Abstract

Objective: To investigate the potential role of β-galactosidase in altering immunoglobulin G (IgG) galactosylation in serum of rheumatoid arthritis (RA).Methods: The expression level and activity of β-galactosidase in serum and CD 19+ B cells were measured by enzyme-linked immune sorbent assay (ELISA). The effect of β-galactosidase on the N-glycan changes in serum from mice intravenously treated with β-galactosidase was observed by linear ion-trap quadrupole-electrospray ionization mass spectrometry (LTQ-ESI-MS). We established a collagen-induced arthritis (CIA) rat model to explore the biological function of β-galactosidase in RA.Results: The expression level of β-galactosidase in serum of 32 patients was elevated when compared with those of 30 healthy controls. The activity and expression level of β-galactosidase in CD19+ B cells from RA patients was higher than those from healthy controls. The ratio of m/z 1142/937 was reduced in mice treated with β-galactosidase when compared with normal mice. We found that β-galactosidase was implicated in the development of inflammation by affecting body weight and elevating the expression level of interleukin-6, tumor necrosis factor-α, and rheumatoid factor in the serum.Conclusions: Our results suggested the high level of β-galactosidase in B cells and serum of RA patients and revealed that altered β-galactosidase may be implicated in the progression of inflammation.

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