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Infection and Immunity, November 2009, p. 4868-4876, Vol. 77, No. 11
0019-9567/09/$08.00+0     doi:10.1128/IAI.00503-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

B Cells Are Essential for Moderating the Inflammatory Response and Controlling Bacterial Multiplication in a Mouse Model of Vaccination against Chlamydophila abortus Infection{triangledown}

Antonio J. Buendía,1* Nieves Ortega,2 María R. Caro,2 Laura Del Río,2 María C. Gallego,2 Joaquín Sánchez,1 Jose A. Navarro,1 Francisco Cuello,2 and Jesús Salinas2

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

Received 6 May 2009/ Returned for modification 10 June 2009/ Accepted 18 August 2009

The use of inactivated vaccines associated with suitable adjuvants has been demonstrated to confer a good level of protection against Chlamydophila abortus. However, the basis of the immune protective response induced by these vaccines has been poorly studied. B cells act as an immune regulatory population during primary infection by C. abortus. Thus, it was considered of interest to study the role of B cells in an infection after immunization with a killed vaccine. For this, C57BL/6 and B-cell-deficient mice were immunized with a killed vaccine against C. abortus using QS-21 as the adjuvant. After challenge, the course of infection was established by analysis of morbidity, C. abortus burden in the liver, and histopathological changes. The immune response induced was studied by real-time PCR techniques. Experiments involving transfer of immune serum from vaccinated or previously infected mice were also carried out. The lack of B cells reduced the protection conferred by the QS-21 adjuvant vaccine. Vaccinated B-cell-deficient mice showed a 1,000-fold-greater bacterial burden in the liver than their wild-type counterparts. Obvious differences existed in the liver, where a severe neutrophilic reaction and extended areas of necrosis were observed with vaccinated B-cell-deficient mice. An analysis of the immune response pointed to a significant increase in inflammatory cytokines and chemokines and the deficient production of transforming growth factor beta. The transfer of antibodies restored the level of protection. This study demonstrates that B cells play a crucial role in controlling C. abortus multiplication and prevent an exacerbated inflammatory response.

* Corresponding author. Mailing address: Departamento de Anatomía y Anatomía Patológica Comparadas, Facultad de Veterinaria, Universidad de Murcia, Campus de Espinardo, 30100 Murcia, Spain. Phone: 34 868 884336. Fax: 34 868 884147. E-mail: abuendia{at}um.es

{triangledown} Published ahead of print on 24 August 2009.

Editor: R. P. Morrison

Infection and Immunity, November 2009, p. 4868-4876, Vol. 77, No. 11
0019-9567/09/$08.00+0     doi:10.1128/IAI.00503-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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