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Infection and Immunity, March 2001, p. 1883-1888, Vol. 69, No. 3
Department of Bacteriology, School of
Medicine,1 and School of Allied Medical
Sciences,2 Hirosaki University, Hirosaki, and
Veterinary Teaching Hospital, Azabu University,
Sagamihara,3 Japan
Received 7 July 2000/Returned for modification 18 October
2000/Accepted 20 November 2000
Listeria monocytogenes promotes the induction of the
T-helper 1 (Th1) cell response, while ovalbumin (OVA) induces a Th2
cell response and allergic reactions, such as airway hyperreactivity and immunoglobulin E (IgE) production. When mice were immunized with
OVA on day 7 after L. monocytogenes infection, eosinophilia in bronchoalveolar lavage and the production of total IgE, OVA-specific IgE, interleukin-4 (IL-4), and IL-5 in the circulation were markedly suppressed. Cytokine responses, including IL-4, IL-5, IL-10, IL-13, and
gamma interferon, to OVA were decreased in the spleen cell cultures
obtained from OVA-immunized mice that had been infected with L. monocytogenes. Conversely, when OVA-immunized mice were infected
with L. monocytogenes, conversion from the nonlethal infection to the lethal infection occurred. Host resistance to L. monocytogenes infection in OVA-immunized mice was enhanced by the
administration of anti-IL-10 monoclonal antibody. The present study
indicates that striking interference is observed between Th1-inducing
L. monocytogenes infection and Th2-driven OVA-induced airway hyperreactivity.
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.3.1883-1888.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Interference between Host Resistance to
Listeria monocytogenes Infection and Ovalbumin-Induced
Allergic Responses in Mice
*
Corresponding author. Mailing address: Department of
Bacteriology, School of Medicine, Hirosaki University, Zaifu-cho 5, Hirosaki, Aomori 036-8562, Japan. Phone: 81-172 39-5032. Fax: 81-172 39-5034. E-mail: a27k03n0{at}cc.hirosaki-u.ac.jp.
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