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Infection and Immunity, November 2001, p. 6981-6986, Vol. 69, No. 11
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.11.6981-6986.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Reciprocal Protective Immunity against Bordetella pertussis and Bordetella parapertussis in a Murine Model of Respiratory Infection

Mineo Watanabe1,* and Masaaki Nagai2

Department of Microbiology and Biologics, Daiichi College of Pharmaceutical Sciences, Fukuoka 815-8511,1 and Research Center for Biologicals, The Kitasato Institute, Kitamoto 364-0026,2 Japan

Received 23 April 2001/Returned for modification 25 June 2001/Accepted 20 August 2001

The protective immunity induced by infection with Bordetella pertussis and with Bordetella parapertussis was examined in a murine model of respiratory infection. Convalescent mice that had been infected by aerosol with B. pertussis or with B. parapertussis exhibited a protective immune response against B. pertussis and also against B. parapertussis. Anti-filamentous hemagglutinin (anti-FHA) serum immunoglobulin G (IgG) and anti-FHA lung IgA antibodies were detected in both mice infected with B. pertussis and those infected with B. parapertussis. Antibodies against pertussis toxin (anti-PT) and against killed B. pertussis cells were detected in mice infected with B. pertussis. Pertactin-specific antibodies and antibodies against killed B. parapertussis cells were detected in mice infected with B. parapertussis. Spleen cells from mice infected with B. pertussis secreted interferon-gamma (IFN-gamma ) in response to stimulation by FHA or PT. Spleen cells from mice infected with B. parapertussis also secreted IFN-gamma in response to FHA. Interleukin-4 was not produced in response to any of the antigens tested. The profiles of cytokine secretion in vitro revealed induction of a Th1-biased immune response during convalescence from infection by B. pertussis and by B. parapertussis. It is possible that Th1 and Th2 responses against FHA might be related to the reciprocal protection achieved in our murine model.

* Corresponding author. Mailing address: Department of Microbiology and Biologics, Daiichi College of Pharmaceutical Sciences, 22-1 Tamagawa-cho, Minami-ku, Fukuoka 815-8511, Japan. Phone: 81-92-541-0161. Fax: 81-92-553-5698. E-mail: min-ind{at}umin.ac.jp.

Infection and Immunity, November 2001, p. 6981-6986, Vol. 69, No. 11
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.11.6981-6986.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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