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Immunomodulatory effect of fosfomycin on human B-lymphocyte function
K Morikawa1, F Oseko, S Morikawa
1Department of Internal Medicine, Shimane Medical University, Japan.
Antimicrobial Agents and Chemotherapy
|February 1, 1993
Summary
Fosfomycin (FOM) inhibits human B-cell proliferation and immunoglobulin secretion by arresting cells in the G0 to G1 phase. This antibiotic may not impede B-cell antigen presentation roles.
Area of Science:
- Immunology
- Microbiology
- Pharmacology
Background:
- Fosfomycin (FOM) is a unique antibiotic with no known chemical relatives.
- Recent studies indicate FOM inhibits histamine release from basophils.
- The impact of FOM on human B-cell functions remains largely unexamined.
Purpose of the Study:
- To investigate the effects of Fosfomycin (FOM) on human B-cell functions.
- To determine if FOM influences B-cell proliferation, cell cycle progression, and immunoglobulin secretion.
Main Methods:
- Human B cells were stimulated with Staphylococcus aureus Cowan 1.
- Cell proliferation was assessed using cell cycle analysis.
- Immunoglobulin secretion and cell surface antigen expression (CD25, CD71, Ia) were measured.
Main Results:
- FOM demonstrated a dose-dependent inhibition of B-cell proliferation induced by S. aureus Cowan 1.
- FOM caused cell cycle arrest at the G0 to G1 transition.
- FOM suppressed immunoglobulin secretion from antibody-producing B cells.
- FOM did not inhibit the expression of CD25 or CD71 activation antigens.
- FOM sustained increased Ia expression on B cells stimulated by S. aureus Cowan 1.
Conclusions:
- Fosfomycin (FOM) significantly impairs human B-cell proliferation and antibody production.
- FOM-induced cell cycle arrest affects both resting and activated B cells.
- FOM's sustained Ia expression suggests it may not hinder B-cell antigen presentation capabilities.