ArticleHistochemistry and cell biology2017
Localization and pneumococcal alteration of junction proteins in the human alveolar-capillary compartment.
Article in Histochemistry and cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 37 citations in OpenAlex.
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- Microenvironmental acidification by pneumococcal sugar consumption fosters barrier disruption and immune suppression in the human alveolus.The European respiratory journal · 2024Article
- Occludin Is Essential to Maintain Normal Alveolar Barrier Integrity and Its Protective Role During ARDS Progression.International journal of molecular sciences · 2024Article
- Impaired upper respiratory tract barrier function during postnatal development predisposes to invasive pneumococcal disease.PLoS pathogens · 2024Article
- Involvement and repair of epithelial barrier dysfunction in allergic diseases.Frontiers in immunology · 2024Review
- Impact of Endogenous Pneumococcal Hydrogen Peroxide on the Activity and Release of Pneumolysin.Toxins · 2023Article
- Pore-forming activity ofInfection and immunity · 2023Article
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- Airway Epithelial Cell Junctions as Targets for Pathogens and Antimicrobial Therapy.Pharmaceutics · 2022Review
- Human alveolar progenitors generate dual lineage bronchioalveolar organoids.Communications biology · 2022Article
- Dynamic Python-Based Method Provides Quantitative Analysis of Intercellular Junction Organization DuringFrontiers in cellular and infection microbiology · 2022Article
- Neutrophil Recruitment in Pneumococcal Pneumonia.Frontiers in cellular and infection microbiology · 2022Review
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- Functional comparison of MERS-coronavirus lineages reveals increased replicative fitness of the recombinant lineage 5.Nature communications · 2021Article
- Microvesicles released from pneumolysin-stimulated lung epithelial cells carry mitochondrial cargo and suppress neutrophil oxidative burst.Scientific reports · 2021Article
- Pneumococcal Extracellular Serine Proteases: Molecular Analysis and Impact on Colonization and Disease.Frontiers in cellular and infection microbiology · 2021Review
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Loss of alveolar barrier function with subsequent respiratory failure is a hallmark of severe pneumonia. Although junctions between endo- and epithelial cells regulate paracellular fluid flux, little is known about their composition and regulation in the human alveolar compartment. High autofluorescence of human lung tissue in particular complicates the determination of subcellular protein localization. By comparing conventional channel mode confocal imaging with spectral imaging and linear unmixing, we demonstrate that background fluorescent spectra and fluorophore signals could be rigorously separated resulting in complete recovery of the specific signal at a high signal-to-noise ratio. Using this technique and Western blotting, we show the expression patterns of tight junction proteins occludin, ZO-1 as well as claudin-3, -4, -5 and -18 and adherence junction protein VE-cadherin in naive or Streptococcus pneumoniae-infected human lung tissue. In uninfected tissues, occludin and ZO-1 formed band-like structures in alveolar epithelial cells type I (AEC I), alveolar epithelial cells type II (AEC II) and lung capillaries, whereas claudin-3, -4 and -18 were visualised in AEC II. Claudin-5 was detected in the endothelium only. Claudin-3, -5, -18 displayed continuous band-like structures, while claudin-4 showed a dot-like expression. Pneumococcal infection reduced alveolar occludin, ZO-1, claudin-5 and VE-cadherin but did not change the presence of claudin-3, -4 and -18. Spectral confocal microscopy allows for the subcellular structural analysis of proteins in highly autofluorescent human lung tissue. The thereby observed deterioration of lung alveolar junctional organisation gives a structural explanation for alveolar barrier disruption in severe pneumococcal pneumonia.
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