Publications by authors named "K Kalsi"

Airway diseases can disrupt tight junction proteins, compromising the epithelial barrier and making it more permeable to pathogens. In people with pulmonary disease who are prone to infection with Pseudomonas aeruginosa, pro-inflammatory leukotrienes are increased and anti-inflammatory lipoxins are decreased. Upregulation of lipoxins is effective in counteracting inflammation and infection.

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New technologies such as single-cell RNA sequencing (scRNAseq) has enabled identification of the mRNA transcripts expressed by individual cells. This review provides insight from recent scRNAseq studies on the expression of glucose transporters in the epithelial cells of the airway epithelium from trachea to alveolus. The number of studies analyzed was limited, not all reported the full range of glucose transporters and there were differences between cells freshly isolated from the airways and those grown in vitro.

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Electronic nicotine delivery systems, or e-cigarettes, utilize a liquid solution that normally contains propylene glycol (PG) and vegetable glycerin (VG) to generate vapor and act as a carrier for nicotine and flavorings. Evidence indicated these "carriers" reduced growth and survival of epithelial cells including those of the airway. We hypothesized that 3% PG or PG mixed with VG (3% PG/VG, 55:45) inhibited glucose uptake in human airway epithelial cells as a first step to reducing airway cell survival.

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Article Synopsis
  • Airway epithelial tight junction (TJ) proteins typically protect against external threats, but during bacterial infections like those from Staphylococcus aureus, these TJs get disrupted, allowing glucose to accumulate and feed bacteria.
  • Metformin, a diabetes medication, enhances the barrier function of these TJs by stabilizing proteins like ZO-1 and occludin, potentially through pathways involving AMPK and PKCζ.
  • The study found that metformin speeds up TJ reassembly after disruption and increases the presence of full-length occludin, signifying its beneficial role in maintaining airway epithelial integrity during bacterial infections.
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Intense, large muscle mass exercise increases circulating microvesicles, but our understanding of microvesicle dynamics and mechanisms inducing their release remains limited. However, increased vascular shear stress is generally thought to be involved. Here, we manipulated exercise-independent and exercise-dependent shear stress using systemic heat stress with localized single-leg cooling (low shear) followed by single-leg knee extensor exercise with the cooled or heated leg (Study 1,  = 8) and whole-body passive heat stress followed by cycling (Study 2,  = 8).

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