Streptococcus pneumoniae stimulated mouse peritoneal macrophagc to release tumor necrosis factor-α (TNFα) in vitro. When penicillin was added into the medium with bacteria, TNFα release was accelerated. Pentoxifyll...Streptococcus pneumoniae stimulated mouse peritoneal macrophagc to release tumor necrosis factor-α (TNFα) in vitro. When penicillin was added into the medium with bacteria, TNFα release was accelerated. Pentoxifylline (PTX), a phosphodiesterase inhibitor, significantly attenuated TNFα release caused either by Streptococcus pneumoniae or by its lysates. In this experiment, 150 Kunming mice were infected with Streptococcus peumoniae through inspiration. Dynamic changes of TNFα concentration in serum and bronchoalveolar lavage fluid were determined, and pulmonary pathological changes were also observed. It was found that PTX significantly attenuated TNFα 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 TNFα which is probably the major mediater that causes tissue damage during Streptococcus pneumoniae infection. The mechanism is probably that Steptococcus pneumoniae and its lysates activate TNFα gene transcription. As penicillin accelerates TNFα release, treatment with penicillin alone may aggravate the tissue damage. Combined treatment with PTX may be more reasonable.展开更多
文摘Streptococcus pneumoniae stimulated mouse peritoneal macrophagc to release tumor necrosis factor-α (TNFα) in vitro. When penicillin was added into the medium with bacteria, TNFα release was accelerated. Pentoxifylline (PTX), a phosphodiesterase inhibitor, significantly attenuated TNFα release caused either by Streptococcus pneumoniae or by its lysates. In this experiment, 150 Kunming mice were infected with Streptococcus peumoniae through inspiration. Dynamic changes of TNFα concentration in serum and bronchoalveolar lavage fluid were determined, and pulmonary pathological changes were also observed. It was found that PTX significantly attenuated TNFα 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 TNFα which is probably the major mediater that causes tissue damage during Streptococcus pneumoniae infection. The mechanism is probably that Steptococcus pneumoniae and its lysates activate TNFα gene transcription. As penicillin accelerates TNFα release, treatment with penicillin alone may aggravate the tissue damage. Combined treatment with PTX may be more reasonable.
