title: Differential modulation of allergic eye disease by chronic and acute ascaris infection.
abstract: OBJECTIVE
  To assess alterations in allergic ocular responses to nonparasite antigens in an experimental system in which mice were skewed toward a Th2 cytokine profile by helminth infection.
  
  
  METHODS
  Mice were inoculated with Ascaris suum (A. suum) eggs concurrent with ragweed (RW) sensitization (RW/acute) or by repeated inoculation before RW sensitization (RW/chronic). Control subjects were divided into RW, A. suum, and sham-sensitized groups. Animals were RW-challenged in the eye and examined for changes in ocular responses, inflammatory cell infiltrates, and in vitro assessment of cytokines after antigen restimulation. In subsequent experiments, CD4(+)/CD25+ T regulatory and CD4(+)/CD25- control T cells were adoptively transferred into mice before ocular challenge.
  
  
  RESULTS
  RW sensitization and challenge increased ocular symptoms and eosinophil infiltration into the conjunctiva over PBS control eyes. Acute A. suum infection significantly increased RW-induced clinical symptoms and eosinophil infiltrates in the conjunctiva (P = 0.0001) and resulted in the development of anterior uveitis. In contrast, RW/chronic infection provided protection from allergic responses to RW with significantly fewer eosinophils in the eye and reduced eotaxin levels. Transfer of CD4(+)/CD25+ T cells from RW/chronic mice into RW/acute animals also decreased disease intensity, suggesting that T regulatory cells may contribute to protection from allergic eye disease.
  
  
  CONCLUSIONS
  The current studies suggest acute parasitic infections exacerbate allergic symptoms, whereas chronic infections offer protection and provide possible explanations for the role of parasitic infection in susceptibility and resistance to nonparasite allergens.
authors.affiliation: Agricultural Research Service, Beltsville Human Nutrition Research Center, Nutrient Requirements and Functions Laboratory, U.S. Department of Agriculture, Beltsville, MD, USA.
authors.forename: Lisa
authors.initials: L
authors.lastname: Schopf
authors.forename: Stefano
authors.initials: S
authors.lastname: Luccioli
authors.forename: Virgilio
authors.initials: V
authors.lastname: Bundoc
authors.forename: Paul
authors.initials: P
authors.lastname: Justice
authors.forename: Chi-Chao
authors.initials: CC
authors.lastname: Chan
authors.forename: Brittany J
authors.initials: BJ
authors.lastname: Wetzel
authors.forename: Hillary H
authors.initials: HH
authors.lastname: Norris
authors.forename: Joseph F
authors.initials: JF
authors.lastname: Urban
authors.forename: Andrea
authors.initials: A
authors.lastname: Keane-Myers
mesh_terms: D000208:Acute Disease; D019264:Adoptive Transfer; D000485:Allergens / Q000276:immunology; D031164:Ambrosia / Q000276:immunology; D000818:Animals; D001196:Ascariasis / Q000276:immunology*; D017165:Ascaris suum / Q000276:immunology*; D001762:Blepharitis / Q000276:immunology*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D054413:Chemokine CCL11; D019742:Chemokines, CC / Q000097:blood; D002908:Chronic Disease; D003233:Conjunctivitis, Allergic / Q000276:immunology*; D004797:Enzyme-Linked Immunosorbent Assay; D004802:Eosinophilia / Q000276:immunology; D004804:Eosinophils / Q000276:immunology; D006967:Hypersensitivity / Q000276:immunology*; D007073:Immunoglobulin E / Q000097:blood; D015850:Interleukin-6 / Q000096:biosynthesis; D008407:Mast Cells / Q000276:immunology; D051379:Mice; D008805:Mice, Inbred A; D008807:Mice, Inbred BALB C; D018345:Mice, Knockout; D018418:Th2 Cells / Q000276:immunology; D014606:Uveitis, Anterior / Q000276:immunology*
chemical_list: D000485:Allergens; C515457:Ccl11 protein, mouse; D054413:Chemokine CCL11; D019742:Chemokines, CC; D015850:Interleukin-6; D007073:Immunoglobulin E