A B-cell mitogen of Brucella abortus is a proline-racemase

SPERA JUAN MANUEL, DIEGO COMERCI, JUAN UGALDE, NORA IÑÓN AND RODOLFO UGALDE.

Puerto Iguazu, Misiones, Argentina

Congreso; SAIB XL; 2004

Brucellosis is characterized by an early acute phase followed by a subvertion of the host innate and adaptive response that allows a chronic infection. The isolation and characterization of molecules essential in pathogens metabolism with host immune defenses are keyed issues for the understanding of the pathology and for the development of rational strategies for vaccination, immunotherapy and drug design. Recently a proline-racemase was reported in Trypanosoma cruzi to act as a B-cell polyclonal activtor. It has been demosntrated that mitogens are assoiated with immunomodulation and immunoevasion by many pathogenic microorganisms. In this study we have cloned, sequenced and expressed a putative prolineracemase (rac1) of B. abortus. Enzymatic activity of rRAC1 showed that it is capable of racemizing only L-Pro. Stimulation of murine naive spleen-purified B-cells with 50ug/ml of rRAC1 induced a 78- fold increase in tritiated timidine incorporation. Experimental infection of Balb/c mice with 2308 and rac1 showed that RAC1 might be involved in a B-cell depletion mechanism during the first stage of infection, as seen by flow cytometry analysis of infected spleens. These results suggest that RAC1 is a B-cell polyclonal activator that strongly contributes to brucellosis. that it is capable of racemizing only L-Pro. Stimulation of murine naive spleen-purified B-cells with 50ug/ml of rRAC1 induced a 78- fold increase in tritiated timidine incorporation. Experimental infection of Balb/c mice with 2308 and rac1 showed that RAC1 might be involved in a B-cell depletion mechanism during the first stage of infection, as seen by flow cytometry analysis of infected spleens. These results suggest that RAC1 is a B-cell polyclonal activator that strongly contributes to brucellosis. that it is capable of racemizing only L-Pro. Stimulation of murine naive spleen-purified B-cells with 50ug/ml of rRAC1 induced a 78- fold increase in tritiated timidine incorporation. Experimental infection of Balb/c mice with 2308 and rac1 showed that RAC1 might be involved in a B-cell depletion mechanism during the first stage of infection, as seen by flow cytometry analysis of infected spleens. These results suggest that RAC1 is a B-cell polyclonal activator that strongly contributes to brucellosis. demosntrated that mitogens are assoiated with immunomodulation and immunoevasion by many pathogenic microorganisms. In this study we have cloned, sequenced and expressed a putative prolineracemase (rac1) of B. abortus. Enzymatic activity of rRAC1 showed that it is capable of racemizing only L-Pro. Stimulation of murine naive spleen-purified B-cells with 50ug/ml of rRAC1 induced a 78- fold increase in tritiated timidine incorporation. Experimental infection of Balb/c mice with 2308 and rac1 showed that RAC1 might be involved in a B-cell depletion mechanism during the first stage of infection, as seen by flow cytometry analysis of infected spleens. These results suggest that RAC1 is a B-cell polyclonal activator that strongly contributes to brucellosis. that it is capable of racemizing only L-Pro. Stimulation of murine naive spleen-purified B-cells with 50ug/ml of rRAC1 induced a 78- fold increase in tritiated timidine incorporation. Experimental infection of Balb/c mice with 2308 and rac1 showed that RAC1 might be involved in a B-cell depletion mechanism during the first stage of infection, as seen by flow cytometry analysis of infected spleens. These results suggest that RAC1 is a B-cell polyclonal activator that strongly contributes to brucellosis. that it is capable of racemizing only L-Pro. Stimulation of murine naive spleen-purified B-cells with 50ug/ml of rRAC1 induced a 78- fold increase in tritiated timidine incorporation. Experimental infection of Balb/c mice with 2308 and rac1 showed that RAC1 might be involved in a B-cell depletion mechanism during the first stage of infection, as seen by flow cytometry analysis of infected spleens. These results suggest that RAC1 is a B-cell polyclonal activator that strongly contributes to brucellosis. demosntrated that mitogens are assoiated with immunomodulation and immunoevasion by many pathogenic microorganisms. In this study we have cloned, sequenced and expressed a putative prolineracemase (rac1) of B. abortus. Enzymatic activity of rRAC1 showed that it is capable of racemizing only L-Pro. Stimulation of murine naive spleen-purified B-cells with 50ug/ml of rRAC1 induced a 78- fold increase in tritiated timidine incorporation. Experimental infection of Balb/c mice with 2308 and rac1 showed that RAC1 might be involved in a B-cell depletion mechanism during the first stage of infection, as seen by flow cytometry analysis of infected spleens. These results suggest that RAC1 is a B-cell polyclonal activator that strongly contributes to brucellosis. that it is capable of racemizing only L-Pro. Stimulation of murine naive spleen-purified B-cells with 50ug/ml of rRAC1 induced a 78- fold increase in tritiated timidine incorporation. Experimental infection of Balb/c mice with 2308 and rac1 showed that RAC1 might be involved in a B-cell depletion mechanism during the first stage of infection, as seen by flow cytometry analysis of infected spleens. These results suggest that RAC1 is a B-cell polyclonal activator that strongly contributes to brucellosis. that it is capable of racemizing only L-Pro. Stimulation of murine naive spleen-purified B-cells with 50ug/ml of rRAC1 induced a 78- fold increase in tritiated timidine incorporation. Experimental infection of Balb/c mice with 2308 and rac1 showed that RAC1 might be involved in a B-cell depletion mechanism during the first stage of infection, as seen by flow cytometry analysis of infected spleens. These results suggest that RAC1 is a B-cell polyclonal activator that strongly contributes to brucellosis. to act as a B-cell polyclonal activtor. It has been demosntrated that mitogens are assoiated with immunomodulation and immunoevasion by many pathogenic microorganisms. In this study we have cloned, sequenced and expressed a putative prolineracemase (rac1) of B. abortus. Enzymatic activity of rRAC1 showed that it is capable of racemizing only L-Pro. Stimulation of murine naive spleen-purified B-cells with 50ug/ml of rRAC1 induced a 78- fold increase in tritiated timidine incorporation. Experimental infection of Balb/c mice with 2308 and rac1 showed that RAC1 might be involved in a B-cell depletion mechanism during the first stage of infection, as seen by flow cytometry analysis of infected spleens. These results suggest that RAC1 is a B-cell polyclonal activator that strongly contributes to brucellosis. that it is capable of racemizing only L-Pro. Stimulation of murine naive spleen-purified B-cells with 50ug/ml of rRAC1 induced a 78- fold increase in tritiated timidine incorporation. Experimental infection of Balb/c mice with 2308 and rac1 showed that RAC1 might be involved in a B-cell depletion mechanism during the first stage of infection, as seen by flow cytometry analysis of infected spleens. These results suggest that RAC1 is a B-cell polyclonal activator that strongly contributes to brucellosis. that it is capable of racemizing only L-Pro. Stimulation of murine naive spleen-purified B-cells with 50ug/ml of rRAC1 induced a 78- fold increase in tritiated timidine incorporation. Experimental infection of Balb/c mice with 2308 and rac1 showed that RAC1 might be involved in a B-cell depletion mechanism during the first stage of infection, as seen by flow cytometry analysis of infected spleens. These results suggest that RAC1 is a B-cell polyclonal activator that strongly contributes to brucellosis. B. abortus. Enzymatic activity of rRAC1 showed that it is capable of racemizing only L-Pro. Stimulation of murine naive spleen-purified B-cells with 50ug/ml of rRAC1 induced a 78- fold increase in tritiated timidine incorporation. Experimental infection of Balb/c mice with 2308 and rac1 showed that RAC1 might be involved in a B-cell depletion mechanism during the first stage of infection, as seen by flow cytometry analysis of infected spleens. These results suggest that RAC1 is a B-cell polyclonal activator that strongly contributes to brucellosis.