Regulation of Na+and Cl−Transport and Mucous Gland Secretion in Airway Epithelium

2008 ◽  
pp. 133-153 ◽  
Author(s):  
Jay. A. Nadel ◽  
Brian Davis
Keyword(s):  
Airway Epithelium ◽  
Gland Secretion ◽  
Mucous Gland ◽  
Cl Transport

Alpha-adrenergic regulation of Na-Cl cotransport in human airway epithelium

1989 ◽  
Vol 257 (2) ◽  
pp. L125-L129 ◽  
Author(s):  
C. M. Liedtke
Keyword(s):  
Epithelial Cells ◽  
Airway Epithelium ◽  
Initial Rate ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Adrenergic Agonist ◽  
Beta Adrenergic ◽  
Human Airway ◽  
Cl Transport ◽  
Human Airway Epithelium

The demonstration of abnormal beta-adrenergic and cAMP-modulated apical Cl- channels in cystic fibrosis (CF) airway epithelial cells suggests that other transporters, which are required for Cl- secretion, may also be abnormally regulated. A basolateral cotransporter was investigated by determining the initial rate of 36Cl efflux from cells isolated from CF nasal polyps or trachea and non-CF trachea. Cells were preequilibrated with radioactive tracer at 25 degrees C, and tracer transport was initiated by 10-fold dilution of an aliquot of cells in radioisotope-free medium. The initial rate of Cl transport was calculated from the linear portion of the efflux curves. In CF and non-CF cells, base-line Cl- transport was not blocked by furosemide but was stimulated twofold by l-epinephrine in Ca2+-deficient and Ca2+-replete transport medium. In both types of cells, furosemide blocked 70 and 77%, respectively, of the stimulated Cl- transport. Prazosin, an alpha 1-adrenergic antagonist, blocked the effects of l-epinephrine and methoxamine, an alpha 1-adrenergic agonist, stimulated prazosin- and furosemide-sensitive Cl transport. Ionomycin mimicked the effects of l-epinephrine. l-Isoproterenol, a beta-adrenergic agonist, did not affect Cl transport. The results of this study indicate an alpha 1-adrenergic stimulation of furosemide-sensitive Cl transport in human airway epithelium that functions normally in CF airway epithelial cells. The transport mechanism is probably a Na-Cl or Na-K-2Cl cotransport located in the basolateral membrane and requires elevated intracellular Ca2+ for activation.

scholarly journals Synergistic mucus secretion by histamine and IL-4 through TMEM16A in airway epithelium

2017 ◽  
Vol 313 (3) ◽  
pp. L466-L476 ◽  
Author(s):  
Ju Wan Kang ◽  
Yong Hyuk Lee ◽  
Min Jeong Kang ◽  
Hyun Jae Lee ◽  
Ryung Oh ◽  
...  
Keyword(s):  
Allergic Rhinitis ◽  
Epithelial Cells ◽  
Airway Epithelium ◽  
Short Circuit ◽  
Fluid Secretion ◽  
Mucus Secretion ◽  
Gland Secretion ◽  
Allergic Symptom ◽  
Control Group ◽  
Human Nasal Epithelial Cells

Histamine is an important mediator of allergic reactions, and mucus hypersecretion is a major allergic symptom. However, the direct effect of histamine on mucus secretion from airway mucosal epithelia has not been clearly demonstrated. TMEM16A is a Ca2+-activated chloride channel, and it is closely related to fluid secretion in airway mucosal epithelia. We investigated whether histamine directly induces fluid secretion from epithelial cells or submucosal glands (SMG) and mechanisms related, therewith, in allergic airway diseases. In pig airway tissues from the nose or trachea, histamine was a potent secretagogue that directly induced strong responses. However, gland secretion from human nasal tissue was not induced by histamine, even in allergic rhinitis patients. Histamine type 1 receptor (H1R) and histamine type 2 receptor (H2R) were not noted in SMG by in situ hybridization. Cultured primary human nasal epithelial (NHE) cells were used for the measurement of short-circuit current changes with the Ussing chamber. Histamine-induced slight responses of anion secretions under normal conditions. The response was enhanced by IL-4 stimulation through TMEM16A, which might be related to fluid hypersecretion in allergic rhinitis. Pretreatment with IL-4 augmented the histamine response that was suppressed by a TMEM16A inhibitor. TMEM16A expression was enhanced by 24-h treatment of IL-4 in human nasal epithelial cells. The expression of TMEM16A was significantly elevated in an allergic rhinitis group, compared with a control group. We elucidated histamine-induced fluid secretions in synergy with IL-4 through TMEM16A in the human airway epithelium. In addition, we observed species differences between pigs and humans in terms of gland secretion of histamine.

New Ultrastructural Observations on Injury and Regeneration of Cilia in Mammalian Conducting Airway Epithelium

1981 ◽  
Vol 39 ◽  
pp. 624-625
Author(s):  
J.L. Carson ◽  
A.M. Collier
Keyword(s):  
Respiratory Tract ◽  
Airway Epithelium ◽  
Defense Mechanisms ◽  
Normal Growth ◽  
Fetal Lung ◽  
Secretory Cells ◽  
Airway Epithelial ◽  
Ciliated Cells ◽  
Conducting Airway ◽  
Conducting Airways

The ciliated cells lining the conducting airways of mammals are integral to the defense mechanisms of the respiratory tract, functioning in coordination with secretory cells in the removal of inhaled and cellular debris. The effects of various infectious and toxic agents on the structure and function of airway epithelial cell cilia have been studied in our laboratory, both of which have been shown to affect ciliary ultrastructure.These observations have led to questions about ciliary regeneration as well as the possible induction of ciliogenesis in response to cellular injury. Classical models of ciliogenesis in the conducting airway epithelium of the mammalian respiratory tract have been based primarily on observations of the developing fetal lung. These observations provide a plausible explanation for the embryological generation of ciliary beds lining the conducting airways but do little to account for subsequent differentiation of ciliated cells and ciliogenesis during normal growth and development.

Cigarette smoke exposure induces substantial changes in the airway epithelium of a Drosophila COPD model

Pneumologie ◽  
2016 ◽  
Vol 70 (07) ◽  
Author(s):  
M Thiedmann ◽  
R Prange ◽  
A Bhandari ◽  
K Kallsen ◽  
C Fink ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Airway Epithelium ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure
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