Résumé
Objective To invetigate the correlation between Kawasaki disease (KD) and mycoplasma pneumomiae (MP). Methods The medical records of 84 children diagnosed as KD in our hospital from March 2012 to February 2014 were retrospectively analyzed, and according to whether with mycoplasma infection or not ,they were divided into observation group and control group. The observation group included 43 cases with mycoplasma infection, and the control group in-cluded 41 KD patients without MP infection. White blood cell count (WBC), high sensitive C reactive protein (CRP), erythrocyte sedimentation rate (ESR), hemoglobin (HB), platelet count (PLT) were detected and analyzed in two groups. Patients of the two groups were compared in whether the existence of coronary artery lesions. Results Patients of the observation group without coronary artery injury accounted for 34.9%(15/43), significantly lower than that of the con trol group 58.5%(24/41), and the observation group with coronary lesions accounted for 65.1%(28/43), significantly higher than that of the control group 41.5%(17/41). The differences were statistically significant (P<0.05); CRP of the observation group was (68.9±14.7) mg/L, significantly higher than that of the control group (52.8±8.2) mg/L, and ESR of the observation group was (42.6 ±15.9) mm/h, significantly higher than that of the control group (21.6 ±6.1) mm/h. The differences were statistically significant (P<0.05). Conclusion MP is one of the causes of KD and has positive corre-lation with coronary artery injury of patients. The injury and inflammation reaction mediated by autoimmune reaction caused by MP is an important way to KD.
Résumé
<p><b>BACKGROUND</b>Non-small cell lung cancer (NSCLC) is the most common lung malignancy worldwide. The metastatic potential of NSCLC cells has been shown to be associated with the tumor microenvironment, which consists of tumor cells, stroma, blood vessels, immune infiltrates and the extracellular matrix. Fibroblasts can produce numerous extracellular matrix molecules and growth factors. Gefitinib has been evaluated as a first-line treatment in selected patients, and it has shown favorable efficacy especially in NSCLC, but it is not effective for everyone.</p><p><b>METHODS</b>In this study, we examined the antitumor activity of gefitinib on lung fibroblasts co-cultured of lung cancer cells. A series of co-culture experiments that employed cell counting kit-8 (CCK8), transwells, real-time polymerase chain reaction (RT-PCR) and Western blotting with HFL-1 fibroblasts and A549 human lung carcinoma cells were performed to learn more about tumor cell proliferation, migration and invasion; and to determine any change of epithelial mesenchymal transition (EMT)-associated tumor markers vimentin, matrix metallopro-teinase 2 (MMP2) and chemotaxis cytokines receptor 4 (CXCR4) mRNA levels.</p><p><b>RESULTS</b>A549 cell proliferation in the presence of HFL-1 cells was not significantly increased compared with A549 cells alone, but A549 cell spheroid body formation was increased after co-culture, and treatment with gefitinib increased further. Our study also revealed that fibroblasts attenuated the lung cancer cell inhibition ratio of migration and invasion after gefitinib treatment in vitro. To further study this mechanism, RT-PCR analysis showed that vimentin, MMP2 and CXCR4 mRNA levels were more highly expressed in the lung cancer cells after co-culture, but did not obviously decrease compared with the control cells following gefitinib treatment. This suggests the mechanism by which fibroblasts attenuate gefitinib-induced expression of EMT-associated tumor markers. Finally, our results demonstrated that co-culture with A549 lung cancer cells does not alter the cell cycle distribution of HFL-1 fibroblasts. Furthermore, HFL-1 fibroblasts had no effect on the cell cycle distribution of HFL-1 cells treated with gefitinib.</p><p><b>CONCLUSION</b>Gefitinib has lower anti-tumor activity on A549 lung cancer cells when co-cultured with HFL-1 fibroblasts.</p>