This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Barrett, E. G. Articles by Bice, D. E. Search for Related Content PubMed PubMed Citation Articles by Barrett, E. G. Articles by Bice, D. E.

Cigarette Smoke-induced Airway Hyperresponsiveness Is Not Dependent on Elevated Immunoglobulin and Eosinophilic Inflammation in a Mouse Model of Allergic Airway Disease

Respiratory Immunology Program, Lovelace Respiratory Research Institute; and Department of Pathology, University of New Mexico, Albuquerque, New Mexico

Correspondence and requests for reprints should be addressed to Edward G. Barrett, Ph.D, Lovelace Respiratory Research Institute, 2425 Ridgecrest Drive SE, Albuquerque, NM 87108. E-mail: tbarrett{at}lrri.org

Epidemiologic studies suggest that children raised in homes of cigarette smokers have a higher incidence of asthma than children who are raised in homes of nonsmokers. We sought to develop an experimental model to understand the mechanisms involved. Female BALB/c mice were paired with male DO11.10 ovalbumin (OVA)-T cell receptor hemizygous (+/-) mice such that the offspring were either transgene positive (+/-) or negative (-/-). Mice were exposed to either air or mainstream cigarette smoke (100 mg/m³ total particulate matter, 6 hours/day, 7 days/week) during pregnancy. Immediately after birth, newborn mice were exposed for 4 weeks to either air or sidestream cigarette smoke (SS; 5 mg/m³ total particulate matter, 6 hours/day, 5 days/week) and then exposed for the following 6 weeks to either air, SS, OVA (5 mg/m³, 6 hours/day, 5 days/week) or a combination of OVA-SS. DO11.10 +/- offspring exposed to OVA had increased airway hyperresponsiveness (AHR) to methacholine challenge, total IgE, OVA-specific IgE and IgG₁, lymphocytes, and neutrophils in bronchoalveolar lavage and perivascular and peribronchiolar inflammation. Exposure to SS alone caused a significant increase in AHR in both +/- and -/- mice. Transgene -/- mice did not exhibit AHR after OVA exposure unless it was delivered in combination with SS. When compared with OVA-only exposure, OVA-SS exposure decreased total IgE, OVA-specific IgE, and IgG₁ amounts in +/- mice. These results indicate that exposure to SS after birth enhanced AHR in offspring that are both predisposed (+/-) and nonpredisposed (-/-) to develop an allergic response to OVA, but this AHR was not associated with elevated lung eosinophilia or OVA-specific Ig amounts.

Key Words: asthma • sensitization • environmental • pollution • tobacco

This article has been cited by other articles:

				S. P. Singh, N. C. Mishra, J. Rir-sima-ah, M. Campen, V. Kurup, S. Razani-Boroujerdi, and M. L. Sopori Maternal Exposure to Secondhand Cigarette Smoke Primes the Lung for Induction of Phosphodiesterase-4D5 Isozyme and Exacerbated Th2 Responses: Rolipram Attenuates the Airway Hyperreactivity and Muscarinic Receptor Expression but Not Lung Inflammation and Atopy J. Immunol., August 1, 2009; 183(3): 2115 - 2121. [Abstract] [Full Text] [PDF]

				T. Wang, Y. Liu, L. Chen, X. Wang, X-R. Hu, Y-L. Feng, D-S. Liu, D. Xu, Y-P. Duan, J. Lin, et al. Effect of sildenafil on acrolein-induced airway inflammation and mucus production in rats Eur. Respir. J., May 1, 2009; 33(5): 1122 - 1132. [Abstract] [Full Text] [PDF]

				K.-a. Moon, S. Y. Kim, T.-B. Kim, E. S. Yun, C.-S. Park, Y. S. Cho, H.-B. Moon, and K.-Y. Lee Allergen-induced CD11b+ CD11cint CCR3+ macrophages in the lung promote eosinophilic airway inflammation in a mouse asthma model Int. Immunol., December 1, 2007; 19(12): 1371 - 1381. [Abstract] [Full Text] [PDF]

				V. Phaybouth, S.-Z. Wang, J. A. Hutt, J. D. McDonald, K. S. Harrod, and E. G. Barrett Cigarette smoke suppresses Th1 cytokine production and increases RSV expression in a neonatal model Am J Physiol Lung Cell Mol Physiol, February 1, 2006; 290(2): L222 - L231. [Abstract] [Full Text] [PDF]

				Y. Tesfaigzi, J. D. McDonald, M. D. Reed, S. P. Singh, G. T. De Sanctis, P. R. Eynott, F. F. Hahn, M. J. Campen, and J. L. Mauderly Low-Level Subchronic Exposure to Wood Smoke Exacerbates Inflammatory Responses in Allergic Rats Toxicol. Sci., December 1, 2005; 88(2): 505 - 513. [Abstract] [Full Text] [PDF]

				Y. Chiba, M. Murata, H. Ushikubo, Y. Yoshikawa, A. Saitoh, H. Sakai, J. Kamei, and M. Misawa Effect of Cigarette Smoke Exposure In Vivo on Bronchial Smooth Muscle Contractility In Vitro in Rats Am. J. Respir. Cell Mol. Biol., December 1, 2005; 33(6): 574 - 581. [Abstract] [Full Text] [PDF]

				U. Frey, C. Kuehni, H. Roiha, M. Cernelc, B. Reinmann, J. H. Wildhaber, and G. L. Hall Maternal Atopic Disease Modifies Effects of Prenatal Risk Factors on Exhaled Nitric Oxide in Infants Am. J. Respir. Crit. Care Med., August 1, 2004; 170(3): 260 - 265. [Abstract] [Full Text] [PDF]

				A. J. Archer, J. L. H. Cramton, J. C. Pfau, G. Colasurdo, and A. Holian Airway responsiveness after acute exposure to urban particulate matter 1648 in a DO11.10 murine model Am J Physiol Lung Cell Mol Physiol, February 1, 2004; 286(2): L337 - L343. [Abstract] [Full Text] [PDF]

				S. P. Singh, E. G. Barrett, R. Kalra, S. Razani-Boroujerdi, R. J. Langley, V. Kurup, Y. Tesfaigzi, and M. L. Sopori Prenatal Cigarette Smoke Decreases Lung cAMP and Increases Airway Hyperresponsiveness Am. J. Respir. Crit. Care Med., August 1, 2003; 168(3): 342 - 347. [Abstract] [Full Text] [PDF]

				M. J. Tobin Asthma, Airway Biology, and Nasal Disorders in AJRCCM 2002 Am. J. Respir. Crit. Care Med., February 1, 2003; 167(3): 319 - 332. [Full Text] [PDF]