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[Streptococcus pneumoniae-induced pulmonary consolidation prevented with tumor necrosis factor alpha monoclonal
1Laboratory of Pulmonary Disease, Union Hospital, Tongji Medical University, Wuhan.
Abstract:
Streptococcus pneumoniae stimulate mouse peritoneal macrophages to release tumor necrosis factor alpha (TNF alpha) in vitro. When penicillin was added to lysate bacterium, TNF alpha release was accelerated. 150 Kunming mice were infected with streptococcus pnumoniae through inspiration. Dynamic changes of TNF alpha concentration in serum and bronchoalveolar lavage fluid were detected; pulmonary pathological changes were also observed. It was found that TNF alpha monoclonal antibody significantly attenuates TNF alpha activity in serum and bronchoalveolar lavage fluid, white blood cell chemotaxis, emigation, and infiltration were inhibited. We conclude that streptococcus pneumoniae infection stimulates TNF alpha release, and TNF alpha is probably the major mediator that causes tissue damage during streptococcus pneumoniae infection. As penicillin accelerates TNFa release, single therapy of penicillin may worse tissue damage.
Insights
Streptococcus pneumoniae infection triggers tumor necrosis factor alpha (TNF alpha) release, a key factor in tissue damage. Penicillin may worsen this damage by accelerating TNF alpha release.
Area of Science:
- Immunology
- Microbiology
- Pathology
Context:
- Streptococcus pneumoniae is a leading cause of bacterial pneumonia.
- Tumor necrosis factor alpha (TNF alpha) plays a critical role in inflammatory responses.
- Understanding the host-pathogen interaction is crucial for effective treatment.
Purpose:
- To investigate the role of TNF alpha in Streptococcus pneumoniae infection.
- To examine the effect of penicillin on TNF alpha release.
- To evaluate the therapeutic potential of TNF alpha inhibition.
Summary:
- In vitro studies showed that Streptococcus pneumoniae stimulates macrophages to release TNF alpha, with penicillin accelerating this release.
- In vivo, S. pneumoniae infection in mice led to increased TNF alpha levels in serum and bronchoalveolar lavage fluid.
- Administration of TNF alpha monoclonal antibody reduced inflammatory cell infiltration and tissue damage.
Impact:
- TNF alpha is identified as a major mediator of tissue damage in pneumococcal pneumonia.
- Penicillin monotherapy might exacerbate lung injury due to accelerated TNF alpha release.
- Targeting TNF alpha presents a potential therapeutic strategy for severe pneumococcal infections.