Regulation of ciliary beat frequency by the nitric oxide signaling pathway in mouse nasal and tracheal epithelial cells

2011 ◽  
Vol 317 (17) ◽  
pp. 2548-2553 ◽  
Author(s):  
Jian Jiao ◽  
Hong Wang ◽  
Wei Lou ◽  
Shanzhe Jin ◽  
Erzhong Fan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Epithelial Cells ◽  
Signaling Pathway ◽  
Beat Frequency ◽  
Ciliary Beat Frequency ◽  
Nitric Oxide Signaling ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial ◽  
Ciliary Beat

Effects of albuterol enantiomers on ciliary beat frequency in ovine tracheal epithelial cells

2002 ◽  
Vol 92 (6) ◽  
pp. 2396-2402 ◽  
Author(s):  
Jeffrey I. Frohock ◽  
Corrine Wijkstrom-Frei ◽  
Matthias Salathe
Keyword(s):  
Epithelial Cells ◽  
Intracellular Calcium ◽  
Single Cells ◽  
Beat Frequency ◽  
Ciliary Beat Frequency ◽  
Airway Epithelial Cells ◽  
Racemic Mixture ◽  
Dependent Manner ◽  
Tracheal Epithelial Cells ◽  
Ciliary Beat

β2-Adrenergic agonists stimulate ciliary beat frequency (CBF), an integral part of mucociliary clearance. To evaluate the differential effects of albuterol enantiomers and their racemic mixture on ciliary function, CBF and intracellular calcium were measured at room temperature from single ovine airway epithelial cells with use of digital videomicroscopy. Baseline CBF was 7.2 ± 0.2 (SE) Hz ( n = 80 measurements). R-albuterol (10 μM to 1 mM) stimulated CBF in a dose-dependent manner to maximally 24.4 ± 5.4% above baseline. Racemic albuterol stimulated CBF to maximally 12.8 ± 3.6% above baseline, a significantly lower increase compared with R-albuterol alone, despite identical R-enantiomer amounts in both groups. Simultaneous recordings of intracellular calcium concentration and CBF from single cells indicated that the CBF increase in response to R-albuterol was mediated through β-receptors and stimulation of protein kinase A, in a calcium-dependent and -independent fashion. S-albuterol had a negligible effect on CBF and did not change intracellular calcium. Together, these results suggest that R-albuterol is more efficacious than racemic albuterol in stimulating CBF. Thus S-albuterol may interfere with the ability of R-albuterol to increase CBF.

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.

Muscarinic signaling in ciliated tracheal epithelial cells: dual effects on Ca2+ and ciliary beating

1997 ◽  
Vol 272 (2) ◽  
pp. L301-L310 ◽  
Author(s):  
M. Salathe ◽  
E. J. Lipson ◽  
P. I. Ivonnet ◽  
R. J. Bookman
Keyword(s):  
Epithelial Cells ◽  
Muscarinic Receptors ◽  
Single Cells ◽  
Beat Frequency ◽  
Ciliary Beat Frequency ◽  
Tracheal Epithelial Cells ◽  
M3 Receptors ◽  
Tracheal Epithelial ◽  
M3 Subtype ◽  
Microscopy Techniques

To examine cholinergic signal transduction pathways that modulate ciliary beat frequency (CBF), cultured ovine tracheal epithelial cells were imaged using a combination of phase-contrast (CBF) and fluorescence (Ca2+) microscopy techniques. In single cells, acetylcholine (ACh) transiently increased CBF and intracellular Ca2+ concentration ([Ca2+]i), mainly by Ca2+ release from internal stores, with a small delayed contribution from Ca2+ influx. Nicotinic agonists did not alter CBF or [Ca2+]i, whereas atropine blocked the ACh-stimulated transients, consistent with the involvement of muscarinic receptors. 4-Diphenylacetoxy-N-methylpiperidine methiodide was approximately 100 times more potent than pirenzepine in inhibiting the ACh-induced [Ca2+]i peaks, suggesting that the receptor is a pharmacologically defined (M3) subtype. Interestingly, after depletion of intracellular Ca2+ stores by thapsigargin, ACh caused a rapid transient decrease in both CBF and [Ca2+]i, again with an antagonist profile of M3 receptors. We conclude that activation of M3 muscarinic receptors initiates specific signaling pathways that act simultaneously to increase and decrease [Ca2+]i and CBF.

Propofol Stimulates Ciliary Motility via  the Nitric Oxide–Cyclic GMP Pathway in Cultured Rat Tracheal Epithelial Cells

2000 ◽  
Vol 93 (2) ◽  
pp. 482-488 ◽  
Author(s):  
Gotaro Shirakami ◽  
Dechun Li ◽  
Xinhua Zhan ◽  
Roger A. Johns
Keyword(s):  
Nitric Oxide ◽  
Epithelial Cells ◽  
Kinase Inhibitor ◽  
Beat Frequency ◽  
Soluble Guanylyl Cyclase ◽  
Guanosine Monophosphate ◽  
Ciliary Motility ◽  
Tracheal Epithelial Cells ◽  
Cgmp Pathway ◽  
Tracheal Epithelial

Background Airway ciliary motility is impaired by inhaled anesthetics. Recent reports show that nitric oxide (NO) induces upregulation in ciliary beat frequency (CBF), and others report that propofol, an intravenous anesthetic, stimulates NO release; this raises the possibility that propofol increases CBF by stimulating the NO-cyclic guanosine monophosphate (cGMP) signal pathway. In this study, the authors investigated the effects of propofol on CBF and its relation with the NO-cGMP pathway using the pharmacologic blockers NG-monomethyl-l-arginine (l-NMMA), an NO synthase inhibitor; 1H-[1,2,4]oxidazole[4,3-a]quinoxalin-1-one (ODQ), a soluble guanylyl cyclase inhibitor; and KT5823, a cGMP-dependent protein kinase inhibitor, in cultured rat tracheal epithelial cells. Methods Rat tracheal tissues were explanted and cultured for 3-5 days. Images of ciliated cells were videotaped using a phase-contrast microscope. Baseline CBF and CBF 25 min after exposure to propofol or blocker were measured using video analysis. Results Vehicle (0.1% dimethyl sulfoxide; n = 11) increased CBF by 0.2 +/- 1.7% (mean +/- SD) from baseline. Propofol stimulated CBF significantly (P < 0.01) and dose dependently (1 microM, 2.0 +/- 1. 9%, n = 6; 10 microM, 8.2 +/- 6.7%, n = 9; 100 microM, 14.0 +/- 4.7%, n = 10). Intralipid (0.05%), the clinical vehicle of propofol, did not affect CBF (-0.2 +/- 2.2%; n = 5). The enhancement of CBF with use of 100 microm propofol was abolished (P < 0.01) by coadministration of 10 mmicroM l-NMMA (2.4 +/- 3.6%; n = 5), 100 microM ODQ (-0.3 +/- 2.2%; n = 6) or 30 microM KT5823 (-0.1 +/- 4. 1%; n = 8). l-NMMA, ODQ, or KT5823 alone did not change CBF. Conclusions These results show that propofol stimulates CBF viathe NO-cGMP pathway in rat tracheal epithelial cells, suggesting a possible advantage of propofol in decreasing respiratory risk.

Betadine has a ciliotoxic effect on ciliated human respiratory cells

2014 ◽  
Vol 129 (S1) ◽  
pp. S45-S50 ◽  
Author(s):  
J H Kim ◽  
J Rimmer ◽  
N Mrad ◽  
S Ahmadzada ◽  
R J Harvey
Keyword(s):  
Epithelial Cells ◽  
High Speed ◽  
Imaging System ◽  
Beat Frequency ◽  
Ciliary Beat Frequency ◽  
Positive Control ◽  
Clinical Dose ◽  
Significant Difference ◽  
Sinonasal Mucosa ◽  
Ciliary Beat

AbstractObjective:This study investigated the effect of Betadine on ciliated human respiratory epithelial cells.Methods:Epithelial cells from human sinonasal mucosa were cultured at the air–liquid interface. The cultures were tested with Hanks' balanced salt solution containing 10 mM HEPES (control), 100 µM ATP (positive control), 5 per cent Betadine or 10 per cent Betadine (clinical dose). Ciliary beat frequency was analysed using a high-speed camera on a computer imaging system.Results:Undiluted 10 per cent Betadine (n = 6) decreased the proportion of actively beating cilia over 1 minute (p < 0.01). Ciliary beat frequency decreased from 11.15 ± 4.64 Hz to no detectable activity. The result was similar with 5 per cent Betadine (n = 7), with no significant difference compared with the 10 per cent solution findings.Conclusion:Betadine, at either 5 and 10 per cent, was ciliotoxic. Caution should be applied to the use of topical Betadine solution on the respiratory mucosal surface.

Nature of the mammalian ciliary metachronal wave

1993 ◽  
Vol 75 (1) ◽  
pp. 458-467 ◽  
Author(s):  
L. B. Wong ◽  
I. F. Miller ◽  
D. B. Yeates
Keyword(s):  
Beat Frequency ◽  
Longitudinal Direction ◽  
Longitudinal Axis ◽  
Ciliary Beat Frequency ◽  
Metachronal Wave ◽  
Epithelial Tissues ◽  
Tracheal Epithelial ◽  
The Mean ◽  
Temporal And Spatial ◽  
Ciliary Beat

The temporal and spatial coordination of ciliary beat (metachronicity) is fundamental to effective mucociliary transport. Metachronal wave period (MWP) and ciliary beat frequency (CBF) of fresh excised sheep and canine tracheal epithelial tissues were measured with the use of a newly developed alternating focal spot laser light scattering system. MWP was determined from cross correlation of the heterodyne signals from the alternating focal spots. CBF was determined by autocorrelation of the heterodyne signals from each of the spots. MWP and CBF were measured in four sheep tracheal epithelial tissues with the use of longitudinal interfocal spot distances of 6 and 18 microns. In three canine tracheal epithelial tissues MWP and CBF were measured both longitudinally and circumferentially with interfocal spot distances of 5, 15, 65, 87, and 96 microns. For the sheep tracheal epithelial tissues the mean CBF was 5.9 +/- 0.4 Hz (mean of means; range 3.6 +/- 0.5 to 9.9 +/- 1.5 Hz), whereas the mean MWPs for 6- and 18-microns interfocal spot distances were 0.50 +/- 0.1 and 0.47 +/- 0.1 s, respectively. For the canine tracheal epithelial tissues the mean CBF was 4.0 +/- 0.2 Hz (2.0 +/- 0.8 to 7.2 +/- 3.2 Hz), whereas the mean longitudinal MWP was 1.5 s and the mean circumferential MWP was 2.1 s. Geometric combination of the MWP components leads to a derived MWP of 2.6 s with a propagation direction of 54 degrees with respect to the longitudinal axis of the trachea. MWP was found to be episode modulated with 12- to 20-min intervals in the longitudinal direction, but modulation was not as apparent in the circumferential direction. These data suggest that MWP and CBF are regulated by separate intracellular, intercellular, and intraciliary mechanisms.

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