The effect of antibiotics on the production of superantigen from Staphylococcus aureus isolated from atopic dermatitis.
Staphylococcus aureus (S. aureus) often colonizes on the skin of patients with atopic dermatitis. It is known that superantigens which are staphylococcal enterotoxins can activate T cells without processing by antigen presenting cells. It has been suggested that activated T cells release various cytokines which may exacerbate or prolong the cutaneous inflammation associated with atopic dermatitis. Reduction of bacterial colonization from skin lesions has been reported to be effective in the treatment of atopic dermatitis. Therefore, antimicrobial therapy using antibiotics may be a treatment option for atopic dermatitis in selected patients. We examined the effect of antibiotics on the production of superantigen from S. aureus in vitro to determine the action mechanism of antibiotics in the treatment of atopic dermatitis. It was found that antibiotics with inhibitory effect on protein synthesis can suppress the production of superantigen. On the other hand, the superantigen production was not suppressed by antibiotics having either the inhibitory effect on cell wall synthesis or on nucleic acid synthesis. Levels of the suppressive effect on superantigen production by S. aureus varied with strains tested in this study. Moreover, we demonstrated that replication of DNA coding of superantigen produced by S. aureus was suppressed only by roxithromycin (ROX), which is a new macrolide. This finding suggests that ROX may have an effect at the gene level. These results suggested that the suppressive effects of antimicrobial agents that act as inhibitors of protein synthesis on superantigen production from S. aureus may be useful in the treatment of atopic dermatitis.
Adachi
Y
Y
Department of Dermatology, Kansai Medical University, Osaka, Japan.
Akamatsu
H
H
Horio
T
T
D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D000942:Antigens, Bacterial / Q000096:biosynthesis* / Q000737:chemistry / Q000187:drug effects; D003876:Dermatitis, Atopic / Q000276:immunology / Q000382:microbiology*; D006801:Humans; D016106:Methicillin Resistance; D010446:Peptide Fragments / Q000037:antagonists & inhibitors; D015575:Roxithromycin / Q000494:pharmacology; D013211:Staphylococcus aureus / Q000254:growth & development / Q000276:immunology* / Q000302:isolation & purification* / Q000502:physiology; D018089:Superantigens / Q000096:biosynthesis* / Q000737:chemistry / Q000187:drug effects
D000900:Anti-Bacterial Agents; D000942:Antigens, Bacterial; D010446:Peptide Fragments; D018089:Superantigens; D015575:Roxithromycin