Abstract

We have attempted to examine the cause of lowering phagocytic activity of phagocytes on clearance of bacteria in SLE patients. The experiments were performed in SLE model mice, NZB/WF1 female mice (BWF1). The ratio of the cells which phagocytized fluorescent microspheres and possessed Mac-1 on both peripheral blood leukocytes (PBL) and peritoneal macrophages (PMo) in BWF1 female mice was shown decreasing by using the flow cytometric method before the present of typical symptoms of SLE (under 25 weeks-old), i.e., the appearance of ANA and IgG deposits in glomeruli. In a period of showing the symptoms of SLE (over 25 weeks-old), the ratio of Mac-1 positive cells on PBL increased, but phagocytic function of these cells did not increase. On the other hand, on PMo, they decreased together in that period. Moreover, the phagocytosis of PMo in 15, 25, 35 weeks-old mice against fluorescent microspheres showed a significant increase (1.7 times) by replacing opsonin with normal (ddY) murine serum instead of BWF1 murine serum, and the phagocytosis of PMo treated with anti-Mac-1 antibody (M1/70) showed a significant inhibition (46%) against that of untreated PMo. These results indicate that lowering phagocytic activity of phagocytes on primary defence against microbial infections in SLE patients is due possibly to decrease of C3 activity in the serum rather than a decrease of positive percentage and function of Mac-1 on these cells.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.