Role of Neutrophil Elastase in Endotoxin-Induced Mucus Hypersecretion in Rat Nasal Epithelium

Shimizu, Takeshi; Takahashi, Yukimitsu; Majima, Yuichi; Takeuchi, Kazuhiko; Sakakura, Yasuo

doi:10.1177/000348940010901111

Cited by 13 publications

(6 citation statements)

References 23 publications

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“…Previous in vivo and in vitro studies have shown that LPS stimulates mucin secretion and upregulates the mucin gene. [36][37][38] Consistently, our data revealed that LPS induces excessive synthesis and secretion of mucin by LS174T cells. Besides, ICA and pICA also restore mucin synthesis and secretion to normal levels.…”

Section: Discussionsupporting

confidence: 85%

The protective effect of icariin and phosphorylated icariin against LPS-induced intestinal goblet cell dysfunction

Xiong

Zhu

et al. 2019

Innate Immun

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In this study, we used LS174T cells as a model to investigate the protective effects of icariin and phosphorylated icariin on LPS-induced goblet cell dysfunction. Our results indicated that icariin and phosphorylated icariin increased the cell viability and decreased lactate dehydrogenase activity in LPS-treated LS174T cells. Icariin and phosphorylated icariin attenuated LPS-induced changes in mucin 2 synthesis and secretion. Besides, Icariin and phosphorylated icariin reduced the levels of ROS, MDA, and H2O2 and increased the activity of SOD, GPx, CAT, and T-AOC in LPS-treated LS174T cells. Moreover, the levels of IL-1β, IL-6, IL-8, and TNF-α were reduced in the Icariin and phosphorylated icariin group. Furthermore, Icariin and phosphorylated icariin decreased gene abundance or enzyme activity of Bip, XBP1, GRP78, CHOP, caspase-3, and caspase-4 in LPS-treated LS174T cells. Our data suggest that Icariin and phosphorylated icariin effectively attenuate LPS-induced intestinal goblet cell function damage through regulating oxidative stress, inflammation, apoptosis, and mucin expression.

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Section: Discussionsupporting

confidence: 85%

The protective effect of icariin and phosphorylated icariin against LPS-induced intestinal goblet cell dysfunction

Xiong

Zhu

et al. 2019

Innate Immun

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“…Neutrophil elastase inhibitor ONO 5046 partially inhibited LPSinduced change, and elastase-induced mucus production was not inhibited by neutrophil depletion (28). These results indicate that neutrophil, especially neutrophil elastase, is an important mediator of LPS-induced mucus production and that the in vivo effects of 14-member macrolides may be partly caused indirectly through the suppression of neutrophil infiltration.…”

Section: Discussionmentioning

confidence: 77%

In VivoandIn VitroEffects of Macrolide Antibiotics on Mucus Secretion in Airway Epithelial Cells

Shimizu

Hattori

et al. 2003

Am J Respir Crit Care Med

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146

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To examine the in vivo effects of macrolide antibiotics on mucus hypersecretion, we induced hypertrophic and metaplastic changes of goblet cells in rat nasal epithelium by intranasal instillation of ovalbumin (OVA) in OVA-sensitized rats and by intranasal LPS instillation. Oral administration of clarithromycin (CAM) (5-10 mg/kg) significantly inhibited OVA- and LPS-induced mucus production and neutrophil infiltration, whereas josamycin and ampicillin showed no effect. In vitro effects of macrolide antibiotics on airway epithelial cells were examined using NCI-H292 cells and human nasal epithelial cells cultured in air-liquid interface. Mucus secretion was evaluated by ELISA using anti-mucin monoclonal antibodies (anti-MUC5AC and HCS18). CAM and erythromycin significantly inhibited spontaneous and tumor necrosis factor-alpha (20 ng/ml)-induced mucus secretion from NCI-H292 cells at 10-6 to 10-7 M and from human nasal epithelial cells at 10-4 to 10-5 M. MUC5AC messenger RNA expression was also significantly inhibited. These results indicate that the 14-member macrolide antibiotics, CAM and erythromycin, exert direct inhibitory effects on mucus secretion from airway epithelial cells and that they may be useful for the treatment of mucus hypersecretion caused by allergic inflammation and LPS stimulation.

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“…This degranulation can be explained by the release of elastase from the azurophilic granules of heterophils in the regions where goblet cells are degranulating. Elastase is a powerful secretagogue on the glands and goblet cells of the airways [43]. …”

Section: Discussionmentioning

confidence: 99%

Ultrastructural Comparison of the Nasal Epithelia of Healthy and Naturally Affected Rabbits withPasteurella multocidaA

Esquinas

Botero

Patiño

et al. 2013

Veterinary Medicine International

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An ultrastructural comparison between the nasal cavities of healthy rabbits and those suffering from two forms of spontaneous infection with Pasteurella multocida was undertaken. Twelve commercially produced rabbits of different ages and respiratory health status were divided into four groups: healthy from 0 to 21 days (G1, n = 2); healthy from 23 to 49 days (G2, n = 2); healthy from 51 to 69 days (G3, n = 2); diseased rabbits with septicemia and the rhinitic form of P. multocida infection (G4, n = 3). The main ultrastructural changes observed were a widening of the interepithelial spaces, increased activity and number of goblet cells, the formation of two types of vacuoles in epithelial cells, the degranulation and migration of heterophils between the epithelial cells, and the association of this migration with some of the other changes. No bacteria were observed adhering to the epithelium, and very few were observed free in the mucus. Scant inter-epithelial spaces were found in healthy rabbits, but they were not as large and numerous as those found in diseased animals. We discuss the origin and meaning of these changes but, we focus on the significance of the inter-epithelial spaces and goblet cells for the defense of the upper respiratory airways against the bacterium and its lipopolysaccharide.

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Role of Neutrophil Elastase in Endotoxin-Induced Mucus Hypersecretion in Rat Nasal Epithelium

Cited by 13 publications

References 23 publications

The protective effect of icariin and phosphorylated icariin against LPS-induced intestinal goblet cell dysfunction

The protective effect of icariin and phosphorylated icariin against LPS-induced intestinal goblet cell dysfunction

In VivoandIn VitroEffects of Macrolide Antibiotics on Mucus Secretion in Airway Epithelial Cells

Ultrastructural Comparison of the Nasal Epithelia of Healthy and Naturally Affected Rabbits withPasteurella multocidaA

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