Surfactant Composition in Lung Tissue and Lavage Fluid after Standardized Polytrauma followed by 14 Days Parenteral Nutrition with Different Nutrition Regimens

Black ginseng (BG), which is ginseng that has been steamed and dried nine times, and its main protopanaxatriol-type ginsenosides Rg4, Rg6, Rh4, and Rg2 have been reported to exhibit various forms of biological activity, including antiseptic, antidiabetic, wound-healing, immune-stimulatory, and anti-oxidant activity. The aim of the this study was to examine the effects of [Formula: see text] (a rare protopanaxatriol-type ginsenoside fraction; Rg2, Rg4, Rg6, Rh1, and Rh4) on heme oxygenase-1 (HO-1) induction and on the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX-)2 in lipopolysaccharide (LPS)-activated human pulmonary artery endothelial cells (HPAECs). [Formula: see text] was tested to determine its effect on iNOS protein expression and inflammatory markers (interleukin [IL]-1[Formula: see text] and tumor necrosis factor [TNF]-[Formula: see text] in the lung tissue of LPS-treated mice. The results showed that [Formula: see text] induced the expression of HO-1, reduced LPS-activated NF-[Formula: see text]B-luciferase activity, and inhibited iNOS/NO and COX-2/PGE2, which contributed to the inhibition of STAT-1 phosphorylation. In particular, [Formula: see text] induced the translocation of Nrf2 from the cytosol to the nucleus by increasing Nrf2-ARE activity and decreased IL-1[Formula: see text] production in LPS-activated HPAECs. This reduction in iNOS/NO expression due to [Formula: see text] was reversed by siHO-1 RNA transfection. In LPS-treated mice, [Formula: see text] significantly reduced lung tissue iNOS protein levels and TNF-[Formula: see text] levels in the bronchoalveolar lavage fluid. In conclusion, these findings indicate that [Formula: see text] has a critical anti-inflammatory effect due to its ability to regulate iNOS via the inhibition of p-STAT-1 and NF-[Formula: see text]B, and thus it may be suitable for the treatment of inflammatory disease.

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Effects of CX3CL1 inhibition on murine bleomycin-induced interstitial pneumonia

European Journal of Inflammation ◽

10.1177/2058739220959903 ◽

2020 ◽

Vol 18 ◽

pp. 205873922095990

Author(s):

Soichi Yamada ◽

Shion Miyoshi ◽

Junko Nishio ◽

Satoshi Mizutani ◽

Zento Yamada ◽

...

Keyword(s):

Interstitial Pneumonia ◽

T Cell Activation ◽

Lung Tissue ◽

Cell Activation ◽

Immunohistochemical Analysis ◽

Inflammatory Cells ◽

Lavage Fluid ◽

Novel Therapy ◽

Tissue Sections

Background: Treatment for interstitial pneumonia (IP) associated with collagen diseases has not been established. There is a need to elucidate the pathogenesis of IP and develop a novel therapy. We aimed to clarify the role of chemokine (C-X3-C motif) ligand 1 (CX3CL1, also known as fractalkine) in IP. Methods: Bleomycin (BLM) was intratracheally administered to C57BL/6 mice to induce IP. For treatment with control Ab or anti-CX3CL1 mAb, the mice were administered either Ab three times per week for 2 weeks from the day of BLM administration until euthanasia. Expressions of CX3CL1 and its unique receptor CX3CR1 in the lung tissue were examined by immunohistochemical analysis. Cellular infiltration and lung fibrosis were evaluated based on hematoxylin-eosin-staining and Sirius red staining of the lung tissue sections, respectively. Bronchoalveolar lavage fluid (BALF) cells were analyzed by flow cytometry. Results: CX3CL1 and CX3CR1 were strongly expressed in the lung tissue from mice with BLM-induced IP (BLM-IP). Treatment with anti-CX3CL1 mAb did not significantly alter inflammatory cell infiltration or fibrosis in the lung tissue. However, the number of M1-like macrophages in BALF was decreased and surface CD3 expression on T cells was increased by anti-CX3CL1 mAb treatment. Conclusions: Inhibition of CX3CL1 decreased inflammatory cells and may attenuate T cell activation in BALF. CX3CL1 inhibitor may have the potential to suppress the infiltration and activation of immune cells in IP.

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Strain dependence of airway hyperresponsiveness reflects differences in eosinophil localization in the lung

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.2001.281.2.l394 ◽

2001 ◽

Vol 281 (2) ◽

pp. L394-L402 ◽

Cited By ~ 86

Author(s):

K. Takeda ◽

A. Haczku ◽

J. J. Lee ◽

C. G. Irvin ◽

E. W. Gelfand

Keyword(s):

Lung Tissue ◽

Airway Hyperresponsiveness ◽

Bronchoalveolar Lavage Fluid ◽

Dynamic Compliance ◽

Lavage Fluid ◽

Antibody Responses ◽

Small Airways ◽

Peripheral Lung ◽

Lung Resistance ◽

Different Strains

Different strains of mice exhibit different degrees of airway hyperresponsiveness after sensitization to and airway challenge with ovalbumin. Antibody responses in BALB/c mice far exceeded those in C57BL/6 mice; in contrast, although responsiveness to methacholine was much higher in the BALB/c mice, the number of eosinophils in the bronchoalveolar lavage fluid was higher in C57BL/6 animals. Sensitized and challenged BALB/c mice developed increases in lung resistance and decreases in dynamic compliance after methacholine or 5-hydroxytryptamine inhalation. C57BL/6 mice only exhibited significant levels of responsiveness when dynamic compliance was monitored in response to inhaled 5-hydroxytryptamine. Eosinophils accumulated in the peribronchial and peripheral lung tissue in BALB/c mice but were distributed diffusely in the peripheral lung tissue of C57BL/6 mice. Thus, in addition to differences in antibody responses and cholinergic agonist reactivity, differences in the responses of large and small airways may reflect the selective distribution of eosinophils in lung tissue.

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Differential NF-κB activation after intratracheal endotoxin

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.1999.277.4.l823 ◽

1999 ◽

Vol 277 (4) ◽

pp. L823-L830 ◽

Cited By ~ 10

Author(s):

Timothy S. Blackwell ◽

Lisa H. Lancaster ◽

Thomas R. Blackwell ◽

Annapurna Venkatakrishnan ◽

John W. Christman

Keyword(s):

Lung Tissue ◽

Lavage Fluid ◽

Lung Lavage ◽

Binding Activity ◽

Cytokine Gene Expression ◽

Dna Binding Activity ◽

Factor Α ◽

The Relationship ◽

Second Peak ◽

Necrosis Factor

We examined the relationship between nuclear factor (NF)-κB DNA binding activity, cytokine gene expression, and neutrophilic alveolitis in rats after intratracheal (IT) instillation of endotoxin [lipopolysaccharide (LPS)]. NF-κB activation in lung tissue mirrored neutrophilic alveolitis after IT LPS instillation, with NF-κB activation and neutrophilic influx beginning 2 h after IT LPS doses of 0.01 mg/kg or greater. In lung lavage fluid cells, however, transient NF-κB activation was present in alveolar macrophages by 15 min after IT LPS instillation, followed by a second peak of NF-κB activation corresponding to the onset on neutrophilic alveolitis. For cytokines thought to be NF-κB dependent, two different patterns of mRNA expression were found. Interleukin (IL)-1α, IL-1β, and tumor necrosis factor-α showed increased mRNA by 30 min after IT LPS instillation, but IL-6- and cytokine-induced neutrophil chemoattractant mRNAs were not substantially increased until 2 h after IT LPS instillation. Therefore, IT LPS causes differential NF-κB activation in air space cells and lung tissue, which likely determines production of key cytokines and directs the evolution of neutrophilic alveolitis.

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Effects of hypoxia and reoxygenation on lung glutathione system

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1990.259.2.h518 ◽

1990 ◽

Vol 259 (2) ◽

pp. H518-H524 ◽

Cited By ~ 1

Author(s):

R. M. Jackson ◽

C. F. Veal

Keyword(s):

Glutathione Peroxidase ◽

Lung Tissue ◽

Neutrophil Infiltration ◽

Lavage Fluid ◽

Glutathione System ◽

Glutathione Disulfide ◽

Lung Collapse ◽

Total Glutathione ◽

Reexpansion Pulmonary Edema ◽

The Right

Reexpansion pulmonary edema (RPE) parallels reperfusion (reoxygenation) injuries in other organs in that hypoxic and hypoperfused lung tissue develops increased vascular permeability and neutrophil infiltration after reexpansion. This study investigated the lung cellular glutathione system during hypoxia (produced by lung collapse) and after reoxygenation (produced by reexpansion). Two separate groups of rabbits were studied to determine effects of lung hypoxia-reoxygenation on 1) lung glutathione peroxidase and reductase enzyme activities and 2) lung tissue, plasma, and alveolar lavage fluid total (reduced glutathione plus glutathione disulfide) and oxidized glutathione. Neither lung collapse for 3-7 days nor reexpansion for 2 h after 7 days of collapse affected glutathione peroxidase [controls, 0.36 +/- 0.04 (left), 0.38 +/- 0.03 U/mg DNA (right)] or reductase [controls, 0.12 +/- 0.01 (left), 0.14 +/- 0.01 U/mg DNA (right)] activities. The concentration of glutathione disulfide increased markedly in right alveolar lavage fluid, but not in plasma, after right lung reexpansion. Right lung total glutathione decreased significantly (-19%) after 7 days of collapse. After right lung reexpansion, both left (-65%) and right (-68%) lung total glutathione decreased significantly. The percent of total glutathione present in the oxidized form increased significantly in both left (to 15.5 +/- 4.0% of total) and right (to 18.7 +/- 6.3% of total) lungs after reexpansion of the right lung. These data indicate that lung tissue hypoxia, produced by unilateral lung collapse, was associated with a unilateral decrease in lung total glutathione content. Right lung reoxygenation, due to rapid reexpansion, caused a bilateral decrease in lung total glutathione content and an increase in right lung and alveolar lavage fluid glutathione disulfide concentration.

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