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Pentoxifylline ameliorates pulmonary damage caused by Streptococcus pneumoniae infection in mouse
1Respiratory Disease Research Laboratory, Union Hospital, Tongji Medical University, Wuhan.
Abstract:
Streptococcus pneumoniae stimulated mouse peritoneal macrophage to release tumor necrosis factor-alpha (TNF alpha) in vitro. When penicillin was added into the medium with bacteria, TNF alpha release was accelerated. Pentoxifylline (PTX), a phosphodiesterase inhibitor, significantly attenuated TNF alpha release caused either by Streptococcus pneumoniae or by its lysates. In this experiment, 150 Kunming mice were infected with Streptococcus pneumoniae through inspiration. Dynamic changes of TNF alpha concentration in serum and bronchoalveolar lavage fluid were determined, and pulmonary pathological changes were also observed. It was found that PTX significantly attenuated TNF alpha activity in serum and bronchoalveolar lavage fluid, and inhibited white blood cell chemotaxis, emigration and infiltration. In conclusion, Streptococcus pneumoniae infection stimulates the release of TNF alpha which is probably the major mediater that causes tissue damage during Streptococcus pneumoniae infection. The mechanism is probably that Streptococcus pneumoniae and its lysates activate TNF alpha gene transcription. As penicillin accelerates TNF alpha release, treatment with penicillin alone may aggravate the tissue damage. Combined treatment with PTX may be more reasonable.
Insights
Streptococcus pneumoniae infection increases tumor necrosis factor-alpha (TNF alpha). Pentoxifylline (PTX) reduces this inflammatory response and associated tissue damage, suggesting combined PTX and penicillin treatment may be beneficial.
Area of Science:
- Immunology
- Microbiology
- Pharmacology
Background:
- Streptococcus pneumoniae infection triggers inflammatory responses.
- Tumor necrosis factor-alpha (TNF alpha) plays a key role in infection-induced tissue damage.
- Penicillin's effect on TNF alpha release during infection is not fully understood.
Purpose of the Study:
- To investigate the role of TNF alpha in Streptococcus pneumoniae infection.
- To evaluate the effect of Pentoxifylline (PTX) on TNF alpha production and related inflammatory processes.
- To assess the potential of combined PTX and penicillin therapy.
Main Methods:
- In vitro studies using mouse peritoneal macrophages stimulated with Streptococcus pneumoniae.
- In vivo studies involving intranasal infection of Kunming mice with Streptococcus pneumoniae.
- Measurement of TNF alpha concentrations in serum and bronchoalveolar lavage fluid.
- Histopathological examination of lung tissues and observation of white blood cell activity.
Main Results:
- Streptococcus pneumoniae and its lysates stimulated TNF alpha release from macrophages.
- Penicillin accelerated TNF alpha release in vitro.
- PTX significantly attenuated TNF alpha release and inhibited inflammatory cell infiltration in vivo.
- PTX reduced TNF alpha levels in serum and bronchoalveolar lavage fluid.
Conclusions:
- TNF alpha is a major mediator of tissue damage in Streptococcus pneumoniae infection.
- Penicillin treatment alone may exacerbate infection-related tissue damage by accelerating TNF alpha release.
- Combined therapy with PTX and penicillin may offer a more effective treatment strategy by mitigating inflammation and tissue damage.