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.
Acknowledgements
We thank Dr. Elizabeth DeLyria for critical reading of the manuscript. We also thank the Suzhou hospital of traditional Chinese medicine, the Huaian Second People’s Hospital, and The First Affiliated Hospital of Soochow University for providing samples.
Conflict of interest
None.