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- Jevnikar, Z., et al.
(författare)
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Epithelial IL-6 trans-signaling defines a new asthma phenotype with increased airway inflammation
- 2019
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Ingår i: Journal of Allergy and Clinical Immunology. - : Elsevier BV. - 0091-6749 .- 1097-6825. ; 143:2, s. 577-590
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Tidskriftsartikel (refereegranskat)abstract
- Background: Although several studies link high levels of IL-6 and soluble IL-6 receptor (sIL-6R) to asthma severity and decreased lung function, the role of IL-6 trans-signaling (IL-6TS) in asthmatic patients is unclear. Objective: We sought to explore the association between epithelial IL-6TS pathway activation and molecular and clinical phenotypes in asthmatic patients. Methods: An IL-6TS gene signature obtained from air-liquid interface cultures of human bronchial epithelial cells stimulated with IL-6 and sIL-6R was used to stratify lung epithelial transcriptomic data (Unbiased Biomarkers in Prediction of Respiratory Disease Outcomes [U-BIOPRED] cohorts) by means of hierarchical clustering. IL-6TS-specific protein markers were used to stratify sputum biomarker data (Wessex cohort). Molecular phenotyping was based on transcriptional profiling of epithelial brushings, pathway analysis, and immunohistochemical analysis of bronchial biopsy specimens. Results: Activation of IL-6TS in air-liquid interface cultures reduced epithelial integrity and induced a specific gene signature enriched in genes associated with airway remodeling. The IL-6TS signature identified a subset of patients with IL-6TS-high asthma with increased epithelial expression of IL-6TS-inducible genes in the absence of systemic inflammation. The IL-6TS-high subset had an overrepresentation of frequent exacerbators, blood eosinophilia, and submucosal infiltration of T cells and macrophages. In bronchial brushings Toll-like receptor pathway genes were upregulated, whereas expression of cell junction genes was reduced. Sputum sIL-6R and IL-6 levels correlated with sputum markers of remodeling and innate immune activation, in particular YKL-40, matrix metalloproteinase 3, macrophage inflammatory protein 1 beta, IL-8, and IL-1 beta. Conclusions: Local lung epithelial IL-6TS activation in the absence of type 2 airway inflammation defines a novel subset of asthmatic patients and might drive airway inflammation and epithelial dysfunction in these patients.
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| 2. |
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| 3. |
- Devda, V., et al.
(författare)
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Recovery of resources from industrial wastewater employing electrochemical technologies : status, advancements and perspectives
- 2021
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Ingår i: Bioengineered. - : Taylor & Francis Group. - 2165-5979 .- 2165-5987. ; 12:1, s. 4697-4718
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Tidskriftsartikel (refereegranskat)abstract
- In the last two decades, water use has increased at twice the rate of population growth. The freshwater resources are getting polluted by contaminants like heavy metals, pesticides, hydrocarbons, organic waste, pathogens, fertilizers, and emerging pollutants. Globally more than 80% of the wastewater is released into the environment without proper treatment. Rapid industrialization has a dramatic effect on developing countries leading to significant losses to economic and health well-being in terms of toxicological impacts on humans and the environment through air, water, and soil pollution. This article provides an overview of physical, chemical, and biological processes to remove wastewater contaminants. A physical and/or chemical technique alone appears ineffective for recovering useful resources from wastewater containing complex components. There is a requirement for more processes or processes combined with membrane and biological processes to enhance operational efficiency and quality. More processes or those that are combined with biological and membrane-based processes are required to enhance operational efficiencies and quality. This paper intends to provide an exhaustive review of electrochemical technologies including microbial electrochemical technologies. It provides comprehensive information for the recovery of metals, nutrients, sulfur, hydrogen, and heat from industrial effluents. This article aims to give detailed information into the advancements in electrochemical processes to energy use, improve restoration performance, and achieve commercialization. It also covers bottlenecks and perspectives of this research area.
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| 5. |
- Singhania, Akul, et al.
(författare)
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CD4+CCR6+ T cells dominate the BCG-induced transcriptional signature
- 2021
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Ingår i: EBioMedicine. - : Elsevier. - 2352-3964. ; 74
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Tidskriftsartikel (refereegranskat)abstract
- Background: The century-old Mycobacterium bovis Bacillus Calmette-Guerin (BCG) remains the only licensed vaccine against tuberculosis (TB). Despite this, there is still a lot to learn about the immune response induced by BCG, both in terms of phenotype and specificity. Methods: We investigated immune responses in adult individuals pre and 8 months post BCG vaccination. We specifically determined changes in gene expression, cell subset composition, DNA methylome, and the TCR repertoire induced in PBMCs and CD4 memory T cells associated with antigen stimulation by either BCG or a Mycobacterium tuberculosis (Mtb)-derived peptide pool. Findings: Following BCG vaccination, we observed increased frequencies of CCR6+ CD4 T cells, which includes both Th1* (CXCR3+CCR6+) and Th17 subsets, and mucosal associated invariant T cells (MAITs). A large number of immune response genes and pathways were upregulated post BCG vaccination with similar patterns observed in both PBMCs and memory CD4 T cells, thus suggesting a substantial role for CD4 T cells in the cellular response to BCG. These upregulated genes and associated pathways were also reflected in the DNA methylome. We described both qualitative and quantitative changes in the BCG-specific TCR repertoire post vaccination, and importantly found evidence for similar TCR repertoires across different subjects. Interpretation: The immune signatures defined herein can be used to track and further characterize immune responses induced by BCG, and can serve as reference for benchmarking novel vaccination strategies. (C) 2021 The Author(s). Published by Elsevier B.V.
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