Helminth infection inhibits airway allergic reaction and dendritic cells are involved in the modulation process

Abstract

Several previous studies have demonstrated that some helminth infections can inhibit allergic reactions, but the examination on the effect of live Schistosoma japonicum (SJ) infection on allergic inflammation remains limited. The aim of this study was to examine the effect and mechanism of chronic SJ infection on airway allergic inflammation in a murine model. The data showed that chronic SJ infection suppressed airway eosinophilia, mucus production and antigen-specific IgE responses induced by ovalbumin (OVA) sensitization and challenge. Cytokine production analysis showed that chronic SJ infection reduced allergen-driven interleukin (IL)-4 and IL-5 production, but had no significant effect on IFN-gamma production. More importantly, we found that the adoptive transfer of dendritic cells (DCs) from SJ-infected mice dramatically decreased airway allergic inflammation in the recipients, which was associated with significant decrease of IL-4/IL-5 production and increase of IL-10 production. The results suggest that SJ infection may inhibit the development of allergy and that DCs may be involved in the process of helminth infection-mediated modulation of allergic inflammation.

Helminth Infections Decrease Host Susceptibility to Immune-Mediated Diseases

“…Exposure to other helminths such as S. mansoni (97–99), S. japonicum (100) or T. spiralis (101) also affords protection from allergic airway reactivity and inflammation. Helminth exposure is associated with decreased OVA-stimulated IL4 and IL5, but increased IL10 and TGFβ production as measured in either bronchoalveolar lavage fluid or supernatants from cultured pulmonary draining lymph node cells or splenocytes.…”

Role of dendritic cells: a step forward for the hygiene hypothesis

“…The role of Tregs in infection-mediated inhibition of allergy has been documented in studies on parasitic infections, especially helminth infections. [58][59][60][61][62][63] The involvement of Tregs in bacterial infectionmediated modulation of allergy/asthma has been reported, but is much less studied. [64][65][66] In particular, subcutaneous treatment with heat-killed Mycobacterium vaccae was reported to induce CD4 1 CD45RB low T cells, which inhibited asthma through IL-10 and TGF-b production.…”

“…34,36,38,57,63,64,66,104 We recently showed that the adoptive transfer of DCs from Schistosoma japonicum-infected mice dramatically decreased airway allergic inflammation and was associated with a significant decrease in IL-4/ IL-5 production and an increase in IL-10 production. 63 The DCs' modulating effect on allergy was related to enhanced CD4…”

“…[33][34][35][36][37][38]63 These studies suggested that different infections may 'educate' DCs to become DC1-like cells, which promote a Th1 response and subsequently inhibit allergic Th2 responses (immune deviation), and/or these DC1-like cells become tolerogenic DCs/DCregs, which induce Tregs or have a direct inhibitory effect on allergic Th2 cells (immune regulation) (Figure 2). We first reported that DCs freshly isolated from C. muridarum-infected mice, but not DCs from naive mice, could inhibit the systemic and cutaneous eosinophilia inflammation normally induced by exposure to an allergen upon adoptive transfer.…”

Perfil de sensibilización alérgica en inmigrantes residentes en la zona centro de España

“…Corroboraría la tendencia ya marcada en otros estudios previos, en los que el tiempo medio de evolución desde el momento de la inmigración oscilaba alrededor de los 5 años 16 . Una de las hipótesis para justificar esta rápida sensibilización se basaría en un cierto carácter protector por parte de las infecciones por helmintos, que estos sujetos sufrirían en sus países de origen, para modular la intensidad de la reacción alér-gica respiratoria 17,18 . Al desaparecer este efecto al llegar a los países más desarrollados, acabarían por sensibilizarse frente a los alérgenos a los que se ven expuestos.…”