Pentoxifylline ameliorates pulmonary damage caused by Streptococcus pneumoniae infection in mouse.

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.