Acetylcholine and substance P stimulate bronchial epithelial cells to release eosinophil chemotactic activity

1998 ◽  
Vol 84 (5) ◽  
pp. 1528-1534 ◽  
Author(s):  
Sekiya Koyama ◽  
Etsuro Sato ◽  
Hiroshi Nomura ◽  
Keishi Kubo ◽  
Sonoko Nagai ◽  
...  
Keyword(s):  
Substance P ◽  
Epithelial Cells ◽  
Receptor Antagonist ◽  
Platelet Activating Factor ◽  
Bronchial Epithelial Cells ◽  
Chemotactic Activity ◽  
Dependent Manner ◽  
Bronchial Epithelial ◽  
Lipoxygenase Inhibitors

We investigated a role of neuroregulation in the release of eosinophil chemotactic activity (ECA) from bovine bronchial epithelial cells (BBEC). BBEC were stimulated with acetylcholine (ACh) and substance P (SP), and the supernatant fluids were tested for ECA by a blind-well chemotactic chamber technique. BBEC released ECA in response to ACh and SP in a dose- and time-dependent manner. Checkerboard analysis showed that ECA in regard to ACh and SP was chemotactic rather than chemokinetic. Partial characterization revealed that ECA involved both lipids and peptides. The release of ECA in response to ACh and SP was inhibited by nonspecific and 5-specific lipoxygenase inhibitors and by cycloheximide ( P < 0.01). Molecular-sieve column chromatography revealed that these mediators induced three molecular mass peaks (near 25 kDa, 9 kDa, and 400 Da, respectively). The lowest peak, which represented the predominant activity, was blocked by leukotriene B4-receptor antagonist ( P < 0.01) but not by platelet-activating factor-receptor antagonist. The release of leukotriene B4 in the supernatant fluids was increased in response to ACh and SP stimulation ( P < 0.01). Platelet-activating factor was not detected. These results raise the possibility of a role of neuroregulation for the elaboration of ECA in the airway.

Bradykinin stimulates bronchial epithelial cells to release neutrophil and monocyte chemotactic activity

1995 ◽  
Vol 269 (1) ◽  
pp. L38-L44 ◽  
Author(s):  
S. Koyama ◽  
S. I. Rennard ◽  
R. A. Robbins
Keyword(s):  
Epithelial Cells ◽  
Receptor Antagonist ◽  
Platelet Activating Factor ◽  
Leukotriene B4 ◽  
Bronchial Epithelial Cells ◽  
Chemotactic Activity ◽  
Dependent Manner ◽  
Bronchial Epithelial ◽  
Lipoxygenase Inhibitors ◽  
Molecular Weight Peak

In the present investigation, we evaluated the potential of bradykinin (BK), histamine, and serotonin to induce the release of neutrophil and monocyte chemotactic activity (NCA and MCA) from bronchial epithelial cells (BEC). BK significantly stimulated BEC to release NCA and MCA in a dose- and time-dependent manner. Histamine weakly but significantly induced the release of both NCA and MCA in a similar fashion. Serotonin did not stimulate BEC. Checkerboard analysis showed that the NCA and MCA released in response to BK were chemotactic. Molecular-sieve column chromatography by Sephadex G-75 revealed that BK induced a single low-molecular-weight peak (approximately 400 Da) for both NCA and MCA. The releases of NCA and MCA in response to BK and histamine were inhibited by lipoxygenase inhibitors (P < 0.01). The released NCA was inhibited by leukotriene B4 (LTB4) receptor antagonist (P < 0.01) and was slightly inhibited by platelet-activating factor receptor antagonist. LTB4 was increased in BK-stimulated BEC supernatant (P < 0.01). BK B2-receptor antagonist attenuated the release of NCA and MCA. These data suggest that BK and histamine may stimulate BEC to release NCA and MCA and may modulate neutrophil and monocyte recruitment into the airways in patients with asthma.

Cigarette Smoke Stimulates Release of Neutrophil Chemotactic Activity from Cultured Bovine Bronchial Epithelial Cells

1995 ◽  
Vol 88 (3) ◽  
pp. 337-344 ◽  
Author(s):  
Shunsuke Shoji ◽  
Ronald F. Ertl ◽  
Sekiya Koyama ◽  
Richard Robbins ◽  
George Leikauf ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Cyclic Amp ◽  
Cigarette Smoke ◽  
Fetal Calf Serum ◽  
Calf Serum ◽  
Bronchial Epithelial Cells ◽  
Chemotactic Activity ◽  
Bronchial Epithelial ◽  
Lipoxygenase Inhibitors ◽  
Neutrophil Chemotactic Activity

1. Recruitment of neutrophils into the airway is a prominent feature of chronic bronchitis, a syndrome often associated with exposure to cigarette smoke. Since bronchial epithelial cells are the ‘first’ lung cells to come into contact with smoke, these cells may be responsible for neutrophil recruitment into the airway by release of neutrophil chemotactic activity in response to cigarette smoke. 2. To evaluate this hypothesis, we prepared bovine bronchial epithelial cells and measured their ability to release neutrophil chemotactic activity following exposure to cigarette smoke. Bronchial epithelial cells were prepared by overnight digestion with protease, filtered through 100-μm Nitex mesh and resuspended in Dulbecco's modified Eagle medium supplemented with 10% fetal calf serum and antibiotics and cultured at 2×106 cells in 2 ml of medium in 35-mm culture dishes. After 4 days, dishes were rinsed and refed with medium without fetal calf serum and incubated with and without 1:10 diluted smoke extract for 6 h at 37°C. The neutrophil chemotactic activity of the supernatant fluids was measured by the blindwell chamber technique. 3. Cigarette smoke itself added to medium did not stimulate chemotaxis. In contrast, cigarette smoke did stimulate the release of neutrophil chemotactic activity from bovine bronchial epithelial cells [15 ± 3 (control) versus 74 ± 5 (smoke), P < 0.01]. 4. This neutrophil chemotactic activity was dialysable, pepsin and acid stable, heat sensitive and lipid extractable. Sephadex G-75 column chromatography demonstrated two peaks of neutrophil chemotactic activity. 5. The lipoxygenase inhibitors diethylcarbamazine and nordihydroguaratic acid both diminished the release of chemotactic activity, suggesting that the activity may be a lipoxygenase product(s). 6. Dibutyryl cyclic AMP also blocked the smoke-stimulated release of neutrophil chemotactic activity, suggesting that its release may be regulated by intracellular cyclic AMP. 7. Thus, bovine bronchial epithelial cells release neutrophil chemotactic activity in response to cigarette smoke, suggesting that bronchial epithelial cells may be modulators of the airway inflammatory response caused by cigarette smoke.

Acetylcholine stimulates bronchial epithelial cells to release neutrophil and monocyte chemotactic activity

1992 ◽  
Vol 262 (4) ◽  
pp. L466-L471 ◽  
Author(s):  
S. Koyama ◽  
S. I. Rennard ◽  
R. A. Robbins
Keyword(s):  
Molecular Weight ◽  
Epithelial Cells ◽  
Receptor Antagonist ◽  
Muscarinic Receptor ◽  
Bronchial Asthma ◽  
Bronchial Epithelial Cells ◽  
Chemotactic Activity ◽  
Low Molecular Weight ◽  
Bronchial Epithelial ◽  
Ach Receptors

Bronchial asthma is accompanied by inflammatory cell infiltration in the airway. Increased bronchial reactivity to cholinergic stimulation is well recognized in patients with bronchial asthma. Thus, we postulated that acetylcholine (ACh) stimulates bronchial epithelial cells (BEC) to release neutrophil and monocyte chemotactic activity (NCA and MCA). To test this hypothesis, bovine BEC monolayers were tested for NCA and MCA by a blind-well chemotactic chamber technique. BEC released NCA and MCA in response to ACh in a dose-dependent and time-dependent manner. Molecular sieve column chromatography revealed that ACh induced a single low-molecular-weight peak (near 400) for NCA and two low-molecular-weight peaks (near 12,000 and 400) for MCA. The release of NCA and MCA was inhibited by the lipoxygenase inhibitors, nordihydroguaiaretic acid and diethylcarbamazine. Cigarette smoke is a well-recognized stimulus for airway inflammation. To determine whether smoke might activate BEC to release NCA by stimulating nicotinic ACh receptors, we further characterized the ACh receptors, using nicotine and nicotinic and muscarinic receptor antagonists. Nicotine, the nicotinic receptor antagonist d-tubocurarine, and the M2 receptor antagonist gallamine did not modulate the release of NCA in response to ACh. In contrast, atropine and the M1 receptor antagonist, pirenzepine, inhibited the release of NCA. These data demonstrate that ACh stimulates BEC to release lipoxygenase-derived NCA and MCA through the muscarinic receptor.

Viral Infection of Bovine Bronchial Epithelial Cells Induces Increased Neutrophil Chemotactic Activity and Neutrophil Adhesion

1993 ◽  
Vol 85 (6) ◽  
pp. 753-760 ◽  
Author(s):  
Meir Raz ◽  
Richard A. Robbins ◽  
Clayton L. Kelling ◽  
Lisa C. Stine ◽  
George D. Leikauf ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Viral Infection ◽  
Herpes Virus ◽  
Bronchial Epithelial Cells ◽  
Chemotactic Activity ◽  
Bronchial Epithelial ◽  
Lipoxygenase Inhibitors ◽  
Bovine Herpes Virus 1 ◽  
Herpès Virus ◽  
Neutrophil Chemotactic Activity

1. Acute bronchitis secondary to viral infection is associated with an influx of neutrophils. We hypothesized that bronchial epithelial cells are capable of releasing neutrophil chemotactic activity in response to viral infection. 2. To test this hypothesis, primary cultures of bovine bronchial epithelial cells were inoculated with a bovine respiratory pathogen, bovine herpes virus-1. 3. Supernatants collected from inoculated cells, before signs of toxicity, demonstrated significant neutrophil chemotactic activity using a blind well chamber neutrophil chemotaxis assay. Lipoxygenase inhibitors markedly reduced the amount of neutrophil chemotactic activity released after bovine herpes virus-1 inoculation. Analysis of arachidonic acid metabolites in cell supernatants by reverse-phase h.p.l.c. confirmed that leukotriene B4, a potent neutrophil chemoattractant, was released. 4. We also confirmed that adhesion of neutrophils to bovine herpes virus-1-inoculated bronchial epithelial cells was increased and mediated in part by the neutrophil integrin, LFA-1. 5. Thus, virally infected airway epithelial cells release leucocyte chemoattractants and hence adhesive interactions, functions that are likely to be important in the inflammatory acute response to viral infection.

scholarly journals TRPC6 contributes to LPS-induced inflammation through ERK1/2 and p38 pathways in bronchial epithelial cells

2018 ◽  
Vol 314 (3) ◽  
pp. C278-C288 ◽  
Author(s):  
Li-Fen Zhou ◽  
Qing-Zi Chen ◽  
Chun-Tao Yang ◽  
Zhao-Di Fu ◽  
Shen-Ting Zhao ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Receptor Potential ◽  
Bronchial Epithelial Cells ◽  
Trpc Channels ◽  
Dependent Manner ◽  
Toll Like Receptor ◽  
Phosphatidylinositol 3 Kinase ◽  
Toll Like Receptor 4 ◽  
Bronchial Epithelial

receptor potential canonical (TRPC) channels are presently an emerging target for airway disorders. Recent evidence has indicated that TRPC6 as a member of the TRPC family plays an important role in airway inflammation, but its precise function in bronchial epithelial cells remains unclear. The aim of this study was to investigate the role of TRPC6 in Toll-like receptor 4 (TLR4)-mediated inflammation in human bronchial epithelial cells stimulated by endotoxin [lipopolysaccharide (LPS)]. Hyp9 is a simplified phloroglucinol derivative of hyperforin that highly selectively activates TRPC6 channels. The results show that the activation of TRPC6 by Hyp9 induced the production of interleukin (IL)-8 and IL-6. LPS was also able to induce the release of IL-8 and IL-6, which was significantly aggravated by Hyp9 and reduced by knockdown of TRPC6. Treatment with LPS not only chronically induced the expression of TRPC6 mRNA and protein in a TLR4-dependent manner but also acutely increased Ca2+ influx through TRPC6 channels. In addition, LPS-induced overexpression of TRPC6 and Ca2+ influx were associated with the phosphorylation of phosphatidylinositol 3-kinase (PI3K) and Akt. Importantly, TRPC6 was required for the activation of ERK1/2, p38, and NF-κB. In conclusion, these data reveal that LPS induced the overexpression of TRPC6 and TRPC6-dependent Ca2+ influx via the TLR4/PI3K/Akt pathway resulting in Ca2+ mobilization, which subsequently promoted the activation of ERK1/2, p38, and NF-κB and the inflammatory response in bronchial epithelial cells.

Role of Bronchial Epithelial Cells in Pathogenesis of COPD

Pneumologie ◽  
2011 ◽  
Vol 65 (12) ◽  
Author(s):  
S Rim ◽  
S Jahan ◽  
G John ◽  
K Kohse ◽  
A Bohla ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Bronchial Epithelial Cells ◽  
Bronchial Epithelial

Flagellin induces innate immune genes in bronchial epithelial cells in vivo: Role of TET2

2021 ◽  
Author(s):  
Wanhai Qin ◽  
Xanthe Brands ◽  
Cornelis Veer ◽  
Alex F. Vos ◽  
Brendon P. Scicluna ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Bronchial Epithelial Cells ◽  
Innate Immune ◽  
Bronchial Epithelial ◽  
Immune Genes ◽  
Innate Immune Genes

Lung fibroblasts produce chemotactic factors for bronchial epithelial cells

1989 ◽  
Vol 257 (2) ◽  
pp. L71-L79 ◽  
Author(s):  
S. Shoji ◽  
K. A. Rickard ◽  
R. F. Ertl ◽  
J. Linder ◽  
S. I. Rennard
Keyword(s):  
Epithelial Cells ◽  
Tissue Repair ◽  
Bronchial Epithelial Cell ◽  
Bronchial Epithelial Cells ◽  
Chemotactic Activity ◽  
Lung Fibroblasts ◽  
Molecular Weight Range ◽  
Bronchial Epithelial ◽  
Chemotactic Factors ◽  
Two Peaks

The interaction between the epithelial cells and the subjacent mesenchymal cells in the airway is thought to play a major role during tissue repair and morphogenesis. To evaluate this interaction, we cultured human lung fibroblasts and bovine bronchial epithelial cells and determined that fibroblast-conditioned medium has chemotactic activity for bronchial epithelial cells. This activity was nondialyzable, heat labile, pepsin labile, acid stable, lipid inextractable, and eluted from Sephadex G-150 column chromatography in the high-molecular-weight range. DEAE-Sephacyl ion exchange and gelatin-Sepharose affinity chromatography revealed two peaks containing chemotactic activity, one of which may be fibronectin, since it binds to gelatin, reacts in a specific immunoassay, and is inhibited of chemotactic activity by anti-fibronectin antiserum, and another of which does not appear to be fibronectin, since it does not bind to gelatin nor react in the immunoassay. Thus lung fibroblasts can produce at least two chemotactic factors for bronchial epithelial cells that may play a role during lung tissue repair and morphogenesis by modulating bronchial epithelial cell migration.

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