The aim of this work was to discover if Mycoplasma fermentans, which is
known to infect B cells, could be the cause of the raised ecto-50-nucleotidase
observed in the synovial fluid of rheumatoid arthritis patients. The
ecto-50-nucleotidase activity in the patients’ serum has been shown to correlate
with the erythrocyte sedimentation rate and DNA from the mycoplasma
has been found in the synovial fluid. B lymphoblastoid cell lines
were exposed to 16 strains of Mycoplasma fermentans and their ecto-
50-nucleotidase, CD73, was measured both biochemically and by mouse
antibodies to human ecto 50-nucleotidase using the fluorescence activated
cell sorter. The type strain, PG 18, did not grow with the B cells. Some of
the mycoplasma strains (9/15) increased the cellular ecto-50-nucleotidase
activity from twice to 17 fold, and usually showed 50-nucleotidase activity
themselves. At least one strain, M106, induced human 50-nucleotidase on
the normally 50-nucleotidase negative Daudi and Raji Burkitt’s lymphoma
cell lines, and increased sevenfold the 50-nucleotidase on the monocyte/
macrophage cell line THP-1. Growing the cells in aged medium increased
the level of mycoplasma infection. This mycoplasma-induced enzyme
showed a conformational change and an increase in activity with a glycosylation
change involving mannose groups. The other group of strains,
mostly of respiratory or cell culture origin, usually did not have any
50-nucleotidase of their own and decreased the B-cell enzyme activity by
about half. Electron microscopy and flow cytometry showed that the
strain M106 was filamentous and could be found inside the B-cells. The
50-nucleotidase-inducing strains of M. fermentans may be important in
the aetiology of rheumatoid arthritis