Abstract
Epidemiological studies suggest an inverse relationship between helminth infections and allergic disease, and several helminth-derived products have been shown to suppress allergic responses in animals. This study was undertaken to evaluate the effect of a crude extract of Caenorhabditis elegans on allergic airway inflammation in a murine model of asthma. Allergic airway inflammation was induced in BALB/c mice by sensitization with ovalbumin. The effect of the C. elegans crude extract on the development of asthma and on established asthma was evaluated by analyzing airway hyperresponsiveness, serum antibody titers, lung histology and cell counts and cytokine levels in the bronchoalveolar lavage fluid. The role of IFN-γ in the suppression of asthma by the C. elegans crude extract was investigated in IFN-γ knockout and wild-type mice. When mice were sensitized with ovalbumin together with the crude extract of C. elegans, cellular infiltration into the lung was dramatically reduced in comparison with the ovalbumin-treated group. Treatment of mice with the C. elegans crude extract significantly decreased methacholine-induced airway hyperresponsiveness and the total cell counts and levels of IL-4, IL-5 and IL-13 in the bronchoalveolar lavage fluid but increased the levels of IFN-γ and IL-12. Sensitization with the C. elegans crude extract significantly diminished the IgE and IgG1 responses but provoked elevated IgG2a levels. However, the suppressive effect of the C. elegans crude extract was abolished in IFN-γ knockout mice, and the Th2 responses in these mice were as strong as those in wild-type mice sensitized with ovalbumin. The crude extract of C. elegans also suppressed the airway inflammation associated with established asthma. This study provides new insights into immune modulation by the C. elegans crude extract, which suppressed airway inflammation in mice not only during the development of asthma but also after its establishment by skewing allergen-induced Th2 responses to Th1 responses.
Highlights
The incidence of allergic diseases such as asthma, allergic rhinitis and eczema has steadily increased during the recent decades, especially in developed countries or urban areas of developing countries where helminth infections are rare or under control [1,2]
crude extract of Caenorhabditis elegans (CEC) inhibits the development of OVA-induced airway inflammation and airway hyperresponsiveness
When mice were sensitized with CEC together with OVA, the cellular infiltration into the lungs was dramatically reduced compared to the infiltration observed in the OVA group (Figure 1A)
Summary
The incidence of allergic diseases such as asthma, allergic rhinitis and eczema has steadily increased during the recent decades, especially in developed countries or urban areas of developing countries where helminth infections are rare or under control [1,2]. Allergic diseases and helminth infections both illicit Th2 responses, helminths have been known to provoke anti-inflammatory responses rather than allergic reactions in humans and animals [1,3,4]. A significant amount of epidemiological evidence from human field studies has suggested the existence of an inverse relationship between helminth infections and asthma and allergic sensitization [5,6,7,8]. Other studies have reported no protective effects or enhanced allergic sensitization in individuals infected with parasites [9,10,11]. Experimental studies using animal models have shown varying effects of parasite infection on the protection of the host against airway inflammation and allergic disease [1]. Infection with Strongyloides stercoralis or Nippostrongylus brasiliensis in mice suppressed experimental airway inflammation [12,13], whereas
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