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Promotion of platelet aggregation by sera from brucellosis patients with antiphosphatidylcholine antibodies

Departamento Microbiología. Universidad de Navarra, Clínica Universitaria de Navarra. 31080, Pamplona and *Departamento Microbiología, Hospital Universitario, Facultad de Medicina, Universidad de Valladolid, Spain

Corresponding author: Dr C. Gamazo (e-mail: cgamazo{at}unav.es).

Received 27 Dec. 2000; revised version accepted 4 May 2001.

Abstract

Results obtained in this study suggest that in human brucellosis there is an antibody response against platelet-activating factor (PAF) and phosphatidylcholine (PC). The specificity of the antiphospholipid response was determined by inhibition assays. The PAF molecule was able to inhibit the anti-PC activity of the brucellosis-control serum. This inhibition capacity of PAF was similar to that of the phosphorylcholine (PYC) group. These results suggest that the inhibition activity could be attributed to the PYC group present in both PAF and PC molecules. Consequently, these findings support an immunodominant role of PYC in the antiphospholipid response of brucellosis. Furthermore, sera from patients infected with Brucella organisms were able to cause platelet aggregation, as were brucella phospholipids, suggesting a possible role of the antiphospholipid antibodies and phospholipids in the inflammatory response in brucellosis.

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