title: Role of breast milk in a mouse model of maternal transmission of asthma susceptibility.
abstract: Epidemiologic data suggest a link between nursing by asthmatic mothers and increased risk of allergy in babies. We sought to experimentally test the potential contribution of breast milk mediator(s) in a mouse model of maternal transmission of asthma risk by evaluating the effect of adoptive nursing on asthma susceptibility in the offspring. We measured airway hyperresponsiveness (AHR) and allergic airway inflammation (AI) after an intentionally suboptimal OVA Ag sensitization, tested the allergen independence of the maternal effect by using a second allergen, casein, for sensitization of the baby mice, and tested the potential role of cytokines by measuring their levels in breast milk. Offspring of asthmatic, but not normal, mothers showed AHR and AI, indicating a maternal transfer of asthma risk. After adoptive nursing, both groups (litters born to asthmatic mothers and nursed by normal mothers, and normal babies nursed by asthmatic mothers) showed AHR (enhanced pause after methacholine aerosol, 50 mg/ml, 3.7 +/- 0.7, 4.2 +/- 0.5, respectively, vs 1.1 +/- 0.1 normal controls, n = 25, p < 0.01) and AI, seen as eosinophilia on histology and bronchoalveolar lavage (40.7 +/- 4.5%, 28.7 +/- 3.7%, vs 1.0 +/- 0.5% normals, n = 25, p < 0.01) after OVA sensitization. Similar results using casein allergen were observed. Multiplex assays for cytokines (IFN-gamma, IL-2, IL-4, IL-5, TNF-alpha, and IL-13) in breast milk were negative. Breast milk is sufficient, but not necessary, to mediate allergen-independent maternal transmission of asthma risk to offspring.
authors.affiliation: Department of Environmental Health, Harvard School of Public Health, Boston, MA 02115, USA.
authors.forename: Adriana S
authors.initials: AS
authors.lastname: Leme
authors.forename: Cedric
authors.initials: C
authors.lastname: Hubeau
authors.forename: Yuhong
authors.initials: Y
authors.lastname: Xiang
authors.forename: Alejandra
authors.initials: A
authors.lastname: Goldman
authors.forename: Kaoru
authors.initials: K
authors.lastname: Hamada
authors.forename: Yasue
authors.initials: Y
authors.lastname: Suzaki
authors.forename: Lester
authors.initials: L
authors.lastname: Kobzik
mesh_terms: D000485:Allergens; D000818:Animals; D000831:Animals, Newborn; D001249:Asthma / Q000209:etiology* / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D001483:Base Sequence; D001942:Breast Feeding / Q000009:adverse effects; D016535:Bronchial Hyperreactivity; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D015870:Gene Expression; D006801:Humans; D007112:Immunity, Maternally-Acquired; D007231:Infant, Newborn; D051379:Mice; D008807:Mice, Inbred BALB C; D008892:Milk / Q000276:immunology; D008895:Milk, Human / Q000276:immunology*; D010047:Ovalbumin / Q000276:immunology; D011247:Pregnancy; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D012307:Risk Factors
chemical_list: D000485:Allergens; D016207:Cytokines; D012333:RNA, Messenger; D010047:Ovalbumin