Regulation of Ciliary Beat Frequency by the Nitric Oxide–Cyclic Guanosine Monophosphate Signaling Pathway in Rat Airway Epithelial Cells

2000 ◽  
Vol 23 (2) ◽  
pp. 175-181 ◽  
Author(s):  
Dechun Li ◽  
Gotaro Shirakami ◽  
Xinhua Zhan ◽  
Roger A. Johns
Keyword(s):  
Nitric Oxide ◽  
Epithelial Cells ◽  
Signaling Pathway ◽  
Beat Frequency ◽  
Ciliary Beat Frequency ◽  
Cyclic Guanosine Monophosphate ◽  
Airway Epithelial Cells ◽  
Guanosine Monophosphate ◽  
Airway Epithelial ◽  
Ciliary Beat

Ethanol stimulates apparent nitric oxide-dependent ciliary beat frequency in bovine airway epithelial cells

1995 ◽  
Vol 268 (4) ◽  
pp. L596-L600 ◽  
Author(s):  
J. H. Sisson
Keyword(s):  
Nitric Oxide ◽  
Epithelial Cells ◽  
Airway Epithelium ◽  
Beat Frequency ◽  
Primary Cultures ◽  
Ciliary Beat Frequency ◽  
Airway Epithelial Cells ◽  
Ethanol Ingestion ◽  
Ciliary Motility ◽  
Ciliary Beat

The mucociliary apparatus of the lung provides an important host-defense function by clearing the upper airway of inhaled particles and infectious microorganisms. Because lung host defenses are impaired in alcoholics, we hypothesized that ethanol would decrease ciliary motility in airway epithelium. Ciliary beat frequency (CBF) was measured by videomicroscopy in primary cultures of ciliated bovine bronchial epithelial cells (BBECs). Ethanol rapidly stimulated ciliary motility in a time-dependent fashion with concentrations as low as 10 mM. No detectable decreases in ciliary motility were noted until ethanol concentrations exceeded 1,000 mM. Because many substances stimulate ciliary motility by releasing nitric oxide (NO) via upregulation of nitric oxide synthase (NOS), we preincubated ciliated BBECs with a stereospecific NOS inhibitor, NG-monomethyl-L-arginine (L-NMMA). L-NMMA completely blocked ethanol-induced stimulation of CBF, which could be subsequently restored by adding either L-arginine or sodium nitroprusside, which is a direct NO donor. These results indicate that ethanol, at clinically relevant concentrations, stimulates the release of NO by airway epithelium that upregulates ciliary motility. The rapidity of this response suggests upregulation of the constitutive NOS, known to be present in airway epithelium, and may explain the increases in mucociliary clearance observed in previous studies of ethanol ingestion in animals and in humans. These data also suggest a novel signal transduction pathway, the NO/NOS system, by which ethanol may exert some of its diverse biologic effects.

Regulation of ciliary beat frequency by both PKA and PKG in bovine airway epithelial cells

1998 ◽  
Vol 275 (4) ◽  
pp. L827-L835 ◽  
Author(s):  
T. A. Wyatt ◽  
J. R. Spurzem ◽  
K. May ◽  
J. H. Sisson
Keyword(s):  
Protein Kinase ◽  
Epithelial Cells ◽  
Beat Frequency ◽  
Ciliary Beat Frequency ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Dependent Protein Kinase ◽  
Dependent Protein ◽  
Ciliary Beat

Ciliary beating is required for the maintenance of lung mucociliary transport. We investigated the role of cyclic nucleotide-dependent protein kinases in stimulating ciliary beat frequency (CBF) in bovine bronchial epithelial cells (BBECs). cAMP-dependent protein kinase (PKA) activity and cGMP-dependent protein kinase (PKG) activity were distinguished after DEAE-Sephacel chromatography of BBEC extracts. cAMP levels and PKA activity are increased in BBECs stimulated with 0.01–1 mM isoproterenol, with a corresponding increase in CBF. cGMP levels and PKG activity are increased in BBECs stimulated with 0.1–10 μM sodium nitroprusside, with a corresponding increase in CBF. Direct protein kinase-activating analogs of cAMP and cGMP (dibutyryl cAMP and 8-bromo-cGMP, respectively) also activate their specific kinases and stimulate CBF. Preincubation of BBECs with inhibitors of PKA or PKG [KT-5720 or Rp-8-( p-chlorophenylthio)-guanosine 3′,5′-cyclic monophosphothioate] results in the inhibition of specific kinase activity as well as in the inhibition of CBF. These studies suggest that the activation of either PKA or PKG can lead to the stimulation of CBF in bovine airway epithelium.

scholarly journals Glycated Albumin Triggers an Inflammatory Response in the Human Airway Epithelium and Causes an Increase in Ciliary Beat Frequency

2021 ◽  
Vol 12 ◽  
Author(s):  
Moira L. Aitken ◽  
Ranjani Somayaji ◽  
Thomas R. Hinds ◽  
Maricela Pier ◽  
Karla Droguett ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Airway Epithelium ◽  
Glycated Albumin ◽  
Beat Frequency ◽  
Ciliary Beat Frequency ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Human Airway ◽  
Human Airway Epithelium ◽  
Ciliary Beat

The role of inflammation in airway epithelial cells and its regulation are important in several respiratory diseases. When disease is present, the barrier between the pulmonary circulation and the airway epithelium is damaged, allowing serum proteins to enter the airways. We identified that human glycated albumin (GA) is a molecule in human serum that triggers an inflammatory response in human airway epithelial cultures. We observed that single-donor human serum induced IL-8 secretion from primary human airway epithelial cells and from a cystic fibrosis airway cell line (CF1-16) in a dose-dependent manner. IL-8 secretion from airway epithelial cells was time dependent and rapidly increased in the first 4 h of incubation. Stimulation with GA promoted epithelial cells to secrete IL-8, and this increase was blocked by the anti-GA antibody. The IL-8 secretion induced by serum GA was 10–50-fold more potent than TNFα or LPS stimulation. GA also has a functional effect on airway epithelial cells in vitro, increasing ciliary beat frequency. Our results demonstrate that the serum molecule GA is pro-inflammatory and triggers host defense responses including increases in IL-8 secretion and ciliary beat frequency in the human airway epithelium. Although the binding site of GA has not yet been described, it is possible that GA could bind to the receptor for advanced glycated end products (RAGE), known to be expressed in the airway epithelium; however, further experiments are needed to identify the mechanism involved. We highlight a possible role for GA in airway inflammation.

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