title: Lactic acid bacteria inhibit TH2 cytokine production by mononuclear cells from allergic patients.
abstract: BACKGROUND
  Among factors potentially involved in the increased prevalence of allergic diseases, modification of the intestinal bacteria flora or lack of bacterial stimulation during childhood has been proposed. Lactic acid bacteria (LAB) present in fermented foods or belonging to the natural intestinal microflora were shown to exert beneficial effects on human health. Recent reports have indicated their capacity to reduce allergic symptoms.
  
  
  OBJECTIVE
  The purpose of this investigation was to determine the effect of LAB on the production of type 2 cytokines, which characterize allergic diseases.
  
  
  METHODS
  PBMCs from patients allergic to house dust mite versus those from healthy donors were stimulated for 48 hours with the related Dermatophagoides pteronyssinus allergen or with a staphylococcal superantigen. The effect of LAB preincubation was assessed by measuring the type 2 cytokine production by means of specific ELISA.
  
  
  RESULTS
  The tested gram-positive LAB were shown to inhibit the secretion of T(H)2 cytokines (IL-4 and IL-5). This effect was dose dependent and was observed irrespective of the LAB strain used. No significant inhibition was induced by the control, gram-negative Escherichia coli TG1. Interestingly, LAB reduced the T(H)2 cytokine production from allergic PBMCs specifically restimulated with the related allergen. The inhibition mechanism was shown to be dependent on antigen-presenting cells (ie, monocytes) and on the involvement of IL-12 and IFN-gamma.
  
  
  CONCLUSIONS
  The tested LAB strains were demonstrated to exhibit an anti-T(H)2 activity, and thus different strains of this family might be useful in the prevention of allergic diseases.
authors.affiliation: Laboratoire de Bactériologie des Ecosystèmes, Institut de Biologie de Lille, Lille, France.
authors.forename: Pierre
authors.initials: P
authors.lastname: Pochard
authors.forename: Philippe
authors.initials: P
authors.lastname: Gosset
authors.forename: Corinne
authors.initials: C
authors.lastname: Grangette
authors.forename: Claude
authors.initials: C
authors.lastname: Andre
authors.forename: André-Bernard
authors.initials: AB
authors.lastname: Tonnel
authors.forename: Joël
authors.initials: J
authors.lastname: Pestel
authors.forename: Annick
authors.initials: A
authors.lastname: Mercenier
mesh_terms: D000485:Allergens / Q000494:pharmacology; D016207:Cytokines / Q000096:biosynthesis*; D004768:Enterotoxins / Q000502:physiology; D006801:Humans; D006967:Hypersensitivity / Q000097:blood / Q000378:metabolism*; D007371:Interferon-gamma / Q000378:metabolism / Q000502:physiology; D018664:Interleukin-12 / Q000502:physiology; D015847:Interleukin-4 / Q000037:antagonists & inhibitors; D007778:Lactobacillus / Q000502:physiology*; D018950:Lipopolysaccharide Receptors / Q000032:analysis; D009000:Monocytes / Q000187:drug effects / Q000378:metabolism*; D012016:Reference Values; D018418:Th2 Cells / Q000378:metabolism*
chemical_list: D000485:Allergens; D016207:Cytokines; D004768:Enterotoxins; D018950:Lipopolysaccharide Receptors; D018664:Interleukin-12; D015847:Interleukin-4; C026066:enterotoxin A, Staphylococcal; D007371:Interferon-gamma