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[Induction by Staphylococcus aureus L-form of tumor necrosis factor-alpha from macrophages]
I Matsu-Ura1, K Kuwano, A Umeda
1Department of Microbiology, Kurume University School of Medicine, Japan.
Abstract:
Induction of tumor necrosis factor-alpha (TNF-alpha) by Staphylococcus aureus L-form was investigated. The supernatant of a macrophage culture mixed with S. aureus L-form showed a potent cytotoxic activity to L cells. Addition of anti TNF-alpha antibody inhibited completely the cytotoxic activity of the supernatant, indicating that the activity might be due mostly to TNF-alpha. To investigate localization of TNF-alpha production, the membranes of hypotonicity treated L-form were layered on a step-gradient composed of an upper and lower layers of 35% and 50% sucrose, respectively. The membranes were banded at the interface of 35% and 50% of sucrose. The activity of TNF-alpha production of the membrane fraction was 10-times higher than that of the soluble fraction.
Insights
Staphylococcus aureus L-form induces tumor necrosis factor-alpha (TNF-alpha), a key inflammatory cytokine. This study found TNF-alpha primarily localized in the bacterial membranes, suggesting a targeted immune response.
Area of Science:
- Immunology
- Microbiology
- Cell Biology
Context:
- Investigating the role of Staphylococcus aureus L-form in immune responses.
- Understanding the mechanisms of cytokine induction by bacterial pathogens.
Purpose:
- To determine if Staphylococcus aureus L-form induces tumor necrosis factor-alpha (TNF-alpha).
- To localize the production of TNF-alpha in Staphylococcus aureus L-form.
Summary:
- Supernatant from macrophage cultures exposed to Staphylococcus aureus L-form exhibited cytotoxic activity against L cells.
- This cytotoxic activity was neutralized by anti-TNF-alpha antibodies, confirming TNF-alpha as the primary mediator.
- Further fractionation revealed that bacterial membranes contained significantly higher TNF-alpha production activity compared to soluble fractions.
Impact:
- Highlights the role of bacterial membranes in initiating inflammatory responses.
- Provides insights into the specific mechanisms by which Staphylococcus aureus L-form interacts with host immune cells.
- Suggests potential targets for therapeutic interventions aimed at modulating TNF-alpha-mediated inflammation.