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Infection and Immunity, December 2002, p. 6911-6918, Vol. 70, No. 12
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.12.6911-6918.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

B-Cell-Deficient Mice Show an Exacerbated Inflammatory Response in a Model of Chlamydophila abortus Infection

Antonio J. Buendía,¹ Laura Del Río,² Nieves Ortega,² Joaquín Sánchez,¹ María C. Gallego,² María R. Caro,² Jose A. Navarro,¹ Francisco Cuello,² and Jesús Salinas^2*

Departamento de Histología y Anatomía Patológica,¹ Departamento de Sanidad Animal, Facultad de Veterinaria, Universidad de Murcia, Campus de Espinardo, 30100 Murcia, Spain²

Received 13 May 2002/ Returned for modification 17 July 2002/ Accepted 12 September 2002

The resolution of Chlamydophila abortus (Chlamydia psittaci serotype 1) infection is dependent on gamma interferon and CD8⁺ T cells, and classically, B cells have been considered to play a minimal role in host defense. The role of B cells in the immune response was studied by using a model of infection in mice with genetically modified immunoglobulin M transmembrane domains (µMT). In the absence of B cells, infection with C. abortus leads to an acute severe fatal disease that involves a disseminated intravascular coagulation syndrome. µMT mice displayed an increased level of proinflammatory cytokines in serum, and an increased number of neutrophils was observed in the lesions. The possible deleterious role of neutrophils in the pathogenesis of disease in µMT mice was determined by depletion of the neutrophils with the monoclonal antibody RB6-8C5. This led to an enhancement of the bacterial burden and early mortality in both µMT and wild-type mice, while necrotic lesions remained. Analysis of the presence of immunoregulatory cytokines showed significantly lower levels of transforming growth factor ß in the sera of µMT mice. However, mice lacking mature B cells were able to establish a specific immune response that protected them from a secondary challenge. Taken together, these data suggest an immunomodulatory role for B cells in the early events of C. abortus primary infection that can protect mice against an exaggerated inflammatory response.

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* Corresponding author. Mailing address: Departamento de Sanidad Animal, Facultad de Veterinaria, Universidad de Murcia, Campus de Espinardo, 30100 Murcia, Spain. Phone: 34 968 364729. Fax: 34 968 364147. E-mail: jsalinas{at}um.es.

Editor: J. D. Clements

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Infection and Immunity, December 2002, p. 6911-6918, Vol. 70, No. 12
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.12.6911-6918.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

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