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C L Rochester

Publications and source records attributed to C L Rochester.

4 recordsLinked to original sources
PubMed1992

Human airway macrophages. A technique for their retrieval and a descriptive comparison with alveolar macrophages.

We developed a technique to isolate and lavage a segment of a large human airway in vivo. Airway lavage and BAL were performed without significant complications 18 times on 17 normal volunteers. The mean +/- SEM volume of instillate used on all subjects totaled 31.3 +/- 2.7 ml with 47.1 +/- 3.8% of the fluid recovered. A total of 1.5 +/- 0.3 x 10(6) cells were retrieved. Cell viability averaged 71.3 +/- 4.6%. The majority of the cells were macrophages, 27.9 +/- 2.7%, and neutrophils, 28.4 +/- 6.0%. A descriptive comparison of airway macrophages using transmission electron microscopy with those retrieved from paired bronchoalveolar lavage (BAL) samples revealed that airway macrophages possessed more vacuoles (p less than 0.0001), fewer long microvilli (p less than 0.0001), and more membrane undulations (p less than 0.0001). In contrast, macrophages from both lavage locations demonstrated similar staining characteristics when stained with a panel of monoclonal antibodies. During lavage, all subjects experienced mild dyspnea that was relieved when the lavage was completed. One of three subjects tested during the procedure revealed O2 desaturation that was prevented by the inhalation of O2. We conclude that viable macrophages can be retrieved safely from airways of normal subjects and that, compared with macrophages present in BAL, these cells bear both similarities and dissimilarities that may portend differing functional capabilities.

Adult↗
PubMed1992

Cytokine regulation of human lung fibroblast hyaluronan (hyaluronic acid) production. Evidence for cytokine-regulated hyaluronan (hyaluronic acid) degradation and human lung fibroblast-derived hyaluronidase.

We characterized the mechanisms by which recombinant (r) tumor necrosis factor (TNF), IFN-gamma, and IL-1, alone and in combination, regulate human lung fibroblast hyaluronic acid (HA) production. Each cytokine stimulated fibroblast HA production. The combination of rTNF and rIFN-gamma resulted in a synergistic increase in the production of high molecular weight HA. This was due to a synergistic increase in hyaluronate synthetase activity and a simultaneous decrease in HA degradation. In contrast, when rTNF and rIL-1 were combined, an additive increase in low molecular weight HA was noted. This was due to a synergistic increase in hyaluronate synthetase activity and a simultaneous increase in HA degradation. Human lung fibroblasts contained a hyaluronidase that, at pH 3.7, depolymerized high molecular weight HA to 10-40 kD end products of digestion. However, hyaluronidase activity did not correlate with fibroblast HA degradation. Instead, HA degradation correlated with fibroblast-HA binding, which was increased by rIL-1 plus rTNF and decreased by rIFN-gamma plus rTNF. Recombinant IL-1 and rTNF weakly stimulated and rIL-1 and rTNF in combination further augmented the levels of CD44 mRNA in lung fibroblasts. In contrast, rIFN-gamma did not significantly alter the levels of CD44 mRNA in unstimulated or rTNF stimulated cells. These studies demonstrate that rIL-1, rTNF, and rIFN-gamma have complex effects on biosynthesis and degradation which alter the quantity and molecular weight of the HA produced by lung fibroblasts. They also show that fibroblast HA degradation is mediated by a previously unrecognized lysosomal-type hyaluronidase whose function may be regulated by altering fibroblast-HA binding. Lastly, they suggest that the CD44 HA receptor may be involved in this process.

Adult↗