Search

Air pollution is a leading cause of increasing infectious lung diseases. Pulmonary cryptococcosis is a fatal fungal pneumonia in acquired immunodeficiency syndrome patients. In some cases, the pathogen Cryptococcus neoformans also develops dormant nodules in immunocompetent individuals. In the present study, we demonstrated that fine particulate matter (PM2.5) increased CD146 expression in alveolar epithelial cells and promoted C. neoformans pulmonary infection. Aryl hydrocarbon receptor (AhR) signaling was required for increased expression of CD146 in epithelial cells treated with PM2.5. In a murine model of pulmonary infection, PM2.5 promoted fungal infection, and CD146 deficiency decreased the fugal burden of C. neoformans. Our study may highlight the importance of air pollution to lung mycosis and CD146 as a target for preventing infectious lung diseases. [ABSTRACT FROM AUTHOR]

Background and Aims: Although long non-coding RNAs (lncRNAs) have been linked to many diseases including asthma, little is known about lncRNA transcriptomes of CD4+ T cells in asthma. The present study aimed to explore the lncRNAs profile in the CD4+T cells from the mouse model of acute asthma. Methods: Next generation sequencing for lncRNAs and mRNAs was performed on CD4+ T cells from asthma and control mice. Gene ontology (GO) and kyoto encyclopedia of genes and genomes (KEGG) pathway analyses were performed to predict the functions and signal pathways for the aberrant lncRNAs. The selected lncRNAs were further measured using quantitative real-time PCR (polymerase chain reaction) and observed in the fluorescence in situ hybridization (FISH). The lncRNA–mRNA co-expression network was constructed via Pearson's correlation coefficient and Cytoscape 3.6. Results: Next generation sequencing revealed 36 up-regulated lncRNAs and 98 down-regulated lncRNAs in acute asthma compared with controls. KEGG pathway analysis showed that cytokine-cytokine receptor interaction had the highest enrichment scores. A co-expression network was constructed in which 23 lncRNAs and 301 mRNAs altered formed a total of 12424 lncRNA and mRNA pairs. To validate the RNA sequencing results, we measured the 4 different lncRNAs using qPCR. The lncRNA fantom3_9230106C11 was significantly reduced in CD4+ T cells of asthma. Bioinformatics analysis showed that lncRNA fantom3_9230106C11 had the potential to interact with many miRNAs and transcription factors related to Th2 differentiation. Conclusion: This study provided the first evidence for different expression of lncRNAs of CD4+T cells in asthma and may serve as a template for further, larger functional in-depth analyses regarding asthma molecular lncRNAs. [ABSTRACT FROM AUTHOR]

Airway remodeling is a key characteristic of allergic asthma. Epithelial-mesenchymal transition (EMT) induced by various factors, particularly transforming growth factor (TGF)-β1, orchestrates airway remodeling. Protein phosphatase 2A (PP2A), an important serine-threonine phosphatase, is involved in TGF-β1 production and EMT. Long noncoding RNAs (lncRNAs) have emerged as novel players in regulating EMT. Here, we aimed to explore the effects and mechanisms of action of lincR-PPP2R5C, a lncRNA that affects PP2A activity, on airway remodeling in a mouse model of chronic allergic asthma. LincR-PPP2R5C knockout (KO) alleviated inflammatory responses in house dust mite (HDM)-induced chronic allergic asthma. Moreover, airway remodeling and EMT were reduced in lung tissues of lincR-PPP2R5C KO mice. HDM extract induced EMT in airway epithelial cells, which was decreased following lincR-PPP2R5C KO. Mechanistically, lincR-PPP2R5C deficiency enhanced PP2A activity, which inhibited TGF-β1 production in epithelial cells. In conclusion, lincR-PPP2R5C deficiency prevented HDM-induced airway remodeling in mice by reversing EMT, which was mediated by the PP2A/TGF-β1 signaling pathway. Thus, lncRNAs, i.e. , lincR-PPP2R5C, may be potential targets to prevent airway remodeling in allergic asthma., Competing Interests: There are no financial or other issues that might lead to a conflict of interest., (Copyright © 2024 The Korean Academy of Asthma, Allergy and Clinical Immunology • The Korean Academy of Pediatric Allergy and Respiratory Disease.)

Objective: To evaluate the efficacy and safety of omalizumab in patients with refractory allergic asthma using meta-analysis. Methods: We searched databases including PubMed, Web of Science, Embase and the website of ClinicalTrials. gov registry for randomized controlled trials (RCTs), using the search terms: ("anti-IgE" OR "anti-immunoglobulin E" OR "anti-IgE antibody" OR "omalizumab" OR "rhuMAb-E25" OR "Xolair") AND ("allergic asthma"). The time was up to September 19th 2020. Review Manager 5.4 software and Stata16 software were used to calculate pooled RR or WMD , perform heterogeneity test, and assess publication bias. Results: Fifteen RCTs with 6 316 patients in total (omalizumab, n =3 469; placebo, n =2 847) met our selection criteria. Comparing with placebo, omalizumab reduced the risk of asthma exacerbations during both stable-inhaled corticosteroid (ICS) phase ( RR =0.69, 95% CI : 0.63-0.75, P <0.001; I 2 =39.0%, P =0.090) and ICS-reduction phase ( RR =0.55, 95% CI : 0.46-0.66, P <0.001; I 2 =41.0%, P =0.180), reduced emergency visits ( RR =0.53, 95% CI : 0.38-0.73, P <0.001; I 2 =0, P =0.420), made a significant reduction in dosage of ICS ( RR= 1.35, 95% CI : 1.25-1.45, P <0.001; I 2 =22.0%, P =0.280) and even withdrew from ICS completely ( RR =1.80, 95% CI : 1.41-2.31, P <0.001; I 2 =57.0%, P =0.070). Omalizumab significantly improved asthma-related quality of life ( RR =1.81, 95% CI : 1.51-2.17). The use of rescue bronchodilators was significantly reduced in the omalizumab group ( RR =0.78, 95% CI : 0.67-0.92) but there was no significant difference in the dosage of rescue bronchodilators (puff per day) ( WMD =-0.32, 95% CI : -0.77-0.13). Patients taking omalizumab did not increase the frequency of any adverse events ( RR =1.01, 95% CI : 0.98-1.03) and serious adverse events ( RR =0.89, 95% CI : 0.74-1.06). Conclusions: Omalizumab is an ideal adjunctive treatment for refractory allergic asthma with good efficacy and safety. Further randomized controlled trials are needed to determine the appropriate duration of treatment.

Air pollution is a leading cause of increasing infectious lung diseases. Pulmonary cryptococcosis is a fatal fungal pneumonia in acquired immunodeficiency syndrome patients. In some cases, the pathogen Cryptococcus neoformans also develops dormant nodules in immunocompetent individuals. In the present study, we demonstrated that fine particulate matter (PM 2 . 5 ) increased CD146 expression in alveolar epithelial cells and promoted C. neoformans pulmonary infection. Aryl hydrocarbon receptor (AhR) signaling was required for increased expression of CD146 in epithelial cells treated with PM 2 . 5 . In a murine model of pulmonary infection, PM 2 . 5 promoted fungal infection, and CD146 deficiency decreased the fugal burden of C. neoformans . Our study may highlight the importance of air pollution to lung mycosis and CD146 as a target for preventing infectious lung diseases., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Sun, Ji, Jiang, Tao, Zhang, Yang, Wang, Chen, Huang and Zhang.)

Background and Aims: Although long non-coding RNAs (lncRNAs) have been linked to many diseases including asthma, little is known about lncRNA transcriptomes of CD4 + T cells in asthma. The present study aimed to explore the lncRNAs profile in the CD4 + T cells from the mouse model of acute asthma., Methods: Next generation sequencing for lncRNAs and mRNAs was performed on CD4+ T cells from asthma and control mice. Gene ontology (GO) and kyoto encyclopedia of genes and genomes (KEGG) pathway analyses were performed to predict the functions and signal pathways for the aberrant lncRNAs. The selected lncRNAs were further measured using quantitative real-time PCR (polymerase chain reaction) and observed in the fluorescence in situ hybridization (FISH). The lncRNA-mRNA co-expression network was constructed via Pearson's correlation coefficient and Cytoscape 3.6., Results: Next generation sequencing revealed 36 up-regulated lncRNAs and 98 down-regulated lncRNAs in acute asthma compared with controls. KEGG pathway analysis showed that cytokine-cytokine receptor interaction had the highest enrichment scores. A co-expression network was constructed in which 23 lncRNAs and 301 mRNAs altered formed a total of 12424 lncRNA and mRNA pairs. To validate the RNA sequencing results, we measured the 4 different lncRNAs using qPCR. The lncRNA fantom3&#95;9230106C11 was significantly reduced in CD4+ T cells of asthma. Bioinformatics analysis showed that lncRNA fantom3&#95;9230106C11 had the potential to interact with many miRNAs and transcription factors related to Th2 differentiation., Conclusion: This study provided the first evidence for different expression of lncRNAs of CD4+T cells in asthma and may serve as a template for further, larger functional in-depth analyses regarding asthma molecular lncRNAs.

Aim: To explore the miRNAs profile of CD4 + T lymphocytes in asthma via next generation sequencing., Methods: In the murine model of acute asthma, spleen CD4 + T lymphocytes were sorted, in which small RNAs were extracted and sequenced. Novel miRNAs were measured with real time quantitative reverse transcription polymerase chain reaction (qRT-PCR)., Results: A total of 127 miRNAs were found to exhibit at least twofold change. In the 262 predicted novel miRNAs, 14 novel miRNAs were measured in qRT-PCR in the sorted CD4 + T cells or in the differentiated Th1/Th2 cells and novel miR-11 (xxx-m0228-3p) was significantly decreased in the sorted CD4 + T cells from the murine model of asthma and in the Th2 cells., Conclusion: Aberrant miRNAs profile in the CD4 + T lymphocytes from acute asthma was documented.