PENTOXIFYLLINE AMELIORATES PULMONARY DAMAGE CAUSED BY STREPTOCOCCUS PNEUMONIAE INFECTION IN MOUSE

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.

Label-free quantitative proteomics reveals fibrinopeptide B and heparin cofactorⅡas potential serum biomarkers in respiratory syncytial virus-infected mice treated with Qingfei oral liquid formula

Respiratory syncytial virus(RSV) is a leading cause of acute lower respiratory tract infections. Qingfei oral liquid(QFOL), a traditional Chinese medicine, is widely used in clinical treatment for RSV-induced pneumonia. The present study was designed to reveal the potential targets and mechanism of action for QFOL by exploring its influence on the host cellular network following RSV infection. We investigated the serum proteomic changes and potential biomarkers in an RSV-infected mouse pneumonia model treated with QFOL. Eighteen BALB/c mice were randomly divided into three groups: RSV pneumonia model group(M), QFOL-treated group(Q) and the control group(C). Serum proteomes were analyzed and compared using a label-free quantitative LC-MS/MS approach. A total of 172 protein groups, 1009 proteins, and 1073 unique peptides were successfully identified. 51 differentially expressed proteins(DEPs) were identified(15 DEPs when M/C and 43 DEPs when Q/M; 7 DEPs in common). Classification and interaction network showed that these proteins participated in various biological processes including immune response, blood coagulation, complement activation, and so forth. Particularly, fibrinopeptide B(FpB) and heparin cofactor Ⅱ(HCII) were evaluated as important nodes in the interaction network, which was closely involved in coagulation and inflammation. Further, the Fp B level was increased in Group M but decreased in Group Q, while the HCII level exhibited the opposite trend. These findings not only indicated FpB and HCII as potential biomarkers and targets of QFOL in the treatment of RSV pneumonia, but also suggested a regulatory role of QFOL in the RSV-induced disturbance of coagulation and inflammation-coagulation interactions.