PubMed · 4446328
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G O Grigor'ian. [Grid for triphasic bronchography].. https://pubmed.ncbi.nlm.nih.gov/4446328/
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Neutrophil recruitment from the blood stream into the airways is one of the important features of many inflammatory disorders in the lung. In this process, neutrophils migrate first from the blood across the ECs in the apical-to-basolateral direction into the tissues and then across airway epithelium in the basolateral-to-apical direction into the lung lumen. We investigated and compared the different mechanisms of neutrophil transmigration in vitro across monolayers of these two cell types in both directions. Neutrophil migration induced by chemoattractants was stronger across resting EC than across resting epithelial cells when both cell types were growing on top of the filters (i.e., migration in the apical-to-basolateral direction). Much higher neutrophil transepithelial migration was found in the physiological, basolateral-to-apical direction (cells hanging underneath the filters) than in the opposite direction across either resting or IL-1 beta-activated epithelial cells. In contrast, no significant difference was observed with EC under these conditions. After a 4-h IL-1 beta activation, neutrophil migration across EC was dependent on IL-8 and PAF. However, the migration across epithelial cells relied, to a greater extent, on IL-8 production, and not on PAF. The adhesion molecule ICAM-1 contributed much less to neutrophil migration across epithelium than that across endothelium. Our study provides evidence of different mechanisms of neutrophil transmigration across monolayers of EC and epithelial cells in vitro, indicating that different processes control neutrophil transmigration across EC and epithelial cells in vivo.
When human respiratory tract epithelial cells were exposed to 100 microM H2O2, there was rapid induction of DNA strand breakage and chemical modifications to all 4 DNA bases suggestive of attack by OH.. The major products were FAPy-adenine, FAPy-guanine, and 8-OH-guanine. Some of the base modifications were removed very quickly from the DNA (e.g., 8-OH-guanine), whereas others persisted for longer (e.g., thymine glycol), probably due to differential activity of different repair enzymes. By contrast, strand breaks continued to increase over the time course of the experiment, perhaps because strand breakage is also implicated in the repair process. One should therefore be cautious in using strand breakage as a sole measure of oxidative DNA damage, and when drawing conclusions about the pattern and biological significance of oxidative DNA damage in cells the relative persistence of different lesions must be considered.
To investigate the role of human bronchial epithelial cells (HBECs) in the maintenance and remodeling of the extracellular matrix, we evaluated the expression by HBECs of 72- and 92-kDa gelatinases under basal conditions and after exposure to bacterial lipopolysaccharides (LPS). Confluent HBECs from explants were cultured in plastic dishes coated with type I and III collagens. Gelatin zymography of HBEC-conditioned media showed constitutive major 92-kDa and minor 72-kDa gelatinases recognized by specific human antibodies and totally inhibited by the metalloproteinase inhibitor EDTA. The identification of the two matrix metalloproteinases was confirmed by quantitative reverse transcription-polymerase chain reaction. Identical patterns of gelatinase expression were observed with repetitive primary cultures issued from the same explants. Zymography showed that exposure of HBECs to LPS induced 2- and 20-fold increases in 92-kDa gelatinase production and activation, respectively, as well as a smaller increase in activated 68-kDa gelatinase. With [3H]gelatin substrate, elevated metallogelatinolytic activity (138 microgram of hydrolyzed gelatin/48 h/10(6) cells) was also observed, whereas no activity was detected in the absence of LPS. A human epithelial cell line (16HBE14o-) exhibited the same basal profile of gelatinase activity, but this profile remained unchanged after exposure to LPS. Quantitative reverse transcription-polymerase chain reaction demonstrated only minimal changes in 92-kDa mRNA levels in response to LPS, but the half-life of 92-kDa gelatinase mRNA was increased with exposure to LPS. In contrast, concomitant slight increases in 72-kDa gelatinase protein and mRNA were found, suggesting that the control mechanisms regulating the expression of 92- and 72-kDa gelatinases by HBECs in response to LPS are divergent. All these data allowed us to propose that HBECs may be actively involved in the physiological and physiopathological remodeling of the airway basement membrane.