PubMed · 13503368
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M B KRESS, O C BRANTIGAN, J H HIRSCHFELD, A STEINER. 1958. Broncholithiasis.. https://pubmed.ncbi.nlm.nih.gov/13503368/
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1. In the human airway epithelium, VIP/PACAP receptors are distributed in nerve fibers and in epithelial cells but their role in transepithelial ion transport have not been reported. Here, we show that human bronchial epithelial Calu-3 cells expressed the VPAC(1) receptor subtype which shares similar high affinity for VIP and PACAP-27. 2. The stoichiometric binding parameters characterizing the (125)I-VIP and (125)I-PACAP-27 binding to these receptors were determined. 3. We found that VIP (EC(50) approximately 7.6 nM) and PACAP-27 (EC(50) approximately 10 nM) stimulated glibenclamide-sensitive and DIDS-insensitive iodide efflux in Calu-3 cells. 4. The protein kinase A (PKA) inhibitor, H-89 and the protein kinase C (PKC) inhibitor, chelerythrine chloride prevented activation by both peptides demonstrating that PKA and PKC are part of the signaling pathway. This profile corresponds to the pharmacological signature of CFTR. 5. In the cystic fibrosis airway epithelial IB3-1 cell lacking functional CFTR but expressing VPAC(1) receptors, neither VIP, PACAP-27 nor forskolin stimulated chloride transport. 6. Ussing chamber experiments demonstrated stimulation of CFTR-dependent short-circuit currents by VIP or PACAP-27 applied to the basolateral but not to the apical side of Calu-3 cells monolayers. 7. This study shows the stimulation in human bronchial epithelial cells of CFTR-dependent chloride secretion following activation by VIP and PACAP-27 of basolateral VPAC(1) receptors.
The Reid index is an instrument for the evaluation of chronic bronchitis. The thickness of the mucosa and of its gland layer are measured and the relationship is expressed as a gland/wall ratio. Specimens were obtained from 124 autopsies from the German National Study on SIDS (GeSID). The cases were divided into three groups: group 1 typical SIDS ( n=47), group 2 SIDS with signs of mild inflammation of the respiratory tract ( n=50) and group 3 unnatural death controls ( n=23). The Reid index was measured in sections from the trachea, bifurcation/main bronchi and bronchioli (staining HE and PAS). The Reid index was remarkably constant throughout the different levels of the respiratory tract (standard deviation range 0.06-0.10). A comparison of the three groups did not show statistically significant differences. Group 1: mean Reid index trachea 0.37, bifurcation/main bronchi 0.38, bronchioli 0.39. Group 2: mean Reid index trachea 0.40, bifurcation/main bronchi 0.38, bronchioli 0.38. Group 3: mean Reid index trachea 0.39, bifurcation/main bronchi 0.38, bronchioli 0.41. It can be concluded that the dimensions of bronchial glands do not vary in cases of SIDS as compared to controls. This demonstrates that the Reid index has no significance in the vast majority of SIDS cases and that acute inflammation commonly does not produce an elevated Reid index. In addition, the Reid index was confirmed to be a valid instrument to study the respiratory tract including the trachea due to its stability and it was found that the Reid index is age-dependent: compared to adults, the ratios in infants were higher.
The influence of two peroxisome proliferator-activated receptor gamma (PPARgamma) ligands, a thiazolidinedione, rosiglitazone (RG) and the prostaglandin D2 metabolite 15-deoxy-Delta(12,14)-prostaglandin J2 (15d-PGJ2) on the proliferation of human cultured airway smooth muscle (HASM) was examined. The increases in HASM cell number in response to basic fibroblast growth factor (bFGF, 300 pm) or thrombin (0.3 U ml-1) were significantly inhibited by either RG (1-10 microM) or 15d-PGJ2 (1-10 microM). The effects of RG, but not 15d-PGJ2, were reversed by the selective PPARgamma antagonist GW9662 (1 microM). Neither RG nor 15d-PGJ2 (10 microM) decreased cell viability, or induced apoptosis, suggesting that the regulation of cell number was due to inhibition of proliferation, rather than increased cell death. Flow-cytometric analysis of HASM cell cycle distribution 24 h after bFGF addition showed that RG prevented the progression of cells from G1 to S phase. In contrast, 15d-PGJ2 caused an increase in the proportion of cells in S phase, and a decrease in G2/M, compared to bFGF alone. Neither RG nor 15d-PGJ2 inhibited ERK phosphorylation measured 6 h post mitogen addition. The bFGF-mediated increase in cyclin D1 protein levels after 8 h was reduced in the presence of 15d-PGJ2, but not RG. Although both RG and 15d-PGJ2 can inhibit proliferation of HASM irrespective of the mitogen used, only the antiproliferative effects of RG appear to be PPARgamma-dependent. The different antimitogenic mechanisms of 15d-PGJ2 and synthetic ligands for PPARgamma may be exploited to optimise the potential for these compounds to inhibit airway remodelling in asthma. British Journal of Pharmacology (2004) 141, 517-525. doi:10.1038/sj.bjp.0705630