Stimulation of Cl Secretion by Lactoferrin across Canine Airway Epithelial Cells in Culture

Respiration ◽  
1992 ◽  
Vol 59 (4) ◽  
pp. 189-192 ◽  
Author(s):  
A. Chiyotani ◽  
J. Tamaoki ◽  
F. Yamauchi ◽  
S. Takeuchi ◽  
T. Kanemura ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Cl Secretion ◽  
Cells In Culture ◽  
Stimulation Of

ICAM-1-independent adhesion of neutrophils to phorbol ester-stimulated human airway epithelial cells

1999 ◽  
Vol 277 (3) ◽  
pp. L465-L471 ◽  
Author(s):  
Alessandro Celi ◽  
Silvana Cianchetti ◽  
Stefano Petruzzelli ◽  
Stefano Carnevali ◽  
Filomena Baliva ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Airway Epithelial Cells ◽  
Bronchial Epithelial Cells ◽  
Neutrophil Adhesion ◽  
Late Time ◽  
Airway Epithelial ◽  
Bronchial Epithelial ◽  
Human Airway ◽  
Stimulation Of ◽  
Human Airway Epithelial Cells

Intercellular adhesion molecule-1 (ICAM-1) is the only inducible adhesion receptor for neutrophils identified in bronchial epithelial cells. We stimulated human airway epithelial cells with various agonists to evaluate whether ICAM-1-independent adhesion mechanisms could be elicited. Phorbol 12-myristate 13-acetate (PMA) stimulation of cells of the alveolar cell line A549 caused a rapid, significant increase in neutrophil adhesion from 11 ± 3 to 49 ± 7% (SE). A significant increase from 17 ± 4 to 39 ± 6% was also observed for neutrophil adhesion to PMA-stimulated human bronchial epithelial cells in primary culture. Although ICAM-1 expression was upregulated by PMA at late time points, it was not affected at 10 min when neutrophil adhesion was already clearly enhanced. Antibodies to ICAM-1 had no effect on neutrophil adhesion. In contrast, antibodies to the leukocyte integrin β-chain CD18 totally inhibited the adhesion of neutrophils to PMA-stimulated epithelial cells. These results demonstrate that PMA stimulation of human airway epithelial cells causes an increase in neutrophil adhesion that is not dependent on ICAM-1 upregulation.

Ambroxol Inhibits Na+ Absorption by Canine Airway Epithelial Cells in Culture

1991 ◽  
Vol 43 (12) ◽  
pp. 841-843 ◽  
Author(s):  
Jun Tamaoki ◽  
Atsushi Chiyotani ◽  
Fumiko Yamauchi ◽  
Satomi Takeuchi ◽  
Takao Takizawa
Keyword(s):  
Epithelial Cells ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Cells In Culture

Effects of vitamin A on proliferation of human distal airway epithelial cells in culture

1994 ◽  
Vol 424 (5) ◽  
Author(s):  
T. Shibagaki ◽  
T. Ogata ◽  
H. Kitamura ◽  
Y. Inayama ◽  
M. Kanisawa
Keyword(s):  
Epithelial Cells ◽  
Vitamin A ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Cells In Culture ◽  
Distal Airway

Basolateral K+ channels in airway epithelia. II. Role in Cl- secretion and evidence for two types of K+ channel

1990 ◽  
Vol 258 (6) ◽  
pp. L343-L348 ◽  
Author(s):  
J. D. McCann ◽  
M. J. Welsh
Keyword(s):  
Epithelial Cells ◽  
Time Course ◽  
Basolateral Membrane ◽  
Airway Epithelial Cells ◽  
K Channel ◽  
Airway Epithelial ◽  
K Channels ◽  
Cl Secretion ◽  
Transient Component ◽  
Permeable Supports

We previously described a Ca2(+)-activated K+ channel (KCLIC) in airway epithelial cells [J. D. McCann, J. Matsuda, M. Garcia, G. Kaczorowski, and M. J. Welsh. Am. J. Physiol 258 (Lung Cell. Mol. Physiol. 2): L334-L342, 1990]. To determine whether the KCLIC channel is a basolateral membrane channel and to understand its role in Cl- secretion, we studied airway epithelial cells grown on permeable supports. When cells were stimulated with A23187, charybdotoxin (ChTX) inhibited Cl- secretion and 86Rb efflux at the same concentrations, indicating that the KCLIC channel is required for Ca2(+)-stimulated Cl- secretion. We also investigated the function of K+ channels in adenosine 3',5'-cyclic monophosphate-stimulated secretion. Addition of isoproterenol caused a biphasic increase in Cl- secretion; the time course of the transient component correlated with the time course of the isoproterenol-induced increase in Ca2+ concentration [( Ca2+]c). ChTX inhibited the transient component, but not the prolonged component of secretion; Ba2+ inhibited the sustained component. These results suggest that when cells are grown on permeable supports isoproterenol-induced secretion depends on activation of two types of K+ channel: the KCLIC channel that is stimulated initially and a ChTX-insensitive K+ channel that is stimulated during sustained secretion. This conclusion was supported by measurement of 86Rb efflux from cell monolayers

scholarly journals Inducible expression of heat shock protein 20 protects airway epithelial cells against oxidative injury involving the Nrf2-NQO-1 pathway

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Aihua Bao ◽  
Aying Ma ◽  
Hui Zhang ◽  
Lihua Qiao ◽  
Suqin Ben ◽  
...  
Keyword(s):  
Heat Shock ◽  
Epithelial Cells ◽  
Heat Shock Protein ◽  
Airway Epithelial Cells ◽  
Inducible Expression ◽  
Ozone Exposure ◽  
Airway Epithelial ◽  
Transfected Cells ◽  
Empty Vector ◽  
Stimulation Of

Abstract Background Heat shock protein (HSP) 20 is a molecular chaperone that exerts multiple protective functions in various kinds of tissues. However, the expression of HSP20 and its specific functions in airway epithelial cells (AECs) remain elusive. Results In current study, we first confirmed the inducible expression of HSP20 in mouse AECs and in a human bronchial epithelial cell line BEAS-2B cells, under different oxidant stressors. Then by establishing a HSP20-abundant mouse model with repeated low-level-ozone exposures and stimulating this model with a single high-level ozone exposure, we found that the HSP20 abundance along with its enhanced phosphorylation potentially contributed to the alleviation of oxidative injuries, evidenced by the decreases in the bodyweight reduction, the BAL neutrophil accumulation, the AECs shedding, and the BAL concentrations of albumin and E-cadherin. The biological function of HSP20 and its molecular mechanisms were further investigated in BEAS-2B cells that were transfected with HSP20-, unphosphorylatable HSP20(Ala) or empty vector plasmids prior to the stimulation of H2O2, of which its oxidant capacity has been proved to be similar with those of ozone in an air–liquid culture system. We found that the H2O2-induced intracellular ROS level and the early cell apoptosis were attenuated in the HSP20- but not HSP20(Ala)- transfected cells. The intracellular expression of NQO-1 (mRNA and protein) and the intranuclear content of Nrf2 were significantly increased in the HSP20- transfected cells but not in the HSP20(Ala)- and empty vector-transfected cells after the stimulation of H2O2. Conclusions The inducible expression of HSP20 in AECs by oxidative stress exerts protective roles against oxidative damages, which may involve the activation of the Nrf2-NQO-1 pathway.

A role for Ca(2+)-conducting ion channels in mechanically-induced signal transduction of airway epithelial cells

1994 ◽  
Vol 107 (11) ◽  
pp. 3037-3044 ◽  
Author(s):  
S. Boitano ◽  
M.J. Sanderson ◽  
E.R. Dirksen
Keyword(s):  
Epithelial Cells ◽  
Mechanical Stimulation ◽  
Airway Epithelial Cells ◽  
Effective Concentration ◽  
Channel Blockers ◽  
Airway Epithelial ◽  
Free Medium ◽  
Half Maximal Effective Concentration ◽  
Induced Signal ◽  
Stimulation Of

Mechanical stimulation of a single cell in a cultured monolayer of airway epithelial cells initiates an intercellularly communicated increase in intracellular Ca2+ concentration ([Ca2+]i) that propagates radically through adjacent cells via gap junctions, forming an intercellular Ca2+ wave. Mechanically-induced intercellular Ca2+ waves also occur in the absence of extracellular Ca2+. However, in Ca(2+)-free medium an increase in [Ca2+]i of the stimulated cell does not occur. Thus, mechanically-induced [Ca2+]i changes in the stimulated cell are influenced by the extracellular Ca2+ concentration. To investigate if a channel-mediated Ca2+ flux across the plasma membrane contributes to the elevation of [Ca2+]i in the stimulated cell we used digital image microscopy to measure mechanically-induced [Ca2+]i changes in the presence of Ca2+ channel blockers. In Ca(2+)-free medium containing Gd3+ (20 microM) mechanical stimulation resulted in an [Ca2+]i increase in the stimulated cell. The delay time between mechanical stimulation and increase in [Ca2+]i of the stimulated cell was dependent on extracellular [Gd3+], with a half-maximal effective concentration of approximately 40 microM. Mechanical stimulation in Ca(2+)-free medium containing La3+ (10 microM) or Ni2+ (100 microM) gave similar results. Mechanical stimulation in Ca(2+)-free medium containing the dihydropyridine Ca2+ channel blockers nifedipine (10 microM) and nimodipine (10 microM) also resulted in an increase of [Ca2+]i of the stimulated cell. Mechanical stimulation of cells treated with thapsigargin to deplete intracellular Ca2+ stores, in the presence of 1.3 mM extracellular Ca2+, results in an increase in [Ca2+]i of the stimulated cell without the propagation of an intercellular Ca2+ wave.(ABSTRACT TRUNCATED AT 250 WORDS)

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