title: Protective effect of Schistosoma mansoni infection on allergic airway inflammation depends on the intensity and chronicity of infection.
abstract: BACKGROUND
  Population studies have suggested that chronic and intense helminth infections, in contrast to acute and mild helminth infections, might suppress allergic airway inflammation.
  
  
  OBJECTIVE
  We sought to address the question of how the chronicity and intensity of helminth infections affect allergic airway inflammation in a well-defined experimental model.
  
  
  METHODS
  C57/Bl6 mice were infected with Schistosoma mansoni, followed by sensitization and challenge with ovalbumin (OVA), and different stages and intensities of infection were studied. To this end, mice were analyzed at 8, 12, or 16 weeks, representing the acute, intermediate, or chronic phases of infection, respectively.
  
  
  RESULTS
  Lung lavage eosinophilia, peribronchial inflammation, and OVA-induced airway hyperresponsiveness were increased during acute infection but significantly decreased when infection progressed into chronicity. Decreases in lung lavage eosinophilia were parasite density-dependent. Similar levels of OVA-specific IgE were found during all phases of infection, whereas both OVA-specific and parasite-specific T(H)2 cytokine levels were significantly reduced during chronic infection. Inhibition of airway inflammation could be transferred to OVA-sensitized recipient mice by B cells and CD4(+) T cells from spleens of chronically, but not acutely, infected mice. This suppression was IL-10-dependent.
  
  
  CONCLUSIONS
  During chronic, but not acute, helminth infections, suppressive mechanisms are induced that regulate immune reactions to inhaled allergens. These data confirm human epidemiologic observations in a well-controlled animal model.
  
  
  CONCLUSIONS
  Characterization of chronic helminth infection-induced regulatory mechanisms will help in the development of future therapeutics to treat or prevent allergic disease.
authors: Department of Parasitology, Leiden University Medical Center, Leiden, The Netherlands. H.H.Smits@lumc.nl
authors: Hermelijn H
authors: HH
authors: Smits
authors: Hamida
authors: H
authors: Hammad
authors: Menno
authors: M
authors: van Nimwegen
authors: Thomas
authors: T
authors: Soullie
authors: Monique A
authors: MA
authors: Willart
authors: Ellen
authors: E
authors: Lievers
authors: Jonathan
authors: J
authors: Kadouch
authors: Mirjam
authors: M
authors: Kool
authors: Janneke
authors: J
authors: Kos-van Oosterhoud
authors: André M
authors: AM
authors: Deelder
authors: Bart N
authors: BN
authors: Lambrecht
authors: Maria
authors: M
authors: Yazdanbakhsh
mesh_terms: D019264:Adoptive Transfer; D000818:Animals; D016535:Bronchial Hyperreactivity / Q000517:prevention & control*; D002908:Chronic Disease; D016207:Cytokines / Q000096:biosynthesis; D004802:Eosinophilia / Q000517:prevention & control*; D005260:Female; D007073:Immunoglobulin E / Q000096:biosynthesis; D016753:Interleukin-10 / Q000502:physiology; D008168:Lung / Q000473:pathology*; D051379:Mice; D008810:Mice, Inbred C57BL; D010047:Ovalbumin / Q000276:immunology; D012555:Schistosomiasis mansoni / Q000276:immunology*
chemical_list: D016207:Cytokines; D016753:Interleukin-10; D007073:Immunoglobulin E; D010047:Ovalbumin