Table 2.
Effects of helminth infections and helminth-derived products/molecules on improvement of symptoms in allergy-related experimental animal models.
| Allergy model | Suppressive mechanism | Reference | |
|---|---|---|---|
| Defined helminth molecules; (from helminth species) | |||
| smCKBP; (S. mansoni) | Hapten-induced contact hypersensitivity | NA3 | [27] |
| Sm22.6, PIII and Sm29; (S. mansoni) | OVA-induced AI1 | CD4+Foxp3+ Treg | [65] |
| As-MIF; (A. simplex) | OVA-induced AI | IL-10, TGF-β, and Treg dependent | [66] |
| PAS-1; (A. suum) | APAS-3-induced AI | Possibly IL-10 | [67] |
| OVA-induced AHR2 | CD4+CD25+ T cell-, CD8+ T cell-dependent and IL-10/TGF-β-, IFN-γ-mediated | [68, 69] | |
| Nippocystatin (NbCys); (N. brasiliensis) | OVA-induced AI | Cathepsin B and cathepsin L-dependent mechanism | [70] |
| AvCystatin (Av17); (A. viteae) | OVA-induced AHR | IL-10, macrophages, partially CD4+CD25+ T cells | [71] |
| ES-62; (A. viteae) | Oxazolone- (Oxa-) induced skin immediate hypersensitivity OVA-induced AHR | Mast cell mediated, TLR4-dependent | [72] |
| Helminth infection and undefined products | |||
| S. mansoni infection; males and females + eggs laid in infection; males (no eggs) | Pen V-induced systemic anaphylaxis | IL-10-producing B cells | [73] |
| S. mansoni infection; males (no eggs) | OVA-induced AHR | B cell- and IL-10-dependent suppression of pulmonary eosinophil infiltration | [74] |
| S. mansoni infection; eggs | OVA-induced AI | Egg-treatment: CD4+CD25+Foxp3+Treg | [75] |
| S. japonicum egg antigen (SEA) | OVA-induced AI | CD4+CD25+ Treg, possibly IL-10 | [76] |
| A. suum adult worm extract (ASC) | OVA-induced AHR | NA | [77] |
| Heligmosomoides polygyrus infection | OVA-induced AHR | IL-10 | [78] |
| OVA-induced AHR HDM-induced AI |
IL-10-independent, CD4+CD25+ T cells IL-10-independent Breg cells |
[79, 80] | |
| Peanut extract-induced food allergy | IL-10 | [81] | |
| H. polygyrus excretory-secretory product (HES) | OVA-induced AI | HES-induced Treg cells | [82] |
| N. brasiliensis infection | OVA-induced AHR | IL-10 from unknown cell source | [83] |
| N. brasiliensis excretory-secretory product (NES) | OVA-induced AI | NA (IL-10 independent) | [84] |
| Strongyloides stercoralis infection | OVA-induced AI | NA | [85] |
| Strongyloides venezuelensis infection | OVA-induced AI | NA | [86] |
| T. spiralis infection | OVA-induced AI | Correlated with increased IL-10, TGF-β, CD4+CD25+ Treg | [87] |
| L. sigmodontis infection | OVA-induced AHR | TGF-β, CD4+CD25+ Treg | [88] |
1 (AI): airway inflammation, associated with inflammatory cell influx into the lungs and local Th2 cytokine production.
2 (AHR): airway hyperreactivity, mainly described as lung bronchiole and smooth-muscle tissue remodelling leading to airflow obstruction, resulting in altered airway function. Chronic airway inflammation may lead to AHR, however, different immunopathological pathways govern the regulation of AI and AHR (discussed elsewhere [89–93]).
3NA data not available.