title: Oral administration of an IL-10-secreting Lactococcus lactis strain prevents food-induced IgE sensitization.
abstract: BACKGROUND
  Because tolerance to food is potentially modulated by IL-10, strategies to prevent food allergy should favor an increased delivery of IL-10 to the gut.
  
  
  OBJECTIVE
  We hypothesized that administration of a Lactococcus lactis transfected to secrete murine IL-10 could prevent sensitization in a mouse model of food allergy.
  
  
  METHODS
  Before each oral sensitization with beta-lactoglobulin in the presence of cholera toxin, young mice were administered the transfected Lactococcus lactis. Antigen-induced anaphylaxis after oral challenge assessed clinical protection achieved by the pretreatment. Serum and feces antigen-specific antibody concentrations were sequentially measured. Antibody titers were correlated with antibody and IL-10-secreting cell numbers in the spleen and in Peyer patches.
  
  
  RESULTS
  Pretreatment with transfected Lactococcus lactis contributed to diminish anaphylaxis significantly, and inhibit antigen-specific serum IgE and IgG(1) production strongly. In addition, transfected Lactococcus lactis increased the production of antigen-specific IgA in the gut. Variations of antibody levels in the serum and the gut correlated with the numbers of antibody-producing cells. In addition, the presence of exogenous IL-10 in the gut by transfected Lactococcus lactis induced IL-10 secretion by Peyer patches cells. Increased IL-10 titers were also measured in the plasma.
  
  
  CONCLUSIONS
  These results suggest that a microorganism bioengineered to deliver IL-10 in the gut can decrease food-induced anaphylaxis and provide an option to prevent IgE-type sensitization to common food allergens.
  
  
  CONCLUSIONS
  Nonpathogenic IL-10-producing microorganisms in the gut could have a potential to prevent systemic food-induced anaphylaxis.
authors.affiliation: University Hospital of Geneva, Department of Pediatrics, Geneva, Switzerland.
authors.forename: Christophe P
authors.initials: CP
authors.lastname: Frossard
authors.forename: Lothar
authors.initials: L
authors.lastname: Steidler
authors.forename: Philippe A
authors.initials: PA
authors.lastname: Eigenmann
mesh_terms: D000284:Administration, Oral; D000818:Animals; D005260:Female; D005512:Food Hypersensitivity / Q000276:immunology* / Q000378:metabolism / Q000517:prevention & control*; D007108:Immune Tolerance / Q000235:genetics; D007073:Immunoglobulin E / Q000009:adverse effects / Q000096:biosynthesis*; D016753:Interleukin-10 / Q000097:blood / Q000235:genetics* / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000276:immunology / Q000378:metabolism; D013294:Lactococcus lactis / Q000235:genetics* / Q000276:immunology* / Q000378:metabolism; D051379:Mice; D008809:Mice, Inbred C3H; D014162:Transfection
chemical_list: D016753:Interleukin-10; D007073:Immunoglobulin E