title: Infection with the roundworm Toxocara canis leads to exacerbation of experimental allergic airway inflammation.
abstract: BACKGROUND
  Epidemiological studies performed in developing as well as in western countries suggest that infection with Toxocara canis contributes to the development of atopic diseases.
  
  
  OBJECTIVE
  To investigate the association between infection with this helminth and allergy, we examined the effect of T. canis infection on experimental allergic airway inflammation.
  
  
  METHODS
  BALB/c mice were infected by oral administration with 500 embryonated T. canis eggs followed by ovalbumin (OVA) sensitization and challenge to induce allergic airway inflammation.
  
  
  RESULTS
  Infection with T. canis in combination with OVA treatment leads to exacerbation of pulmonary inflammation, eosinophilia, airway hyperresponsiveness, OVA specific and total IgE. Relative quantification of cytokine expression in the lungs of these mice showed increased expression of IL-4 compared with mice that were only T. canis infected or OVA treated. Increased expression of IL-5 and IL-10 was measured in the lungs of T. canis-infected or OVA-treated mice compared with controls; however, combining infection and OVA treatment did not significantly change the expression of these cytokines.
  
  
  CONCLUSIONS
  A previous infection with T. canis leads to exacerbation of experimental allergic airway inflammation. These results have important consequences for findings on the helminths-allergy association. Several factors, including parasite species, infection of definitive vs. accidental host, parasite load and timing of infection, may influence whether an infection with helminths protects one from or enhances allergic manifestations.
authors.affiliation: Department of Parasitology and Mycology, Centre for Infectious Disease Control Netherlands, National Institute for Public Health and Environment (RIVM), Bilthoven, The Netherlands. elena.pinelli@rivm.nl
authors.forename: E
authors.initials: E
authors.lastname: Pinelli
authors.forename: S
authors.initials: S
authors.lastname: Brandes
authors.forename: J
authors.initials: J
authors.lastname: Dormans
authors.forename: E
authors.initials: E
authors.lastname: Gremmer
authors.forename: H
authors.initials: H
authors.lastname: van Loveren
mesh_terms: D000818:Animals; D016535:Bronchial Hyperreactivity / Q000276:immunology* / Q000469:parasitology / Q000473:pathology; D018893:Bronchoalveolar Lavage / Q000379:methods; D016207:Cytokines / Q000235:genetics; D004195:Disease Models, Animal; D005260:Female; D007073:Immunoglobulin E / Q000097:blood / Q000276:immunology; D007249:Inflammation; D008168:Lung / Q000276:immunology / Q000469:parasitology / Q000473:pathology; D008174:Lung Diseases, Parasitic / Q000276:immunology* / Q000469:parasitology / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C; D010047:Ovalbumin / Q000008:administration & dosage; D012333:RNA, Messenger / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012307:Risk Factors; D013997:Time Factors; D017166:Toxocara canis / Q000276:immunology / Q000469:parasitology*; D014120:Toxocariasis / Q000276:immunology* / Q000469:parasitology
chemical_list: D016207:Cytokines; D012333:RNA, Messenger; D007073:Immunoglobulin E; D010047:Ovalbumin