Pulmonary fibrosis is a chronic progressive parenchymal lung lesion that is a common outcome of several interstitial lung diseases.Despite some progress in investigation of the etiology and pathogenesis of pulmonary fibrosis,it only achieves palliation and is difficult to cure.Lung macrophages are the most abundant innate immune cells in alveolar tissues,and there exists a great degree of heterogeneity and potential dynamic changes of lung macrophages at different stages of pulmonary fibrosis,whose dysfunction is closely related to the development of pulmonary fibrosis.Macrophages in the early stage of lung tissue injury mainly mediate the inflam-matory response.However,in the fibrotic stage,macrophages would be transformed into macrophages with a reparative phenotype that secrete large amounts of pro-fibrotic mediators and promote the proliferation and differentiation of fibroblasts,contributing to the pro-gression and deterioration of pulmonary fibrosis.The function of lung macrophages during fibrosis is regulated by a variety of mecha-nisms,including epigenetic modifications,metabolic reprogramming,and regulation of complex signaling pathways,etc.Strict func-tional regulation is critical for maintaining lung homeostasis and regulating injury repair.In this review,we will describe the heteroge-neity of macrophage and the underlying regulatory mechanisms during pulmonary fibrosis.

Objective: To assess the presence of vector-borne pathogens [including Zika virus (ZIKV), dengue virus (DENV), chikungunya virus (CHIKV), and Plasmodium (PLAS)] among voluntary blood donors in Wenshan Zhuang and Miao Autonomous Prefecture (referred to as Wenshan), so as to provide a basis for formulating blood safety-related strategies. Methods: Blood samples from voluntary blood donors in Wenshan from June to August 2022 to 2024 were selected. Real-time fluorescent quantitative reverse transcription polymerase chain reaction (RT-qPCR) was used to test 20 426 samples for ZIKV RNA, DENV RNA, and CHIKV RNA; and 19 765 samples were tested for PLAS DNA. Results: All 20 426 samples tested for ZIKV RNA, DENV RNA, and CHIKV RNA were negative; similarly, all 19 765 samples tested for PLAS DNA were negative. Conclusion: The risk of ZIKV, DENV, CHIKV, and PLAS infection among voluntary blood donors in Wenshan is relatively low. Routine surveillance for these pathogens as endemic diseases is not currently warranted. It is recommended to adjust the screening strategy based on the dynamic situation of local epidemiology control and prevention.

Pulmonary fibrosis is a chronic progressive parenchymal lung lesion that is a common outcome of several interstitial lung diseases.Despite some progress in investigation of the etiology and pathogenesis of pulmonary fibrosis,it only achieves palliation and is difficult to cure.Lung macrophages are the most abundant innate immune cells in alveolar tissues,and there exists a great degree of heterogeneity and potential dynamic changes of lung macrophages at different stages of pulmonary fibrosis,whose dysfunction is closely related to the development of pulmonary fibrosis.Macrophages in the early stage of lung tissue injury mainly mediate the inflam-matory response.However,in the fibrotic stage,macrophages would be transformed into macrophages with a reparative phenotype that secrete large amounts of pro-fibrotic mediators and promote the proliferation and differentiation of fibroblasts,contributing to the pro-gression and deterioration of pulmonary fibrosis.The function of lung macrophages during fibrosis is regulated by a variety of mecha-nisms,including epigenetic modifications,metabolic reprogramming,and regulation of complex signaling pathways,etc.Strict func-tional regulation is critical for maintaining lung homeostasis and regulating injury repair.In this review,we will describe the heteroge-neity of macrophage and the underlying regulatory mechanisms during pulmonary fibrosis.

Objective To investigate the role and mechanism of low-dose aspirin concurrent with IFN-a in inducing hepatocellular carcinoma apoptosis in BEL-7402 cells. Methods BEL-7402 cells were cultured and treated with IFN-α,or low dose aspirin or both.MTT and flow cytometry were used to measure the cell proliferation and apoptosis after treatment with a singular drug or the combined regiment.The expressions of the apoptosis-related proteins were detected by Western blot.Results MTT assay revealed after IFN α administration alone or combined with aspirin treatment for 48 h,the proliferation ratio of the IFN-α or aspirin group were 82.45％ ± 1.71％ and 83.22％ ±2.26 ％,compared with the control group.The group which received the combined therapy had a proliferation ratio of 69.84 ％ ±1.18 ％,which was significantly lower than the single groups (P＜0.05).The flow cytometry revealed that the apoptosis ratio in IFN-α group and aspirin group were 14.78 ％ ±1.93％ and 14.00％±0.61％,respectively,while the IFN-α + aspirin group was 21.68％±1.28％,which was also significantly higher than that of the single groups (P＜0.05).Western blot detected that IFN-α and aspirin (1 mmol/L) could promote caspase-3 and caspase-9 protein expressions,and when the two drugs were combined,caspase-3 and caspase-9 were also significantly activated.IFN-α alone or combined with aspirin can promote the expression of pro-apoptotic protein Bax (P＜0.05),while the anti-apoptotic proteins expression of Bcl-2 and Bcl-xl did not change significantly (P＞0.05).Conclusions Low-dose aspirin can cooperate with IFN-α in inhibiting the BEL-7402 cell growth and inducing the cell apoptosis by activating and increasing caspase-3 and caspase-9 levels,which may be related to the increased expression of pro-apoptotic protein Bax.