title: Gastro-intestinal exposure to latex antigens induce allergic responses in mice.
abstract: BACKGROUND
  Natural rubber latex (NRL) has emerged as a major cause of respiratory allergy among specific exposed groups of individuals. Since latex allergens are dispersed in the environment it is conceivable that latex proteins are both inhaled and ingested. The mechanism of latex allergy and the immune responses following reexposure of latex allergens by the intranasal route was studied in a murine model of latex allergy developed by intragastric sensitization with NRL.
  
  
  METHODS
  BALB/c mice were sensitized intragastrically ('ig'), intranasally ('in') or 'ig' followed by 'in' challenge with NRL allergens. The cellular and humoral immune responses, lung function and histological changes were determined.
  
  
  RESULTS
  Peripheral blood eosinophilia was observed in the 'ig' and 'ig/in'-NRL-sensitized animals in comparison to normal controls (p < 0.05). The 'ig' group showed a marked increase over control mice in serum total IgE, NRL-specific IgG and IgG subclasses (p < 0.05). Increased levels of IL-4, IL-5, IL-10, and IL-13 were detected in 'ig'-NRL-sensitized mice. Intranasal exposure with NRL after 'ig' sensitization further enhanced the cytokine levels. A tendency towards enhanced stimulation was determined in 'ig'-sensitized mice; a significant difference was shown in the 'ig/in'-group (p < 0.05). Increased airway hyperreactivity was found in 'ig'-NRL-sensitized-mice (15.1 +/- 2.5 vs. 8.9 +/- 1.7 cm H2O x ml(-1) x s, p < 0.05). Mucus secretion from jejunal epithelium and eosinophilic infiltration into the jejunal lamina propria were observed in the 'ig'-NRL-sensitized-mice.
  
  
  CONCLUSIONS
  The results demonstrate that intragastric NRL sensitization did not induce specific tolerance, and additional intranasal exposure with latex allergens resulted in systemic allergic manifestations in the murine model.
authors.affiliation: Allergy-Immunology Division, Department of Pediatrics, Medical College of Wisconsin, Milwaukee, WI, USA.
authors.forename: Christy S
authors.initials: CS
authors.lastname: Barrios
authors.forename: Viswanath P
authors.initials: VP
authors.lastname: Kurup
authors.forename: David A
authors.initials: DA
authors.lastname: Rickaby
authors.forename: James D
authors.initials: JD
authors.lastname: Henderson
authors.forename: Jordan N
authors.initials: JN
authors.lastname: Fink
authors.forename: Kevin J
authors.initials: KJ
authors.lastname: Kelly
mesh_terms: D000281:Administration, Intranasal; D000818:Animals; D016535:Bronchial Hyperreactivity / Q000139:chemically induced / Q000276:immunology; D001985:Bronchial Provocation Tests; D018946:Chemokine CCL5 / Q000096:biosynthesis; D004195:Disease Models, Animal; D004333:Drug Administration Routes; D004802:Eosinophilia / Q000139:chemically induced / Q000276:immunology; D005260:Female; D007108:Immune Tolerance; D007073:Immunoglobulin E / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D016753:Interleukin-10 / Q000096:biosynthesis; D018793:Interleukin-13 / Q000096:biosynthesis; D015847:Interleukin-4 / Q000096:biosynthesis; D015848:Interleukin-5 / Q000096:biosynthesis; D007422:Intestines / Q000276:immunology* / Q000473:pathology; D007840:Latex / Q000008:administration & dosage* / Q000276:immunology; D020315:Latex Hypersensitivity / Q000276:immunology* / Q000473:pathology; D008168:Lung / Q000276:immunology / Q000473:pathology; D008213:Lymphocyte Activation / Q000276:immunology; D051379:Mice; D013270:Stomach / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D018946:Chemokine CCL5; D007074:Immunoglobulin G; D018793:Interleukin-13; D015848:Interleukin-5; D007840:Latex; D016753:Interleukin-10; D015847:Interleukin-4; D007073:Immunoglobulin E