scholarly journals Cigarette smoke (cs) or degeneration of pulmonary C‐fibers (PCFs) in mice changes alveolar macrophages’ (AM's) NK1Rs and MMP‐12 responses to substance P (SP) in vitro

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Junyang Xu ◽  
Fadi Xu
Keyword(s):  
Substance P ◽  
Cigarette Smoke ◽  
Alveolar Macrophages ◽  
C Fibers

scholarly journals Metalloelastase in lungs and alveolar macrophages is modulated by extracellular substance P in mice

2008 ◽  
Vol 295 (1) ◽  
pp. L162-L170 ◽  
Author(s):  
J. Xu ◽  
F. Xu ◽  
E. Barrett
Keyword(s):  
Animal Models ◽  
Substance P ◽  
Bronchoalveolar Lavage ◽  
Cigarette Smoke ◽  
Alveolar Macrophages ◽  
Control Medium ◽  
Neurokinin 1 Receptor ◽  
Protein Levels ◽  
C Fibers ◽  
Neurokinin 1

Metalloelastase (MMP-12), mainly produced by macrophages, has been shown to play a key role in the pathogenesis of emphysema in animal models. Chronic cigarette smoke increases pulmonary MMP-12, which is closely correlated with an elevation of pulmonary substance P (SP). Because alveolar macrophages (AMs) contain the neurokinin-1 receptor (NK1R), we tested whether SP was able to trigger the upregulation of MMP-12 synthesis in AMs by acting on the NK1R. AMs isolated from bronchoalveolar lavage cells in C3H/HeN mice were cultured with control medium or SP that was coupled without or with NK1R antagonists (CP-99,994 or aprepitant) for 24 h. We found that SP significantly increased the mRNA of MMP-12 and NK1R by 11-fold and 82%, respectively, in AMs ( P < 0.05), and these responses were abolished by NK1R antagonists with little change in the cells' viability. Because pulmonary SP is primarily released by bronchopulmonary C-fibers (PCFs), we further asked whether destruction of PCFs would reduce SP and MMP-12. Two groups of mice were pretreated with vehicle and neonatal capsaicin (NCAP) to degenerate PCFs, respectively. Our results show that NCAP treatment significantly decreased mRNA and protein levels of SP associated with a reduction NK1R and MMP-12 in the lungs and AMs. These findings suggest that SP has a modulatory effect on pulmonary MMP-12 by acting on NK1R to trigger MMP-12 syntheses in the AMs.

Role of C fibers in the inflammatory response to intratracheal lipopolysaccharide

1996 ◽  
Vol 271 (3) ◽  
pp. L425-L431 ◽  
Author(s):  
N. C. Long ◽  
C. W. Frevert ◽  
S. A. Shore
Keyword(s):  
Inflammatory Response ◽  
Alveolar Macrophages ◽  
Tumor Necrosis ◽  
Pulmonary Inflammation ◽  
Intratracheal Instillation ◽  
C Fibers ◽  
Vehicle Treatment ◽  
Necrosis Factor

We proposed that C fibers play a role in mediating the inflammatory response to the intratracheal instillation of lipopolysaccharaide (LPS), a purified form of endotoxin. To test this hypothesis, we compared the inflammatory response to intratracheal LPS (0.1-2.5 mg/kg) in rats whose C fibers had been destroyed by neonatal capsaicin treatment to the response seen in animals that were treated with vehicle. Three hours after the instillation of LPS, we assessed pulmonary inflammation by performing bronchoalveolar lavage (BAL) on the animals. We measured the number of neutrophils, the concentration of protein as an index of vascular permeability, and the concentration of tumor necrosis factor (TNF). Our results indicate that capsaicin treatment resulted in more neutrophils and higher levels of protein and TNF in the BAL fluid in response to intratracheal LPS, compared with vehicle treatment. Using cells from both groups of rats, we also assessed the production of inflammatory mediators by alveolar macrophages incubated with LPS (0.3-30 ng/ml) in vitro. We found a modest increase in the concentration of TNF and nitrite in the supernatant of macrophages collected from capsaicin-treated rats, in comparison with vehicle-treated animals. These results are consistent with the hypothesis that intrinsic differences in the sensitivity of alveolar macrophages of capsaicin and vehicle-treated animals contribute to the greater inflammatory response of capsaicin-treated rat to intratracheal LPS.

Acute cigarette smoke exposure induces apoptosis of alveolar macrophages

2001 ◽  
Vol 281 (6) ◽  
pp. L1392-L1401 ◽  
Author(s):  
Kazutetsu Aoshiba ◽  
Jun Tamaoki ◽  
Atsushi Nagai
Keyword(s):  
Cigarette Smoke ◽  
Alveolar Macrophages ◽  
Critical Role ◽  
Light And Electron Microscopy ◽  
In Vivo Studies ◽  
Cigarette Smoke Exposure ◽  
Protein Accumulation ◽  
Cytochrome C Release ◽  
Bax Protein

Alveolar macrophages (AMs) may play a critical role in cigarette smoke (CS)-related pulmonary diseases. This study was designed to determine whether CS induces apoptosis of AMs. In in vitro studies, mouse, rat, and human AMs and human blood monocyte-derived macrophages cultured with aqueous whole CS extracts underwent apoptosis that was detected by light and electron microscopy and terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling. The gas phase of CSE did not cause apoptosis. The CS-induced apoptosis was associated with increased oxidative stress, Bax protein accumulation, mitochondrial dysfunction, and mitochondrial cytochrome c release but was independent of p53, Fas, and caspase activation. This apoptosis was inhibited by antioxidants such as glutathione, ascorbic acid, and α-tocopherol. In in vivo studies where rats were exposed to the smoke from 10 cigarettes over 5 h in an exposure chamber, ∼3% of AMs obtained by bronchoalveolar lavage after 24 h showed apoptosis. These results suggest that acute CS exposure is capable of inducing apoptosis of AMs.

The influence of cigarette smoke on colour stability and friction property of aesthetic orthodontic wires—In vitro study

2020 ◽  
Vol 18 (3) ◽  
pp. 555-560
Author(s):  
Flávio Mendonça Copello ◽  
Lincoln Issamu Nojima ◽  
Margareth Maria Gomes Souza ◽  
Matheus Melo Pithon ◽  
Antônio Carlos Oliveira Ruellas ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
In Vitro Study ◽  
Vitro Study ◽  
Colour Stability ◽  
Friction Property ◽  
Orthodontic Wires

scholarly journals PSIII-38 Butyric acid and derivatives: In vitro anti-inflammatory effects tested in porcine alveolar macrophages

2020 ◽  
Vol 98 (Supplement_4) ◽  
pp. 370-370
Author(s):  
Lauren L Kovanda ◽  
Monika Hejna ◽  
Yanhong Liu
Keyword(s):  
Organic Acid ◽  
Butyric Acid ◽  
Sodium Butyrate ◽  
Alveolar Macrophages ◽  
Block Design ◽  
Lps Challenge ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Challenge Group

Abstract The aim of this experiment was to examine the anti-inflammatory effects of butyric acid, sodium butyrate, monobutyrin and tributyrin using porcine alveolar macrophages (PAMs). PAMs were isolated from the bronchial lavage of 6 piglets at 6 weeks of age, and then seeded at 106 cells/mL in 24-well plates. After 24 h incubation, cells were treated with different treatments in a randomized complete block design with 10 replicates. The treatments were in a factorial arrangement with 2 doses of lipopolysaccharide (LPS, 0 or 1 μg/mL) and 5 levels of organic acid (0, 0.5, 1, 2, 4 mM for butyric acid and tributyrin and 0, 1, 2, 4, 8 mM for sodium butyrate and monobutyrin). Supernatants were collected after another 24 h incubation and analyzed for tumor necrosis factor alpha (TNF-α). Cell viability was also tested by the MTT assay. Data were analyzed using the MIXED procedure of SAS. No cytotoxic effect was observed in LPS challenge and each organic acid with the percentage of live cells was more than 76% in comparison to the sham control. Sodium butyrate at 2 and 4 mM dose exhibited (P &lt; 0.01) a stimulatory effect on cell proliferation. LPS challenge remarkably stimulated (P &lt; 0.0001) TNF-α secretion from PAMs. In the non-challenge group, butyric acid, monobutyrin, and tributyrin linearly reduced TNF-α production from PAMs, whereas 2 mM sodium butyrate tended to increase (P = 0.056) TNF-α secretion from PAMs. In the LPS challenge group, all tested organic acid dose-dependently reduced (P &lt; 0.001) TNF-α production from LPS-challenged PAMs, with the strongest inhibiting effect observed at the highest dose. Results indicated that butyric acid and its derivatives that were tested in the current experiment all had strong anti-inflammatory activities in vitro.

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