Background Pulmonary fibrosis (PF) is a devastating disease characterized by remodeling of lung architecture and abnormal deposition of fibroblasts in parenchymal tissue and ultimately results in respiratory failure and death. Preclinical studies suggest that mesenchymal stem cell (MSC) administration may be a safe and promising option in treating PF. The objective of our meta-analysis is to assess the efficacy of MSC therapy in preclinical models of PF. Methods We performed a comprehensive literature search in PubMed, EMBASE, Web of Science, and Cochrane Library databases from inception to March 17, 2021. Studies that assessed the efficacy of MSC therapy to animals with PF were included. The SYRCLE bias risk tool was employed to evaluate the bias of included studies. The primary outcomes included survival rate and pulmonary fibrosis scores. Meta-analysis was conducted via Cochrane Collaboration Review Manager (version 5.4) and Stata 14.0 statistical software. Results A total of 1120 articles were reviewed, of which 24 articles met inclusion criteria. Of these, 12 studies evaluated the survival rate and 20 studies evaluated pulmonary fibrosis scores. Compared to the control group, MSC therapy was associated with an improvement in survival rate (odds ratios (OR) 3.10, 95% confidence interval (CI) 2.06 to 4.67, P < 0.001, I2 = 0%) and a significant reduction in pulmonary fibrosis scores (weighted mean difference (WMD) 2.05, 95% CI −2.58 to −1.51, P < 0.001, I2 = 90%). Conclusions MSC therapy is a safe and effective method that can significantly improve the survival and pulmonary fibrosis of PF animals. These results provide an important basis for future translational clinical studies.

The over‐activation of inflammation is involved in the pathogenesis of smoke‐induced lung injury (SILI), while Rb3 treatment may alleviate smoke‐induced lung injury by down‐regulating the expression of H19, a regulator of miR‐29b expression. Moreover, HMGB1 is an important mediator of inflammation. Therefore, in this study, we set up an animal model of SILI and treated it with Rb3 to study the effect of Rb3 on the treatment of SILI and the involvement of H19/miR‐29b/HMGB1/TLR4 signalling. SILI mice treated with Rb3 before H&E staining and TUNEL assay were conducted to observe the pathological damages and status of apoptosis in each group. Real‐time PCR, Western blot, computational analysis and luciferase assays were utilized to establish the signalling pathway involved in the pathogenesis of SILI and the action of Rb3 treatment. Rb3 treatment alleviated pathological changes in the lungs while decreasing the levels of W/D ratio and cell apoptotic index. H19 was validated to sponge miR‐29b‐3p, while HMGB1 mRNA was validated to be a target gene of miR‐29b‐3. As a result, a signalling pathway of H19/miR‐29b‐3p/HMGB1 was established. Cell viability was evidently reduced after 72 hours of treatment with CSE, but the treatment of Rb3 elevated the expression of H19 and HMBG1 in the presence of CSE. Also, CSE‐induced inhibition of miR‐29b‐3p expression was restored by Rb3. The findings of this study collectively demonstrated that Rb3 exhibited its therapeutic effect during the treatment of SILI via modulating the H19/miR‐29b‐3p/HMBG1 signalling pathway.

Clinical characteristics of tuberculosis (TB) patients from southern China with pulmonary tuberculosis hemoptysis (PTH) were analyzed retrospectively in order to improve the diagnosis of TB, reduce mortality and prevent the transmission of TB. A total of 1227 cases of pulmonary TB patients hospitalized in the Third Affiliated Hospital of Sun Yat-sen University and Guangzhou Chest Hospital from January to December of 2011 were analyzed retrospectively. 1) The male/female ratio of the 1227 tuberculosis cases was 2.15:1. There were 403 cases (32.8%) of PTH with a male/ female ratio of 3.03:1. 2) The ratio of patients with PTH to those with TB was designated as Rh. The Rh in the male group (36.2%, 303 cases) was higher than that in the female group (25.6%, 100 cases, risk ratio (RR) = 1.41, P ≤ 0.001). 3) The Rh in the elderly group (≥60 years old, 20.3%, 56 cases) was lower than that in the younger patients group (20-39 years old, 45.4%, 189 cases, RR = 2.51, P ≤ 0.001). 4) The Rh in initial treatment group (29.6%, 296 cases) was lower than that in the retreatment group (46.9%, 107 cases, RR = 1.58, P ≤ 0.001). 5) The Rh in sputum-positive TB patients (44.5%, 297 cases) was significantly higher than that in the smear-negative TB patients (18.9%, 106 cases, RR = 2.35, P ≤ 0.001). 6) The Rh of patients with lung lesions range < 3 lung fields (31.7%, 105 cases) was not significantly different with that of patients with lung lesions range ≥ 3 lung fields (33.3%, 298 cases, RR = 1.05, P = 0.96 > 0.05). 7) The Rh of patients with cavities (51.8%, 309 cases) was higher than that of patients without cavities (14.9%, 94 cases, RR = 3.48, P ≤ 0.001). Male, young, retreated, sputum-positive TB patients and those with cavitary TB * Corresponding authors. S. Y. Tan et al. 174 were more predisposed to PTH in southern China. TB patients with such characteristics should be sensitized and accorded good care.

Coxsackievirus A16 (CV-A16) is one of the viruses that is most frequently associated with hand-foot-and-mouth disease (HFMD). Previous studies have shown that CV-A16 infections are mostly self-limiting, but in recent years, it has been gradually found that CV-A16 infections can also induce neurological complications and eventually cause death in children with HFMD. Moreover, no curative drugs or preventative vaccines have been developed for CV-A16 infection. Therefore, it is particularly important to investigate the mechanism of CV-A16 infection-induced neuropathy. In the current study, transcriptome sequencing technology was used to identify changes in the transcriptome of SH-SY5Y cells infected with CV-A16, which might hide the mechanism of CV-A16-induced neuropathology. The transcriptome profiling showed that 82,406,974, 108,652,260 and 97,753,565 clean reads were obtained in the Control, CV-A16-12 h and CV-A16-24 h groups, respectively. And it was further detected that a total of 136 and 161 differentially expressed genes in CV-A16-12 h and CV-A16-24 h groups, respectively, when compared with Control group. Then, to explore the mechanism of CV-A16 infection, we focused on the common differentially expressed genes at different time points of CV-A16 infection and found that there were 34 differentially expressed genes based on which clustering analysis and functional category enrichment analysis were performed. The results indicated that changes in oxidation levels were particularly evident in the GO term analysis, while only the “Gonadotropin-releasing hormone receptor pathway” was enriched in the KEGG pathway analysis, which might be closely related to the neurotoxicity caused by CV-A16 infection. Meanwhile, the ID2 closely related to nervous system has been demonstrated to be increased during CV-A16 infection. Additionally, the data on differentially expressed non-protein-coding genes of different types within the transcriptome sequencing results were analyzed, and it was speculated that these dysregulated non-protein-coding genes played a pivotal role in CV-A16 infection. Ultimately, qRT-PCR was utilized to validate the transcriptome sequencing findings, and the results of qRT-PCR were in agreement with the transcriptome sequencing data. In conclusion, transcriptome profiling was carried out to analyze response of SH-SY5Y cells to CV-A16 infection. And our findings provide important information to elucidate the possible molecular mechanisms which were linked to the neuropathogenesis of CV-A16 infection.