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Infection and Immunity, January 2000, p. 342-351, Vol. 68, No. 1
0019-9567/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

In Vitro Brucella suis Infection Prevents the Programmed Cell Death of Human Monocytic Cells

Antoine Gross, Annie Terraza, Safia Ouahrani-Bettache, Jean-Pierre Liautard, and Jacques Dornand*

INSERM U431, IFR Eugène Bataillon, Université de Montpellier II, 34095 Montpellier Cedex 5, France

Received 3 June 1999/Returned for modification 29 July 1999/Accepted 29 September 1999

During the complex interaction between an infectious agent and a host organism, the pathogen can interfere with the host cell's programmed death to its own benefit. Induction or prevention of host cell apoptosis appears to be a critical step for determining the infection outcome. Members of the gram-negative bacterial genus Brucella are intracellular pathogens which preferentially invade monocytic cells and develop within these cells. We investigated the effect of Brucella suis infection on apoptosis of human monocytic phagocytes. The present study provides evidence that Brucella infection inhibited spontaneously occurring apoptosis in human monocytes. Prevention of monocyte apoptosis was not mediated by Brucella lipopolysaccharide and required bacterial survival within infected cells. Both invaded and noninvaded cells were protected, indicating that soluble mediators released during infection were involved in the phenomenon. Analysis of Brucella-infected monocytes revealed specific overexpression of the A1 gene, a member of the bcl-2 family implicated in the survival of hematopoietic cells. Brucella infection also rendered macrophage-like cells resistant to Fas ligand- or gamma interferon-induced apoptosis, suggesting that Brucella infection protected host cells from several cytotoxic processes occurring at different steps of the immune response. The present data clearly show that Brucella suis modulated the monocyte/macrophage's apoptotic response to the advantage of the pathogen, thus preventing host cell elimination. This might represent a strategy for Brucella development in infected hosts.

* Corresponding author. Mailing address: INSERM U431, IFR Eugène Bataillon, Université de Montpellier II CC100, Place Eugène Bataillon, 34095 Montpellier Cedex 5, France. Phone: 33 (0)4 67144244. Fax: 33 (0)4 67143338. E-mail: dornand{at}crit.univ-montp2.fr.

Infection and Immunity, January 2000, p. 342-351, Vol. 68, No. 1
0019-9567/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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