BCG infection suppresses allergic sensitization and development of increased airway reactivity in an animal model☆☆☆★★★

Herz, Udo; Gerhold, Kerstin; Grüber, Christoph; Braun, Armin; Wahn, Ulrich; Renz, Harald; Paul, K.

doi:10.1016/s0091-6749(98)70030-2

Cited by 218 publications

(173 citation statements)

References 42 publications

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“…6 Animal studies support an association between response to mycobacteria and allergic responses. 7,8 These data are consistent with BCG's action as a potent adjuvant for induction of cell-mediated immunity, with IFN-␥ as one of the major cytokines induced. 9 IFN-␥ is associated with a Th1-like immune response and counteracts production of IgE antibodies.…”

Section: Introductionsupporting

confidence: 72%

Atopy in children in relation to BCG vaccination and genetic polymorphisms at SLC11A1 (formerly NRAMP1) and D2S1471

et al. 2002

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Section: Introductionsupporting

confidence: 72%

Atopy in children in relation to BCG vaccination and genetic polymorphisms at SLC11A1 (formerly NRAMP1) and D2S1471

et al. 2002

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“…In addition to us, others have demonstrated a suppressive effect on various parameters of allergic inflammation in mouse models after mycobacteria pretreatment (4,5,8,9). However, except for one report from the work of Wang and Rook (7), there is no information as to the potential for these Ags in attenuating a preexisting allergic state.…”

Section: Discussionmentioning

confidence: 99%

Airway Hyperresponsiveness, Late Allergic Response, and Eosinophilia Are Reversed with Mycobacterial Antigens in Ovalbumin-Presensitized Mice

Hopfenspirger

Agrawal

2002

The Journal of Immunology

121

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Pretreatment with mycobacterial Ags has been shown to be effective in preventing allergic airway inflammation from occurring in a mouse model. Because most asthmatics are treated after the development of asthma, it is crucial to determine whether mycobacterial Ags can reverse established allergic airway inflammation in the presensitized state. Our hypothesis, based upon our previous findings, is that mycobacteria treatment in presensitized mice will suppress the allergic airway inflammation with associated clinical correlates of established asthma, with the noted exception of factors associated with the early allergic response (EAR). BALB/c mice sensitized and challenged with OVA were evaluated for pulmonary functions during both the EAR and late allergic response, and airway hyperresponsiveness to methacholine. Following this, sensitized mice were randomized and treated with placebo or a single dose (1 × 105 CFUs) of bacillus Calmette-Guérin (BCG) or Mycobacterium vaccae via nasal or peritoneal injection. One week later, the mice were rechallenged with OVA and methacholine, followed by bronchoalveolar lavage (BAL) and tissue collection. Mice treated with intranasal BCG were most significantly protected from the late allergic response (p < 0.02), airway hypersensitivity (p < 0.001) and hyperreactivity (p < 0.05) to methacholine, BAL (p < 0.05) and peribronchial (p < 0.01) eosinophilia, and BAL fluid IL-5 levels (p < 0.01) as compared with vehicle-treated, sensitized controls. Intranasal M. vaccae treatment was less effective, suppressing airway hypersensitivity (p < 0.01) and BAL eosinophilia (p < 0.05). No changes were observed in the EAR, BAL fluid IL-4 levels, or serum total and Ag-specific IgE. These data suggest that mycobacterial Ags (BCG≫M. vaccae) are effective in attenuating allergic airway inflammation and associated changes in pulmonary functions in an allergen-presensitized state.

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“…Observations from Japan suggesting that positive tuberculin responses in children predict a lower incidence of asthma, lower serum IgE levels, and cytokine pro®le bias toward the Th1 type (75) were supported by animal experiments which demonstrated that the IgE response to ovalbumin in mice could be downregulated by a previous infection with BCG (76,77). Although these observations on the relationship between immune responses to infectious agents and atopic sensitization and disease expression are quite stimulating and challenging, conclusions regarding their relevance to the atopic march should be drawn with caution.…”

Section: The Lifestyle Factors Which Have Been Proposed So Farmentioning

confidence: 93%

What drives the allergic march?

Wahn

2000

Allergy

132

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BCG infection suppresses allergic sensitization and development of increased airway reactivity in an animal model☆☆☆★★★

Cited by 218 publications

References 42 publications

Atopy in children in relation to BCG vaccination and genetic polymorphisms at SLC11A1 (formerly NRAMP1) and D2S1471

Atopy in children in relation to BCG vaccination and genetic polymorphisms at SLC11A1 (formerly NRAMP1) and D2S1471

Airway Hyperresponsiveness, Late Allergic Response, and Eosinophilia Are Reversed with Mycobacterial Antigens in Ovalbumin-Presensitized Mice

What drives the allergic march?

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