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Maternal Transmission of Resistance to Development of Allergic Airway Disease¹

Adam P. Matson^*,, Li Zhu^*, Elizabeth G. Lingenheld^*, Craig M. Schramm, Robert B. Clark^*, Dawn M. Selander^*, Roger S. Thrall^*, Elena Breen^* and Lynn Puddington^2,*

^* Department of Immunology, University of Connecticut Health Center, Farmington, CT 06030; and Division of Neonatology and Division of Pulmonary Medicine, Department of Pediatrics, Connecticut Children’s Medical Center, Hartford, CT 06106

Parental phenotype is known to influence the inheritance of atopic diseases, such as allergic asthma, with a maternal history being a more significant risk factor for progeny than paternal history. We hypothesized that recall Th1- or Th2-type immune responses during pregnancy would result in transfer of maternal factors that would differentially impact development of immune responsiveness in offspring. Following weaning, susceptibility and severity of allergic airway disease (a murine model of human asthma) was evaluated in progeny, disease being elicited by immunization with OVA-Al(OH)₃ and challenge with aerosolized OVA. We found that progeny of mothers with Th1-biased immunity to OVA subjected to recall aerosol challenge during pregnancy had reduced levels of Ag-specific IgE and airway eosinophilia compared with progeny of mothers with Th2-biased immunity to OVA or naive mothers. Interestingly, progeny of mothers with Th1-type immunity to a heterologous albumin, BSA, were not protected from developing OVA-induced allergic airway disease. These findings demonstrated that maternal transfer of protection from development of allergic airway disease to offspring in this model of maternal Th1-type immunity was Ag specific.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by National Institutes of Health Grants HL069083, HL08058, and HL066963 (to L.P.) and American Lung Association of Connecticut Grants (to L.P. and to A.P.M.). D.M.S. was supported in part by National Institutes of Health Training Grant AI007080.

² Address correspondence and reprint requests to Dr. Lynn Puddington, Department of Immunology, Center for Integrative Immunology and Vaccine Research, MC-1319, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030-1319. E-mail address: puddington{at}nso1.uchc.edu

³ Abbreviations used in this paper: E, embryonic day; BAL, bronchoalveolar lavage; Penh, enhanced pause.

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