Integrative study of pulmonary microbiome, transcriptome and clinical outcomes in Mycoplasma pneumoniae pneumonia.

BACKGROUND: This study aimed to investigate the interactions among three core elements of respiratory infection-pathogen, lung microbiome, and host response-and their avocation with the severity and outcomes of Mycoplasma pneumoniae pneumonia (MPP) in children. METHODS: We prospectively collected bronchoalveolar lavage fluid from a cohort of 41 children with MPP, including general MPP (GMPP) and complicated MPP (CMPP), followed by microbiome and transcriptomic analyses to characterize the association among pathogen, lung microbiome, and host response and correlate it with the clinical features and outcomes. RESULTS: The lung microbiome of patients with CMPP had an increased relative abundance of Mycoplasma pneumoniae (MP) and reduced alpha diversity, with 76 differentially expressed species. Host gene analysis revealed a key module associated with neutrophil function and several inflammatory response pathways. Patients with a high relative abundance of MP, manifested by a specific lung microbiome and host response type, were more prone to CMPP and had a long imaging recovery time. CONCLUSION: Patients with CMPP have a more disrupted lung microbiome than those with GMPP. MP, lung microbiome, and host response interacts with each other and are closely related to disease severity and outcomes in children with MPP.

Inhibition of mitochondrial calcium uptake by Ru360 enhances the effect of 1800 MHz radio-frequency electromagnetic fields on DNA damage.

Today, the existence of radio-frequency electromagnetic fields (RF-EMF) emitted from cell phones, wireless routers, base stations, and other sources are everywhere around our living environment, and the dose is increasing. RF-EMF have been reported to be cytotoxic and supposed to be a risk factor for various human diseases, thus, more attention is necessary. In recent years, interfere with mitochondrial calcium uptake by using mitochondrial calcium uniporter (MCU) inhibitor were suggested to be potential clinical treatment in mitochondrial calcium overload diseases, like neurodegeneration, ischemia/reperfusion injury, and cancer, but whether this approach increases the health risk of RF-EMF exposure are unknown. To address our concern, we did a preliminary study to determine whether inhibition of MCU will increase the genotoxicity of RF-EMF exposure in cells, and found that short-time (15 min) exposure to 1800 MHz RF-EMF induced significant DNA damage and cell apoptosis in mouse embryonic fibroblasts (MEFs) treated with Ruthenium 360 (Ru360), a specific inhibitor of MCU, but no significant effects on cell cycle, cell proliferation, or cell viability were observed. In conclusion, our results indicated that inhibiting MCU increases the genotoxicity of RF-EMF exposure, and more attention needs to be paid to the possible health impact of RF-EMF exposure under these treatments.

Intubation at Birth Is Associated with Death after Pulmonary Hemorrhage in Very Low Birth Weight Infants.

OBJECTIVE: This retrospective cohort study was performed to clarify the association between intubation in the delivery room and the mortality after pulmonary hemorrhage in very low birth weight infants (VLBWIs) during hospitalization. METHODS: The study participants were screened from the VLBWIs admitted to the neonatal intensive care unit (NICU) of the Children's Hospital Affiliated to Nanjing Medical University from 31 July 2019 to 31 July 2022. The newborns who ultimately were included were those infants who survived until pulmonary hemorrhage was diagnosed. These subjects were divided into the intubation-at-birth group (n = 29) and the non-intubation-at-birth group (n = 35), retrospectively. RESULTS: Univariate analysis found that the intubation group had a higher mortality and shorter hospital stay than the non-intubation group (p < 0.05) (for mortality: 25/29 (86.21%) in intubation group versus 14/35 (40.00%) in non-intubation group). By multivariate analysis, the result further showed that intubation in the delivery room was related to shorter survival time and higher risk of death (adjusted hazard ratio: 2.341, 95% confidence interval: 1.094-5.009). CONCLUSIONS: Intubation at birth suggested a higher mortality in the VLBWIs when pulmonary hemorrhage occurred in the NICU.

Immune response plays a role in Mycoplasma pneumoniae pneumonia.

Introduction: Mycoplasma pneumoniae (MP) is a major pathogen of community-acquired pneumonia in children. However, the specific pathogenesis of the progression of Mycoplasma pneumoniae pneumonia (MPP) is unclear. We aimed to reveal the landscape of microbiota and the host immune response in MPP. Methods: This self-controlled study analyzed the microbiome and transcriptome of bronchoalveolar lavage fluid (BALF) from the severe side (SD) and opposite side (OD) of 41 children with MPP from January to December 2021 and revealed the differences of the peripheral blood neutrophil function among children with mild MPP, severe MPP, and healthy children through transcriptome sequencing. Results: The MP load or the pulmonary microbiota had no significant difference between the SD group and OD group, and the deterioration of MPP was related to the immune response, especially the intrinsic immune response. Discussion: The immune response plays a role in MPP, which may inform treatment strategies for MPP.

Exposure to 10 Hz Pulsed Magnetic Fields Do Not Induce Cellular Senescence in Human Fetal Lung Fibroblasts.

Rapid population aging has led to a global burden of late-life diseases. As the largest risk factor for a multitude of age-related diseases, aging is not only the result of genotype but also closely related to external factors. With the rapid expansion in the usage of electromagnetic fields (EMFs), the effect of EMFs on aging has also attracted attention. Cells are the basic unit of organs and body tissues, and cellular senescence plays an important role in the aging process. The effect of EMFs on cellular senescence has been investigated in a few studies, but the information is limited, and the results are inconsistent; thus, further investigation is required. In this study, we investigated the effect of 10 Hz pulsed magnetic fields (MFs) on cellular senescence in a 2BS cell line, isolated from human fetal lung fibroblasts, and found that intermittent (1 d on/1 d off) exposure to 10 Hz pulsed MFs at 1.0 mT for 2 weeks induced DNA damage, but no other significant phenotype of cellular senescence in 2BS cells.

Profiling of miRNAs in pediatric asthma: upregulation of miRNA-221 and miRNA-485-3p.

The aim of this study was to investigate the expression profiles of microRNAs (miRNAs) in pediatric asthma and to determine candidate miRNAs responsible for the pathogenesis of this disease. Microarrays were used to detect the differences in the miRNA expression levels between asthmatic children and controls. Airway inflammation was evaluated by cell counting and tissue biopsy in an ovalbumin (OVA)-induced murine asthma model. Real-time polymerase chain reaction (PCR) was used to verify the differentially expressed miRNAs. The targets of the identified miRNAs were analyzed by bioinformatic analysis. The sprouty-related protein with an EVH1 domain-2 (Spred-2) protein content was assessed by western blotting. Differences were observed in the expression of miRNAs between the asthmatic children and controls. Upregulation of miRNA-221 and miRNA-485-3p in pediatric asthmatics and murine asthma models were verified by real-time PCR. Spred-2, a predicted target of miRNA-221 and miRNA-485-3p, was downregulated in murine asthma models. Upregulation of miRNA-221 and miRNA-485-3p may regulate the pathogenesis of asthma.

Inhibition of miRNA-221 suppresses the airway inflammation in asthma.

This study investigated the expression of miRNA-221 in asthmatics in order to determine whether miRNA-221 plays a role in the development of asthma. Real-time PCR was used to detect the miRNA-221 in both asthmatic and control subjects. In addition, airway inflammation was evaluated by cell counting and tissue biopsy in the OVA-induced murine asthma model. miRNA-221 was differentially expressed in asthmatics and control subjects, and miRNA-221 blockade resulted in a reduction of airway inflammation in the OVA-induced murine asthma model. We conclude that miRNA-221 participates in the pathogenesis of asthma and that inhibition of miRNA-221 suppresses airway inflammation in asthmatics.