scholarly journals Methyl Protodioscin from the Roots ofAsparagus cochinchinensisAttenuates Airway Inflammation by Inhibiting Cytokine Production

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Ju Hee Lee ◽  
Hun Jai Lim ◽  
Chan Woo Lee ◽  
Kun-Ho Son ◽  
Jong-Keun Son ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Cytokine Production ◽  
Herbal Remedy ◽  
Oral Treatment ◽  
A549 Cells ◽  
Ethanol Extract ◽  
Lung Epithelial Cells ◽  
Major Constituent ◽  
Pharmacologically Active

The present study was designed to find pharmacologically active compound against airway inflammation from the roots ofAsparagus cochinchinensis. The 70% ethanol extract of the roots ofA. cochinchinensis(ACE) was found to inhibit IL-6 production from IL-1β-treated lung epithelial cells (A549) and the major constituent, methyl protodioscin (MP), also strongly inhibited the production of IL-6, IL-8, and tumor necrosis factor- (TNF-)αfrom A549 cells at 10–100 μM. This downregulating effect of proinflammatory cytokine production was found to be mediated, at least in part, via inhibition of c-Jun N-terminal kinase (JNK) and c-Jun activation pathway. When examined on anin vivomodel of airway inflammation in mice, lipopolysaccharide- (LPS-) induced acute lung injury, ACE, and MP significantly inhibited cell infiltration in the bronchoalveolar lavage fluid by the oral treatment at doses of 100–400 mg/kg and 30–60 mg/kg, respectively. MP also inhibited the production of proinflammatory cytokines such as IL-6, TNF-α, and IL-1βin lung tissue. All of these findings provide scientific evidence supporting the role ofA. cochinchinensisas a herbal remedy in treating airway inflammation and also suggest a therapeutic value of MP on airway inflammatory disorders.

scholarly journals Evodia rutaecarpaand Three Major Alkaloids Abrogate Influenza A Virus (H1N1)-Induced Chemokines Production and Cell Migration

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Wen-Fei Chiou ◽  
Han-Chieh Ko ◽  
Bai-Luh Wei
Keyword(s):  
Cell Migration ◽  
Influenza A Virus ◽  
Influenza A ◽  
Herbal Remedy ◽  
A549 Cells ◽  
Influenza Virus Infection ◽  
Ethanol Extract ◽  
Lung Epithelial Cells ◽  
Virus H1n1 ◽  
Active Components

Evodia rutaecarpais commonly used as an anti-inflammatory herbal remedy in traditional Chinese medicine. In this study, the ethanol extract ofE. rutaecarpa(ER) and three major quinazoline alkaloids dehydroevodiamine (DeHE), evodiamine (Evo) and rutaecarpine (Rut), isolated from ER were employed to study their inhibitory effects against influenza A virus (H1N1)-induced chemokines production in A549 lung epithelial cells as well as on chemokines-evoked cell recruitment in HL-60-differentiated macrophages. The results showed that ER was a potent inhibitor of RANTES secretion by H1N1-inoculated A549 cells (IC50: 1.9 ± 0.4 g ml−1). Three alkaloids, although to differing extents, all concentration dependent, inhibited H1N1-induced RANTES production with Evo consistently being the most potent among these active components. ER also moderately and significantly inhibited H1N1-stimulated MCP-1 production in A549 cells. This was mimicked by Evo and Rut, but not DeHE. In the macrophage recruitment assay, both RANTES and MCP-1 markedly evoked cell migration and this phenomenon was significantly suppressed by ER. Evo and Rut, but not DeHE, also had the ability to inhibit cell migration toward RANTES and MCP-1, respectively. In summary, three major alkaloids displayed different potentials for inhibiting chemokines secretion and subsequently cell migration, which could partially explain the activity of ER. As an effective agent to suppress H1N1-induced chemokines production and block chemokine-attracted leukocytes recruitment,E. rutaecarpaand its active components may be useful in influenza virus infection-related inflammatory disorders.

scholarly journals IL-22 induces Reg3γ and inhibits allergic inflammation in house dust mite–induced asthma models

2017 ◽  
Vol 214 (10) ◽  
pp. 3037-3050 ◽  
Author(s):  
Takashi Ito ◽  
Koichi Hirose ◽  
Aiko Saku ◽  
Kenta Kono ◽  
Hiroaki Takatori ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Airway Inflammation ◽  
House Dust ◽  
House Dust Mite ◽  
Cytokine Production ◽  
Allergic Airway Inflammation ◽  
Lung Epithelial Cells ◽  
Intratracheal Administration ◽  
Lung Epithelial ◽  
Dust Mite

Previous studies have shown that IL-22, one of the Th17 cell–related cytokines, plays multiple roles in regulating allergic airway inflammation caused by antigen-specific Th2 cells; however, the underlying mechanism remains unclear. Here, we show that allergic airway inflammation and Th2 and Th17 cytokine production upon intratracheal administration of house dust mite (HDM) extract, a representative allergen, were exacerbated in IL-22-deficient mice. We also found that IL-22 induces Reg3γ production from lung epithelial cells through STAT3 activation and that neutralization of Reg3γ significantly exacerbates HDM-induced eosinophilic airway inflammation and Th2 cytokine induction. Moreover, exostatin-like 3 (EXTL3), a functional Reg3γ binding protein, is expressed in lung epithelial cells, and intratracheal administration of recombinant Reg3γ suppresses HDM-induced thymic stromal lymphopoietin and IL-33 expression and accumulation of type 2 innate lymphoid cells in the lung. Collectively, these results suggest that IL-22 induces Reg3γ production from lung epithelial cells and inhibits the development of HDM-induced allergic airway inflammation, possibly by inhibiting cytokine production from lung epithelial cells.

scholarly journals Loss of versican and production of hyaluronan in lung epithelial cells are associated with airway inflammation during RSV infection

2020 ◽  
pp. jbc.RA120.016196
Author(s):  
Gerald G. Kellar ◽  
Kaitlyn A. Barrow ◽  
Lucille M. Rich ◽  
Jason S. Debley ◽  
Thomas N. Wight ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Ex Vivo ◽  
Lung Epithelial Cells ◽  
In Vivo Studies ◽  
Critical Feature ◽  
Human Lung Fibroblast ◽  
Rsv Infection ◽  
Syncytial Virus ◽  
Tract Infections

Airway inflammation is a critical feature of lower respiratory tract infections caused by viruses such as respiratory syncytial virus (RSV). A growing body of literature has demonstrated the importance of extracellular matrix (ECM) changes such as the accumulation of hyaluronan (HA) and versican in the subepithelial space in promoting airway inflammation; however, whether these factors contribute to airway inflammation during RSV infection remains unknown. To test the hypothesis that RSV infection promotes inflammation via altered HA and versican production, we studied an ex vivo human bronchial epithelial cell (BEC)/human lung fibroblast (HLF) co-culture model. RSV infection of BEC/HLF co-cultures led to decreased hyaluronidase expression by HLFs, increased accumulation of HA, and enhanced adhesion of U937 cells as would be expected with increased HA. HLF production of versican was not altered following RSV infection; however, BEC production of versican was significantly downregulated following RSV infection. In vivo studies with epithelial-specific versican-deficient mice [SPC-Cre(+) Vcan-/-] demonstrated that RSV infection led to increased HA accumulation compared to control mice which also coincided with decreased hyaluronidase expression in the lung. SPC-Cre(+) Vcan-/- mice demonstrated enhanced recruitment of monocytes and neutrophils in bronchoalveolar lavage fluid and increased neutrophils in the lung compared to SPC-Cre(-) RSV-infected littermates. Taken together, these data demonstrate that altered ECM accumulation of HA occurs following RSV infection and may contribute to airway inflammation. Additionally, loss of epithelial expression of versican promotes airway inflammation during RSV infection further demonstrating that versican’s role in inflammatory regulation is complex and dependent on the microenvironment.

scholarly journals Urban Aerosols Induce Pro-inflammatory Cytokine Production in Macrophages and Cause Airway Inflammation in Vivo

2010 ◽  
Vol 33 (5) ◽  
pp. 780-783 ◽  
Author(s):  
Tokuyuki Yoshida ◽  
Yasuo Yoshioka ◽  
Maho Fujimura ◽  
Hiroyuki Kayamuro ◽  
Kohei Yamashita ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Inflammatory Cytokine Production ◽  
Urban Aerosols

scholarly journals Anti-malarial activity and toxicity of Aspidosperma nitidum Benth: a plant used in traditional medicine in the Brazilian Amazon

2020 ◽  
Vol 9 (10) ◽  
pp. e5059108817
Author(s):  
Dayse Lucia do Nascimento Brandão ◽  
Michel Tavares Martins ◽  
Adreanne Oliveira Silva ◽  
Amanda Dias Almeida ◽  
Renata Cristina de Paula ◽  
...  
Keyword(s):  
Ethanol Extract ◽  
Neutral Fraction ◽  
Antiplasmodial Activity ◽  
Major Constituent ◽  
Acute Oral Toxicity ◽  
Oral Toxicity ◽  
Alkaloid Fraction ◽  
Low Cytotoxicity

The objective of this work was to evaluate the antiplasmodial activity and toxicity of the extract and fractions obtained from the bark of Aspidosperma nitidum. The ethanol extract obtained from the powdered bark of plants was acid-base partitioned and phytochemically analyzed. The antiplasmodial activity, in vivo antimalarial activity and in vitro cytotoxicity were acessed. The selectivity index (SI) was calculated. The acute oral toxicity and pathological effects, of the ethanol extract was evaluated in mice. The major constituent of the ethanol extract was suggestive of a β-carboline chromophore. The alkaloid and neutral fractions contained compounds with an aspidospermine core as the major constituent. The ethanol extract (IC50 = 3.60 µg/mL), neutral fraction (IC50 = 3.34 µg/mL) and alkaloid fraction (IC50= 2.32 µg/mL) showed high activity against P. falciparum (W2 strain). The ethanol extract and the alkaloid fraction reduced 80% of the parasitemia of P. berghei (ANKA)-infected mice (dose of 500 mg/kg) in the 5th day, which was not sustainable at the 8th day. A similar result was obtained for chloroquine. The ethanol extract (CC50 = 410.65 µg/mL; SI = 114.07), neutral fraction (CC50 = 452.53 µg/mL; SI = 135.49), and alkaloid fraction (CC50 =346.73 µg/mL; SI 149.45) demonstrated low cytotoxicity and high SI. The ethanol extract (5000 mg/kg; gavage) presented low acute oral toxicity, with no clinical or anatomopathological modifications being observed (in comparison to the control group). In vitro studies with a chloroquine-resistant clone of P. falciparum confirmed the antiplasmodial activity of the A. nitidum ethanol extract, and its fractions had low cytotoxicity for HepG2 cells. In vivo studies with P. berghei–infected mice and acute toxicity studies corroborated these results.

scholarly journals Therapeutic Management of Pulmonary Tuberculosis by Mannosylated Chitosan Ascorbate Microspheres: Preparation and Characterization

2019 ◽  
Vol 9 (3) ◽  
pp. 13-25
Author(s):  
Archana Bagre ◽  
Narendra Kumar Lariya ◽  
Mohan Lal Kori
Keyword(s):  
Ascorbic Acid ◽  
Pulmonary Tuberculosis ◽  
Alveolar Macrophages ◽  
Antioxidant Properties ◽  
A549 Cells ◽  
Lung Epithelial Cells ◽  
Scanning Calorimetry ◽  
Aerodynamic Properties

Objective: In this study, biodegradable Chitosan Ascorbate Microsphere (CAMs) and mannosylated chitosan ascorbate microsphere (m-CAMs) prepared for targeting towards alveolar macrophages to treatment of pulmonary tuberculosis.  Significance: Ascorbic acid is an antioxidant and reported killing effect on mycobacterium by induces fenton reaction. This study enlightens the possible benefits of adding antioxidant properties of ascorbic acid with chitosan microsphere to an anti-tuberculosis regimen and mannosylation of microsphere significantly induce the targetability of antitubercular drug to alveolar macrophages. Methods: CAMs prepared by firstly salification of chitosan by ascorbic acid then ionic gelation with STPP and m-CAMs prepared by incubation method and purified for further studies. The physicochemical, in vitro and in vivo characterizations of both formulations were carried out. Results: The size of microspheres (both CAMs and m-CAMs) were found to be in range of 3.40-4.81µm. Evident changes were observed in crystallinity and structure of both carrier systems and depicted by Fourier transform infrared (FTIR), Differential scanning calorimetry (DSC) and X-ray diffraction (XRD) studies. In vitro lung deposition study of microspheres showed favourable aerodynamic properties for deep lung delivery (MMAD 2.0- 3.8 μm) and, thus, show potential for an application as inhalable tuberculosis therapy. The drug release showed the biphasic pattern of release, i.e., initial burst (30-45% up to 8 h) followed by a slower sustained release pattern (more than 80% up to 72 h) in both simulated lung fluids. Optimized formulations exhibited lower cytotoxicity and bio distribution studies demonstrated the efficiency of m-CAMs for spatial delivery of INH to alveolar tissues. CAMs and m-CAMs evidenced minor cytotoxicity on lung epithelial cells (A549 cell lines). Conclusion: m-CAMs thus has a promising potential to be explore as an effective carrier system for delivery of antitubercular drugs regimen. Key words: Targetability, alveolar macrophage, lung cancer A549 cells

scholarly journals 3,4-Dicaffeoylquinic Acid, a Major Constituent of Brazilian Propolis, Increases TRAIL Expression and Extends the Lifetimes of Mice Infected with the Influenza A Virus

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Tomoaki Takemura ◽  
Tomohiko Urushisaki ◽  
Mayuko Fukuoka ◽  
Junji Hosokawa-Muto ◽  
Taketoshi Hata ◽  
...  
Keyword(s):  
Influenza A Virus ◽  
Influenza A ◽  
Water Extract ◽  
Ethanol Extract ◽  
Major Constituent ◽  
Chemical Components ◽  
Control Group ◽  
Dicaffeoylquinic Acid ◽  
Brazilian Green Propolis

Brazilian green propolis water extract (PWE) and its chemical components, caffeoylquinic acids, such as 3,4-dicaffeoylquinic acid (3,4-diCQA), act against the influenza A virus (IAV) without influencing the viral components. Here, we evaluated the anti-IAV activities of these compoundsin vivo. PWE or PEE (Brazilian green propolis ethanol extract) at a dose of 200 mg/kg was orally administered to Balb/c mice that had been inoculated with IAV strain A/WSN/33. The lifetimes of the PWE-treated mice were significantly extended compared to the untreated mice. Moreover, oral administration of 3,4-diCQA, a constituent of PWE, at a dose of 50 mg/kg had a stronger effect than PWE itself. We found that the amount of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) mRNA in the mice that were administered 3,4-diCQA was significantly increased compared to the control group, while H1N1 hemagglutinin (HA) mRNA was slightly decreased. These data indicate that PWE, PEE or 3,4-diCQA possesses a novel and unique mechanism of anti-influenza viral activity, that is, enhancing viral clearance by increasing TRAIL.

scholarly journals Transcriptional analysis of lung epithelial cells using WGCNA revealed the role of IRF9 and IFI6 genes in SARS-CoV-2 pathogenicity

2020 ◽  
Author(s):  
Hassan Karami ◽  
Afshin Derakhshani ◽  
Mohammad Fereidouni ◽  
Ebrahim Miri-Moghaddam ◽  
Behzad Baradaran ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Experimental Studies ◽  
A549 Cells ◽  
Lung Epithelial Cells ◽  
Transcriptional Analysis ◽  
Type I ◽  
Hub Genes

Abstract The coronavirus disease 2019 (COVID-19) outbreak is an ongoing global health emergence, but the pathogenesis remains unclear. Here, we applied weighted gene co-expression network analysis to comprehensively characterize transcriptional changes in bronchial epithelium cells (NHBE and A549 cells) during SARS-CoV-2 infection. Our analysis identified a network highly correlated to COVID-19 pathogenicity based on MX1, IFIT1, ISG15, IFI6, DDX60, IRF9, PARP9, PGLYRP4, IL36G, SAA2 and IL-8 hub genes. The results also indicated a unique transcriptional signatures of infected cells including IFI6 and IRF9 as novel gene candidates and suggested their prospective mechanism in COVID-19 pathogenesis. The result of hub genes enrichment showed that the most correlation topic in biological process and KEGG were type I interferon signaling pathway, IL-17 signaling pathway, cytokine mediated signaling pathway, and defense response to virus categories which all play significant roles in restricting viral infection. Also according to the drug-target network, we recognized 54 FDA-approved drug candidates for other indications could potentially use for the treatment of COVID-19 patients through regulation of six hub genes of the co-expression network. Our findings also showed that the 19 experimentally validated miRNAs regulated the co-expression network through 5 hub genes (SLC19A3, FAM13A, PLA2G16, and HRASLS5). In conclusion, these hub genes had potential roles in the translational medicine and might become promising therapeutic targets further in vitro and in vivo experimental studies are needed to evaluate the role of above mentioned genes in COVID-19.

scholarly journals The Ethanol Extract ofOsmanthus fragransFlowers Reduces Oxidative Stress and Allergic Airway Inflammation in an Animal Model

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Chien-Ya Hung ◽  
Fu-Long Huang ◽  
Li-Shian Shi ◽  
Shuk-Man Ka ◽  
Jing-Yao Wang ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Allergic Airway Inflammation ◽  
Ethanol Extract ◽  
Thiobarbituric Acid ◽  
Specific Ige ◽  
Antioxidant Compounds ◽  
Osmanthus Fragrans ◽  
Antioxidative Effects ◽  
Traditional Chinese Medical

TheOsmanthus fragransflower, a popular herb in Eastern countries, contains several antioxidant compounds.Ben Cao Gang Mu, traditional Chinese medical literature, describes the usefulness of these flowers for phlegm and stasis reduction, arrest of dysentery with blood in the bowel, and stomachache and diarrhea treatment. However, modern evidence regarding the therapeutic efficacy of these flowers is limited. This study was aimed at assessing the antioxidative effects of the ethanol extract ofO. fragransflowers (OFE)in vivoand evaluating its antioxidant maintenance and therapeutic effect on an allergic airway inflammation in mice. After OFE’s oral administration to mice, the values obtained in the oxygen radical absorbance capacity assay as well as the glutathione concentration in the lungs and spleens of mice increased while thiobarbituric acid reactive substances decreased significantly, indicating OFE’s significantin vivoantioxidant activity. OFE was also therapeutically efficacious in a mouse model of ovalbumin-induced allergic airway inflammation. Orally administered OFE suppressed ovalbumin-specific IgE production and inflammatory cell infiltration in the lung. Moreover, the antioxidative state of the mice improved. Thus, our findings confirm the ability of theO. fragransflowers to reduce phlegm and suggest that OFE may be useful as an antiallergic agent.

scholarly journals Signaling through FcγRIII is required for optimal T helper type (Th)2 responses and Th2-mediated airway inflammation

2007 ◽  
Vol 204 (8) ◽  
pp. 1875-1889 ◽  
Author(s):  
Hozefa S. Bandukwala ◽  
Bryan S. Clay ◽  
Jiankun Tong ◽  
Purvi D. Mody ◽  
Judy L. Cannon ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Cytokine Production ◽  
Inflammatory Responses ◽  
T Helper ◽  
Fcγ Receptors ◽  
Th2 Responses ◽  
Helper Type

Although inhibitory Fcγ receptors have been demonstrated to promote mucosal tolerance, the role of activating Fcγ receptors in modulating T helper type (Th)2-dependent inflammatory responses characteristic of asthma and allergies remains unclear. Here, we demonstrate that signaling via activating Fcγ receptors in conjunction with Toll-like receptor 4 stimulation modulated cytokine production from bone marrow–derived dendritic cells (DCs) and augmented their ability to promote Th2 responses. Ligation of the low affinity receptor FcγRIII was specifically required for the enhanced Th2 responses, as FcγRIII−/− DCs failed to augment Th2-mediated airway inflammation in vivo or induce Th2 differentiation in vitro. Further, FcγRIII−/− mice had impaired Th2 cytokine production and exhibited reduced airway inflammation, whereas no defect was found in FcγRI−/− mice. The augmentation of Th2 immunity was regulated by interleukin 10 production from the DCs but was distinct and independent of the well-established role of FcγRIII in augmenting antigen presentation. Thus, our studies reveal a novel and specific role for FcγRIII signaling in the regulation of Th cell responses and suggest that in addition to immunoglobulin (Ig)E, antigen-specific IgG also contributes to the pathogenesis of Th2-mediated diseases such as asthma and allergies.

Sign in / Sign up

Export Citation Format

Share Document