no mast cell degranulation occurs when these antibodies, present on mast cells, bind an allergen. 2. one of the important properties of helminth infections, namely their capacity to induce regulatory responses may be responsible for the suppression of the effector phase of the allergic response. Immunologie van de hygiëne-hypothese
Diligentia 131 The regulatory response inhibiting allergic inflammation. In a study carried out in Gabonese schoolchildren, it has been shown that children with an increased parasite induced IL-10 production had a decreased risk of being atopic to house dust mite. The inhibitory cytokine, IL-10, is indeed up regulated during chronic helminth infections, and has been shown to be able to inhibit basophil degranulation. Therefore, it is plausible that during helminth infections regulatory responses and suppressory cytokines such as IL-10, inhibit the inflammatory process that eventually leads to allergic disease outcome, as suggested in the diagram. However, several questions such as whether high levels of IL-10 are present in tissues where mast cells reside, how does the IL-10 reach these tissues and does it work in an antigen specific manner, need to be addressed before this model is accepted. Immuno-epidemiological studies have the problem that it is impossible to control for all confounders. Therefore, it is extremely valuable, if possible, to use animal models and well controlled conditions to prove whether a finding can be confirmed in the experimental system. To study the causal relationship between helminth infections and the development of allergic diseases, several research groups have developed combined murine models of infection and asthma. Either house dust mite antigen or a model antigen (e.g. ovalbumin) is used to induce airway inflammation that involves eosinopilic infiltration. This model is then used to study the effect of helminth infections on the development of airway allergies. Studies with Schistosoma mansoni have demonstrated that this infection, at the chronic stage, leads to strongly reduced eosinophilic airway inflammation. Interestingly, during the acute phase of infection, there was no suppression of the inflammatory response to allergen and if anything, there seemed to be an enhanced eosinophil recruitment into the lungs of acutely infected mice. The latter supports the notion that only chronic helminth Immunologie van de hygiëne-hypothese Histamine, leukotrienes, prostaglandins
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NATUURKUNDIGE VOORDRACHTEN 2008-200
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ISBN 978-90-72644-21-3
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INHOUD Verslag over het seizoen 200
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Diligentia 37 elektrische activitei
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Diligentia 47 BOX 3 Vanwege de rand
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Diligentia 57 D=0.2 voor zowel H 2
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60 Diligentia De dubbele helix van
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74 Diligentia Figuur 1. Ontwikkelin
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76 Diligentia eigen DNA) zijn veel
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