Mucus glycoconjugate secretion in cool and hypertonic solutions

1997 ◽  
Vol 272 (6) ◽  
pp. L1121-L1125 ◽  
Author(s):  
T. M. Dwyer ◽  
J. M. Farley
Keyword(s):  
Average Rate ◽  
Transient Increase ◽  
Productive Cough ◽  
Submucosal Gland ◽  
Basal Secretion ◽  
Cold Air ◽  
Dry Air ◽  
Gland Cells ◽  
Hypertonic Solutions ◽  
Exercise Induced

For sensitive individuals, exercise-induced asthma is triggered by cold and dry air and is often accompanied by a productive cough. In this study, we determined whether cold solutions and/or solutions of increased tonicity directly caused an increase in glycoconjugate (GC) secretion. To test this, we used isolated swine tracheal submucosal gland cells (TSGCs) and measured the rate of GC secretion at 37 and 32 degrees C in isotonic solutions and in solutions made hypertonic by 30 mosM. TSGCs were isolated under conditions that minimized the rate of GC secretion and were perfused with medium 199 equilibrated with 5% CO2 to a pH of 7.4. A lectin-based assay was used to specifically detect GC present in each 2-min fraction of the perfusate. Basal secretion was 3.1-fold greater at 32 degrees C (n = 3) than at 37 degrees C (n = 4; P < 0.05). At 37 degrees C, increasing perfusate osmolarity by 30 mosM increased the average rate of secretion by 41 +/- 11% (n = 4; P < 0.05); return to isotonic perfusate caused a 4.5 +/- 1.8-fold transient increase in secretion (n = 4; P < 0.05) that was complete within 10 min. At 32 degrees C, changing tonicity of the perfusate had no significant effect but returning to isotonic perfusate caused a 2.3 +/- 0.7-fold transient increase in secretion (n = 3; P < 0.05). Thus key stimuli that trigger obstruction of airflow (cold and increased osmolarity) can also directly stimulate GC secretion in the airway. Such increased secretions may contribute to the productive cough observed in some individuals in response to cold air.

A technique for the isolation of submucosal gland cells from cat trachea

1983 ◽  
Vol 55 (3) ◽  
pp. 1035-1041 ◽  
Author(s):  
D. J. Culp ◽  
D. P. Penney ◽  
M. G. Marin
Keyword(s):  
Trypan Blue ◽  
Mechanical Treatment ◽  
Average Rate ◽  
Periodic Acid ◽  
Surface Epithelium ◽  
Submucosal Gland ◽  
Isolated Cells ◽  
Periodic Acid Schiff ◽  
Gland Cells ◽  
Glandular Cells

We have developed a procedure to isolate submucosal gland cells from cat trachea. The excised trachea was stripped of surface epithelium by stroking the luminal surface with a nylon brush. The remaining submucosa was scraped free from underlying cartilage and minced into small fragments. To disperse glandular cells from these fragments, we subjected the minced tissue to both enzymatic (collagenase and elastase) and mechanical treatment. In 23 preparations of cells we yielded an average (+/- SE) of 8.4 +/- 0.9 (X 10(6] cells. In eight cell preparations 95 +/- 1% of the cells stained with periodic acid-Schiff stain, suggesting that the cells are of glandular origin. We used the following criteria to assess cell viability. The dye trypan blue was excluded by 92 +/- 1% of the cells (n = 23). Under the electron microscope, cellular membranes and organelles appeared normal. The isolated cells consumed oxygen at an average rate of 1.34 +/- 0.05 microliters O2 X h -1 X (10(6) cell) -1, (n = 65). Oxygen consumption was constant for at least 4 h after cell isolation, was inhibited 21% by 10(-4) M ouabain, and was subsequently stimulated to 135% above basal levels by 4 X 10(-5) M dinitrophenol.

scholarly journals Exercise Increases Insulin Content and Basal Secretion in Pancreatic Islets in Type 1 Diabetic Mice

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Han-Hung Huang ◽  
Kevin Farmer ◽  
Jill Windscheffel ◽  
Katie Yost ◽  
Mary Power ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Glycemic Control ◽  
Wheel Running ◽  
Insulin Content ◽  
Control Groups ◽  
Basal Secretion ◽  
Exercise Induced ◽  
Old Mice ◽  
Cell Proportion

Exercise appears to improve glycemic control for people with type 1 diabetes (T1D). However, the mechanism responsible for this improvement is unknown. We hypothesized that exercise has a direct effect on the insulin-producing islets. Eight-week-old mice were divided into four groups: sedentary diabetic, exercised diabetic, sedentary control, and exercised control. The exercised groups participated in voluntary wheel running for 6 weeks. When compared to the control groups, the islet density, islet diameter, andβ-cell proportion per islet were significantly lower in both sedentary and exercised diabetic groups and these alterations were not improved with exercise. The total insulin content and insulin secretion were significantly lower in sedentary diabetics compared to controls. Exercise significantly improved insulin content and insulin secretion in islets in basal conditions. Thus, some improvements in exercise-induced glycemic control in T1D mice may be due to enhancement of insulin content and secretion in islets.

Isolation and Culture of Submucosal Gland Cells

1986 ◽  
Vol 7 (2) ◽  
pp. 239-245
Author(s):  
Matthew G. Marin ◽  
David J. Culp
Keyword(s):  
Submucosal Gland ◽  
Gland Cells

Multiple calcium mobilization pathways in single avian salt gland cells

1990 ◽  
Vol 258 (2) ◽  
pp. C289-C298 ◽  
Author(s):  
E. L. Stuenkel ◽  
S. A. Ernst
Keyword(s):  
Salt Gland ◽  
Transient Increase ◽  
Secretory Cells ◽  
Free Medium ◽  
Subsequent Removal ◽  
Intracellular Pool ◽  
Gland Cells ◽  
Agonist Stimulation ◽  
Induced Changes ◽  
Sustained Increase

Agonist-induced changes in intracellular Ca2+ concentration ([Ca2+]i) in individual secretory cells from the avian salt gland were detailed using dual-wavelength microspectrofluorimetry of the Ca2(+)-sensitive fluorescent probe fura-2. Resting [Ca2+]i averaged 42 +/- 5 nM. Stimulation with the cholinergic agonist carbachol (1 microM) resulted in a rapid increase in [Ca2+]i to 308 +/- 26 nM, which was sustained at a nearly constant elevated level (328 +/- 31 nM) throughout agonist application. In the absence of extracellular Ca2+ or in the presence of an inorganic blocker of Ca2+ entry (Ni2+, 1 mM), only a transient increase in [Ca2+]i occurred on agonist stimulation, whereas subsequent readmission of Ca2+ or washout of Ni2+ reinitiated a sustained increase in [Ca2+]i. The initial transient response results from Ca2+ release from intracellular stores, whereas the sustained phase represents entry of extracellular Ca2+ into the cytoplasm. Repetitive stimulations in Ca2(+)-free medium alternating with Ca2(+)-containing medium were performed to examine the mechanisms involved in refilling of the agonist-sensitive intracellular pool. After depletion of the intracellular pool by stimulation in Ca2(+)-free medium, removal of the agonist and readmission of Ca2+ resulted in a rapid transient increase in [Ca2+]i that could be blocked by Ni2+, La3+, or elevated K+. Subsequent removal of extracellular Ca2+ and restimulation nonetheless showed that complete refilling of the intracellular pool had occurred in each case. These results suggest that two separate Ca2(+)-entry mechanisms, one sensitive to Ni2+, La3+, and elevated K+ and responsible for the agonist-induced increase in [Ca2+]i and one insensitive to the blockers and involved in refilling of the intracellular pool, may exist in salt gland cells. Spontaneous oscillations of [Ca2+]i that are independent of extracellular Ca2+ have also been observed in 10% of the cells. The abolition of the oscillations by depletion of the agonist-sensitive pool suggests this pool as the Ca2+ source for the oscillations.

Reduced hyperpnea-induced bronchospasm following repeated cold air challenge

1986 ◽  
Vol 61 (1) ◽  
pp. 210-214 ◽  
Author(s):  
F. Haas ◽  
N. Levin ◽  
S. Pasierski ◽  
M. Bishop ◽  
K. Axen
Keyword(s):  
Base Line ◽  
Maximum Heart Rate ◽  
Cold Air ◽  
Asthma Symptoms ◽  
Rest Periods ◽  
Before And After ◽  
Exercise Induced ◽  
Inflammatory Changes ◽  
Training Protocol

This study assessed reduction in expiratory function in 12 asthmatic subjects both after 5 min of cold air provocation (CAP) with dry air conditioned to approximately 0 degrees C and after exercise (to 85% of predicted maximum heart rate) while breathing ambient room air (approximately 21 degrees C and 40% relative humidity). These assessments were done both before and after the following training protocol. Three 5-min periods of isocapnic cold air hyperpnea separated by 5-min rest periods were performed breathing 0 degrees to -10 degrees C air, for 36 sessions over 12 wk. As expected, pretraining expiratory function was significantly reduced (P less than 0.001) after both CAP and exercise. The posttraining reduction in expiratory function after CAP and exercise, however, was significantly less pronounced (largest P less than 0.05). These data support our hypothesis that repeated bouts of cold air challenge result in airway acclimatization to cold air and consequent decrease in exercise-induced bronchospasm. Acclimatization may result directly either by habituation of the airways or by vasodilation leading to increased bronchial blood flow and consequent reduced airway cooling. An unanticipated finding, though, is that repeated cold air challenge may also cause long-term inflammatory changes in the airways. A significant percentage of subjects experienced reduced base-line pulmonary function and overall exacerbation of asthma symptoms during the training period.

Effects of atropine on potentiation of exercise-induced bronchospasm by cold air

1978 ◽  
Vol 45 (2) ◽  
pp. 238-243 ◽  
Author(s):  
E. C. Deal ◽  
E. R. McFadden ◽  
R. H. Ingram ◽  
J. J. Jaeger
Keyword(s):  
Ambient Air ◽  
Small Airways ◽  
Flow Limitation ◽  
Ambient Conditions ◽  
Cold Air ◽  
Relative Contribution ◽  
Maximal Expiratory Flow ◽  
Before And After ◽  
Expiratory Flow ◽  
Exercise Induced

The role of vagal efferent activity in the cold air potentiation of exercise-induced asthma was assessed by exercising nine subjects who breathed air at ambient and subfreezing temperatures before and after cholinergic blockade. Lung volumes and maximal expiratory flow volume curves with air and with 80% helium-20% oxygen were obtained before and 5--10 min after each challenge. Isovolume comparisons of maximal expiratory flow rates with the two gases were used to assess relative contributions of large and small airways to flow limitation. Exercise under ambient conditions resulted in the expected airway obstruction and cold air exaggerated the response. Atropine pretreatment had no effect on the cold air potentiation. After atropine with ambient air exercise, there was an increase in the relative contribution of large airways to flow limitation, whereas exercise with cold air resulted in an increase in the contribution of small airways. We concluded that the potentiating effects of cold air are local and suggest that the immediate stimulus is related to cooling of intrathoracic airways.

Vitronectin Is Expressed By Submucosal Gland Cells In The Human Airways

2011 ◽  
Author(s):  
Ana M. Herrera ◽  
Maria A. Escobar ◽  
Lina M. Salazar ◽  
Mario A. Correa
Keyword(s):  
Submucosal Gland ◽  
Gland Cells ◽  
Human Airways

Muscarinic stimulation of submucosal glands in swine trachea

1988 ◽  
Vol 64 (1) ◽  
pp. 200-209 ◽  
Author(s):  
C. M. Yang ◽  
J. M. Farley ◽  
T. M. Dwyer
Keyword(s):  
Acetylcholine Receptors ◽  
Relative Proportion ◽  
Muscarinic Acetylcholine Receptors ◽  
Mucus Secretion ◽  
Submucosal Gland ◽  
Isolated Cells ◽  
Gland Cells ◽  
Submucosal Glands ◽  
Tracheal Explants

The properties of muscarinic acetylcholine receptors (mAChR) on tracheal explants and isolated submucosal gland cells were determined using [3H]quinuclidinyl benzilate ([3H]QNB) and N-[3H]methylscopolamine ([3H]NMS) as ligands. Analysis of competitive displacement of ([3H]NMS binding by pirenzepine demonstrated the presence of M1- (27 +/- 2%) and M2G- (73 +/- 2%) receptors on isolated tracheal submucosal gland cells (TSGC's) in control. Daily administration of diisopropylfluorophosphate (DFP) inhibited cholinesterase activity by greater than 95%. After 7 days of DFP treatment, [3H]QNB binding to intact TSGC's decreased from 14.2 +/- 0.6 to 6.3 +/- 0.8 fmol/10(6) cells; similarly, [3H]NMS binding fell from 8.1 +/- 1.9 to 2.0 +/- 0.8 fmol/10(6) cells. The loss of mAChR's was predominantly of the M2G subtype with the relative proportion dropping to 33%. In addition, 90% of the receptors assumed the high-affinity state for carbachol displacement of [3H]NMS. Mucus secretion was quantitated by measuring the release of 3H-labeled mucus macromolecules from explants of tracheal submucosal glands and isolated cells. Acetylcholine (ACh), 2 X 10(-5) M, stimulated mucus secretion by 2.5 and 2.3 times the basal rate, respectively. Elimination of acetylcholinesterase (AChe) by DFP increased the ACh sensitivity by 18- and 5-fold. Tracheal explants or TSGC's obtained 2 h after an in vivo DFP treatment showed a 6- and 3-fold ACh stimulation. This ACh sensitivity decreased during the continued daily dosing with DFP such that only a 1.3- and 1.1-fold ACh stimulation was apparent after 7 days of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

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