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Importance: Measles virus spreads rapidly and efficiently in human airway epithelial cells.
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The regulation of ACE2 release was investigated in polarized human airway epithelia.
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Background: The human airway is believed to be acidified in asthma.
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Methods: Primary BSMC were isolated from human airway tissue of asthmatic and non-asthmatic patients.
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We found that polarized human airway epithelia expressed abundant FR alpha on their apical surface.
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Our results underline the regenerative potential of patient-derived human airway stem cells in lung tissue engineering.
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The ARAF mutations were shown to transform immortalized human airway epithelial cells in a sorafenib-sensitive manner.
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LGL1-conditioned medium increased migration of fetal rat primary lung epithelial cells and human airway epithelial cells.
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Of particular interest, entry independent of FR alpha was observed in primary cultures of human airway epithelia.
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Results: Gram-positive bacteria Staphylococcus aureus or Streptococcus pneumoniae, induced release of CXCL8 from human airway epithelial cells.
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Using a model of well-differentiated human airway epithelia, we found that apical MMP9 significantly increases transepithelial conductance.
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In addition, we sought to determine which immune cells transfer MeV infectivity to the human airway epithelium.
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In human airway samples from two asthma cohorts, we observed altered expression patterns of multiple clock genes.
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PM10 exposure primes human airway epithelial cells to subsequent models of cell damage and influenza A virus exposure.
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The molecular identity of this calcium influx pathway in human airway smooth muscle (HASM) remains unclear.
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Nectin-4 sustains measles virus entry and non-cytopathic lateral spread in well-differentiated primary human airway epithelial sheets infected basolaterally.
