scholarly journals Farnesol, a Sesquiterpene Alcohol in Herbal Plants, Exerts Anti-Inflammatory and Antiallergic Effects on Ovalbumin-Sensitized and -Challenged Asthmatic Mice

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Chi-Mei Ku ◽  
Jin-Yuarn Lin
Keyword(s):  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Peritoneal Macrophages ◽  
Cytokine Secretion ◽  
Dietary Control ◽  
Allergic Asthmatic ◽  
Antiallergic Effect ◽  
Herbal Plants ◽  
Anti Inflammatory ◽  
Necrosis Factor

To investigate the effect of farnesol on allergic asthma, three farnesol doses were extra-added into AIN-76 feed consumed by ovalbumin- (OVA-) sensitized and -challenged mice continuously for 5 weeks, at approximately 5, 25, and 100 mg farnesol/kg, BW/day. The results showed that there were no significant differences in body weight, feed intake, and visceral organ weights between the farnesol supplementation and dietary control groups. Farnesol supplementation decreased interleukin (IL)-6/IL-10 level ratios in bronchoalveolar lavage fluid (BALF). Farnesol supplementation significantly (P<0.05) restored the cytokine secretion ability of peritoneal macrophages that was suppressed as a result of OVA sensitization and challenge and slightly decreased tumor necrosis factor (TNF-α)/IL-10 cytokine secretion ratios. Farnesol supplementation slightly (P>0.05) decreased IL-4 but significantly (P<0.05) increased IL-2 levels secreted by the splenocytes in the presence of OVA, implying that farnesol might have a systemic antiallergic effect on allergic asthmatic mice. Farnesol supplementation significantly (P<0.05) increased IL-10 levels secreted by the splenocytes in the presence of OVA, suggesting that farnesol might have an anti-inflammatory potential to allergic asthmatic mice. Overall, our results suggest that farnesol supplementation may be beneficial to improve the Th2-skewed allergic asthmatic inflammation.

scholarly journals Effects of esculentoside A on turnour necrosis factor production by mice peritoneal macrophages

1992 ◽  
Vol 1 (6) ◽  
pp. 375-377 ◽  
Author(s):  
Fang Jun ◽  
Zheng Qin Yue ◽  
Wang Hong Bin ◽  
Ju Dian Wen ◽  
Yi Yang Hua
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Inflammatory Mediator ◽  
Platelet Activating Factor ◽  
Peritoneal Macrophages ◽  
Dependent Manner ◽  
Anti Inflammatory ◽  
Dose Dependent ◽  
Necrosis Factor ◽  
Inflammatory Effect

Esculentoside A (EsA) is a saponin isolated from the roots of Phytolacca esculenta. Previous experiments showed that it had strong anti-inflammatory effects. Tumour necrosis factor (TNF) is an important inflammatory mediator. In order to study the mechanism of the anti-inflammatory effect of EsA, it was determined whether TNF production from macrophages was altered by EsA under lipopolysaccharide (LPS) stimulated conditions. EsA was found to decrease both extracellular and cell associated TNF production in a dose dependent manner at concentrations higher than 1 μmol/l EsA. Previous studies have showed that EsA reduced the releasing of platelet activating factor (PAF) from rat macrophages. The reducing effects of EsA on the release of TNF and PAF may explain its anti-inflammatory effect.

scholarly journals Role of TNFR1 in the innate airway hyperresponsiveness of obese mice

2012 ◽  
Vol 113 (9) ◽  
pp. 1476-1485 ◽  
Author(s):  
Ming Zhu ◽  
Alison S. Williams ◽  
Lucas Chen ◽  
Allison P. Wurmbrand ◽  
Erin S. Williams ◽  
...  
Keyword(s):  
Airway Hyperresponsiveness ◽  
Bronchoalveolar Lavage Fluid ◽  
Pulmonary Inflammation ◽  
Tumor Necrosis Factor Receptor ◽  
Lavage Fluid ◽  
Forced Oscillation Technique ◽  
Obese Mice ◽  
Wild Type ◽  
Necrosis Factor

The purpose of this study was to examine the role of tumor necrosis factor receptor 1 (TNFR1) in the airway hyperresponsiveness characteristic of obese mice. Airway responsiveness to intravenous methacholine was measured using the forced oscillation technique in obese Cpe fat mice that were either sufficient or genetically deficient in TNFR1 ( Cpe fat and Cpe fat/TNFR1−/− mice) and in lean mice that were either sufficient or genetically deficient in TNFR1 [wild-type (WT) and TNFR1−/− mice]. Compared with lean WT mice, Cpe fat mice exhibited airway hyperresponsiveness. Airway hyperresponsives was also greater in Cpe fat/TNFR1−/− than in Cpe fat mice. Compared with WT mice, Cpe fat mice had increases in bronchoalveolar lavage fluid concentrations of several inflammatory moieties including eotaxin, IL-9, IP-10, KC, MIG, and VEGF. These factors were also significantly elevated in Cpe fat/TNFR1−/− vs. TNFR1−/− mice. Additional moieties including IL-13 were also elevated in Cpe fat/TNFR1−/− vs. TNFR1−/− mice but not in Cpe fat vs. WT mice. IL-17A mRNA expression was greater in Cpe fat/TNFR1−/− vs. Cpe fat mice and in TNFR1−/− vs. WT mice. Analysis of serum indicated that obesity resulted in systemic as well as pulmonary inflammation, but TNFR1 deficiency had little effect on this systemic inflammation. Our results indicate that TNFR1 is protective against the airway hyperresponsiveness associated with obesity and suggest that effects on pulmonary inflammation may be contributing to this protection.

Paeonol attenuates airway inflammation and hyperresponsiveness in a murine model of ovalbumin-induced asthma

2010 ◽  
Vol 88 (10) ◽  
pp. 1010-1016 ◽  
Author(s):  
Qiang Du ◽  
Gan-Zhu Feng ◽  
Li Shen ◽  
Jin Cui ◽  
Jian-Kang Cai
Keyword(s):  
Bronchoalveolar Lavage ◽  
Airway Inflammation ◽  
Bronchoalveolar Lavage Fluid ◽  
Immunoglobulin E ◽  
Therapeutic Potential ◽  
Lavage Fluid ◽  
Interleukin 4 ◽  
Moutan Cortex ◽  
Ifn Γ ◽  
Anti Inflammatory

Paeonol, the main active component isolated from Moutan Cortex, possesses extensive pharmacological activities such as anti-inflammatory, anti-allergic, and immunoregulatory effects. In the present study, we examined the effects of paeonol on airway inflammation and hyperresponsiveness in a mouse model of allergic asthma. BALB/c mice sensitized and challenged with ovalbumin were administered paeonol intragastrically at a dose of 100 mg/kg daily. Paeonol significantly suppressed ovalbumin-induced airway hyperresponsiveness to acetylcholine chloride. Paeonol administration significantly inhibited the total inflammatory cell and eosinophil count in bronchoalveolar lavage fluid. Treatment with paeonol significantly enhanced IFN-γ levels and decreased interleukin-4 and interleukin-13 levels in bronchoalveolar lavage fluid and total immunoglobulin E levels in serum. Histological examination of lung tissue demonstrated that paeonol significantly attenuated allergen-induced lung eosinophilic inflammation and mucus-producing goblet cells in the airway. These data suggest that paeonol exhibits anti-inflammatory activity in allergic mice and may possess new therapeutic potential for the treatment of allergic bronchial asthma.

scholarly journals Effect of Kramecyne on the Inflammatory Response in Lipopolysaccharide-Stimulated Peritoneal Macrophages

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
E. Sánchez-Miranda ◽  
J. Lemus-Bautista ◽  
S. Pérez ◽  
J. Pérez-Ramos
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Responses ◽  
Inflammatory Diseases ◽  
Peritoneal Macrophages ◽  
Anti Inflammatory ◽  
Oxide Synthase ◽  
North And South America ◽  
North And South ◽  
Mouse Peritoneal Macrophages ◽  
Necrosis Factor

Kramecyne is a new peroxide, it was isolated fromKrameria cytisoides, methanol extract, and this plant was mostly found in North and South America. This compound showed potent anti-inflammatory activity; however, the mechanisms by which this compound exerts its anti-inflammatory effect are not well understood. In this study, we examined the effects of kramecyne on inflammatory responses in mouse lipopolysaccharide- (LPS-) induced peritoneal macrophages. Our findings indicate that kramecyne inhibits LPS-induced production of tumor necrosis factor (TNF-α) and interleukin- (IL-) 6. During the inflammatory process, levels of cyclooxygenase- (COX-) 2, nitric oxide synthase (iNOS), and nitric oxide (NO) increased in mouse peritoneal macrophages; however, kramecyne suppressed them significantly. These results provide novel insights into the anti-inflammatory actions and support its potential use in the treatment of inflammatory diseases.

scholarly journals Effect of exogenous surfactant on Paediatric Bronchoalveolar lavage derived macrophages’ cytokine secretion

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Lyné van Rensburg ◽  
Johann M. van Zyl ◽  
Johan Smith ◽  
Pierre Goussard
Keyword(s):  
Bronchoalveolar Lavage ◽  
South African ◽  
Alveolar Macrophages ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Cytokine Secretion ◽  
Exogenous Surfactant ◽  
Normal Children ◽  
African Children ◽  
South African Children

Abstract Background Bronchoalveolar lavage is a useful bronchoscopy technique. However, studies in “normal” children populations are few. Furthermore, the anti-inflammatory effects of exogenous pulmonary surfactants on the bronchoalveolar cellular components are limited. Methods Thirty children, aged 3 to 14 years, underwent diagnostic bronchoscopy and bronchoalveolar lavage. Differential cytology, cytokine and chemokine measurements were performed on the fluid after exogenous surfactant exposure. The aim of the study was to investigate the potential anti-inflammatory effects of exogenous surfactants on the bronchoalveolar lavage fluid, specifically alveolar macrophages of healthy South African children. Results Alveolar macrophages were the predominant cellular population in normal children. Patients with inflammatory pneumonopathies had significantly more neutrophils. Levels of inflammatory cytokines were significantly lower after exogenous surfactant exposure. Moreover, IL-10 and IL-12 cytokine secretion increased after exogenous surfactant exposure. Conclusion This study provides the first data on bronchoalveolar lavage of healthy South African children. Bronchoalveolar lavage fluid from patients with pulmonary inflammation was characterised by neutrophilia. Finally, we propose that exogenous surfactant treatment could help alleviate inflammation in diseased states where it occurs in the tracheobronchial tree.

Low-tidal-volume Mechanical Ventilation Induces a Toll-like Receptor 4–dependent Inflammatory Response in Healthy Mice

2008 ◽  
Vol 109 (3) ◽  
pp. 465-472 ◽  
Author(s):  
Michiel Vaneker ◽  
Leo A. Joosten ◽  
Leo M. A. Heunks ◽  
Dirk G. Snijdelaar ◽  
Feico J. Halbertsma ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Toll Like Receptor ◽  
Necrosis Factor Alpha ◽  
Ventilator Induced Lung Injury ◽  
Factor Alpha ◽  
Necrosis Factor

Background Mechanical ventilation (MV) can induce ventilator-induced lung injury. A role for proinflammatory pathways has been proposed. The current studies analyzed the roles of Toll-like receptor (TLR) 4 and TLR2 involvement in the inflammatory response after MV in the healthy lung. Methods Wild-type (WT) C57BL6, TLR4 knockout (KO), and TLR2 KO mice were mechanically ventilated for 4 h. Bronchoalveolar lavage fluid was analyzed for presence of endogenous ligands. Lung homogenates were used to investigate changes in TLR4 and TLR2 expression. Cytokines were measured in lung homogenate and plasma, and leukocytes were counted in lung tissue. Results MV significantly increased endogenous ligands for TLR4 in bronchoalveolar lavage fluid and relative messenger RNA expression of TLR4 and TLR2 in lung tissue. In lung homogenates, MV in WT mice increased levels of keratinocyte-derived chemokine, interleukin (IL)-1alpha, and IL-1beta. In TLR4 KO mice, MV increased IL-1alpha but not IL-1beta, and the increase in keratinocyte-derived chemokine was less pronounced. In plasma, MV in WT mice increased levels of IL-6, keratinocyte-derived chemokine, and tumor necrosis factor alpha. In TLR4 KO mice, MV did not increase levels of IL-6 or tumor necrosis factor alpha, and the response of keratinocyte-derived chemokine was less pronounced. MV in TLR2 KO mice did not result in different cytokine levels compared with WT mice. In WT and TLR2 KO mice, but not in TLR4 KO mice, MV increased the number of pulmonary leukocytes. Conclusions The current study supports a role for TLR4 in the inflammatory reaction after short-term MV in healthy lungs. Increasing the understanding of the innate immune response to MV may lead to future treatment advances in ventilator-induced lung injury, in which TLR4 may serve as a therapeutic target.

scholarly journals Non-Invasive Delivery of Nano-Emulsified Sesame Oil-Extract of Turmeric Attenuates Lung Inflammation

Pharmaceutics ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 1206
Author(s):  
Sahibzada Tasleem Rasool ◽  
Rajasekhar Reddy Alavala ◽  
Umasankar Kulandaivelu ◽  
Nagaraja Sreeharsha
Keyword(s):  
Lung Injury ◽  
Bronchoalveolar Lavage ◽  
Lung Inflammation ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Treated Group ◽  
Sesame Oil ◽  
Oil Extract ◽  
Anti Inflammatory ◽  
Nano Emulsion

Turmeric, the golden Indian spice, and the edible oil of sesame seeds are the essential ingredients of Indian food created by ancestors and established the belief of the curative effect of food for many generations. Considering the anti-inflammatory effects of turmeric, we formulated a nano-emulsion of turmeric infused in edible sesame oil, with a globule size of 200–250 nm using high-energy microfluidization. The product with a zeta potential of −11.5 mV showed spherical globules when imaged for scanning and transmission electron microscopy. We explored the anti-inflammatory potential of this edible nano-emulsion in lung inflammation. The lungs are the internal organ most vulnerable to infection, injury, and rapid inflammation from the external environment because of their constant exposure to pollutants, pathogenic microorganisms, and viruses. We evaluated the nano-emulsion for efficacy in ovalbumin-induced lung injury in mice with an oral treatment for two weeks. The therapeutic effect of nano-emulsion of the sesame oil-extract of turmeric was evident from biochemical analysis of bronchoalveolar lavage fluid, lung histopathology, and flow cytometric analysis. The developed nano-emulsion significantly reduced the inflammation and damage to the alveolar network in ovalbumin-injured mice. Significant reduction in the levels of neutrophils and inflammatory cytokines like IL-4, IL-6, and IL-13 in bronchoalveolar lavage fluid was observed in the nano-emulsion-treated group. Leukotriene B4 and IgE were also significantly altered in the treated group, thus suggesting the suitability of the formulation for the treatment of allergy and other inflammatory conditions. The nano-emulsification process potentiated the immunoregulatory effect of turmeric, as observed from the elevated levels of the natural anti-inflammatory cytokine, IL-10. The dietary constituents-based nano-emulsion of spice turmeric helped in scavenging the free radicals in the injured lungs, thus modulating the inflammation pathway. This easily scalable formulation technology approach can therefore serve as a potential noninvasive and safe treatment modality for reducing lung inflammation in lung injury cases.

scholarly journals AP-1-Targeted Anti-Inflammatory Activities of the Nanostructured, Self-Assembling S5 Peptide

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Woo Seok Yang ◽  
Young-Jin Son ◽  
Mi-Yeon Kim ◽  
Soochan Kim ◽  
Jong-Hoon Kim ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Positive Charge ◽  
Nuclear Translocation ◽  
Peritoneal Macrophages ◽  
Prostaglandin E ◽  
Signaling Complex ◽  
Self Assembling ◽  
Free Hydroxyl ◽  
Anti Inflammatory ◽  
Necrosis Factor

Peptide-based therapeutics have received increasing attention in medical research. However, the local delivery of such therapeutics poses unique challenges. Self-assembling peptides that use decorated nanofibers are one approach by which these therapeutics may be delivered. We previously found that the self-assembling K5 peptide affects the anti-inflammatory response. The aim of the present study was to investigate another self-assembling peptide, S5. Unlike the K5 peptide which has a positive charge, the S5 peptide has a free hydroxyl (-OH) group. We first examined whether the S5 peptide regulates the inflammatory response in primary cells and found that the S5 peptide reduced the production of prostaglandin E2(PGE2) and tumor necrosis factor (TNF)-αin lipopolysaccharide- (LPS-) treated bone marrow-derived macrophages. Moreover, the S5 peptide significantly downregulatedcyclooxygenase- (COX-) 2, TNF-α, andinterleukin- (IL-) 1βexpression by blocking the nuclear translocation of c-Jun. Consistent with this finding, the S5 peptide diminished the activation of inflammatory signaling enzymes related to p38. The S5 peptide also inhibited the formation of the p38/c-Jun signaling complex in RAW264.7 cells. Similarly, p38 and MKK3/6 were inhibited by the S5 peptide in LPS-activated peritoneal macrophages. Taken together, these results strongly suggest that the S5 peptide could exert anti-inflammatory effects by inhibiting the c-Jun/p38 signaling pathway.

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