scholarly journals Virgin Coconut Oil Supplementation Prevents Airway Hyperreactivity of Guinea Pigs with Chronic Allergic Lung Inflammation by Antioxidant Mechanism

2020 ◽  
Vol 2020 ◽  
pp. 1-16
Author(s):  
Luiz Henrique C. Vasconcelos ◽  
Maria da Conceição C. Silva ◽  
Alana C. Costa ◽  
Giuliana A. de Oliveira ◽  
Iara Leão Luna de Souza ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Guinea Pigs ◽  
Lung Inflammation ◽  
Inflammatory Infiltrate ◽  
Coconut Oil ◽  
Airway Hyperreactivity ◽  
Epithelial Hyperplasia ◽  
Virgin Coconut Oil ◽  
Allergic Lung Inflammation ◽  
Inducible Nos

Asthma is a chronic inflammatory disease of the airways characterized by immune cell infiltrates, bronchial hyperresponsiveness, and declining lung function. Thus, the possible effects of virgin coconut oil on a chronic allergic lung inflammation model were evaluated. Morphology of lung and airway tissue exhibited peribronchial inflammatory infiltrate, epithelial hyperplasia, and smooth muscle thickening in guinea pigs submitted to ovalbumin sensitization, which were prevented by virgin coconut oil supplementation. Additionally, in animals with lung inflammation, trachea contracted in response to ovalbumin administration, showed a greater contractile response to carbachol (CCh) and histamine, and these responses were prevented by the virgin coconut oil supplementation. Apocynin, a NADPH oxidase inhibitor, did not reduce the potency of CCh, whereas tempol, a superoxide dismutase mimetic, reduced potency only in nonsensitized animals. Catalase reduced the CCh potency in nonsensitized animals and animals sensitized and treated with coconut oil, indicating the participation of superoxide anion and hydrogen peroxide in the hypercontractility, which was prevented by virgin coconut oil. In the presence of L-NAME, a nitric oxide synthase (NOS) inhibitor, the CCh curve remained unchanged in nonsensitized animals but had increased efficacy and potency in sensitized animals, indicating an inhibition of endothelial NOS but ineffective in inhibiting inducible NOS. In animals sensitized and treated with coconut oil, the CCh curve was not altered, indicating a reduction in the release of NO by inducible NOS. These data were confirmed by peribronchiolar expression analysis of iNOS. The antioxidant capacity was reduced in the lungs of animals with chronic allergic lung inflammation, which was reversed by the coconut oil, and confirmed by analysis of peribronchiolar 8-iso-PGF2α content. Therefore, the virgin coconut oil supplementation reverses peribronchial inflammatory infiltrate, epithelial hyperplasia, smooth muscle thickening, and hypercontractility through oxidative stress and its interactions with the NO pathway.

scholarly journals Cutaneous, But Not Airway, Latex Exposure Induces Allergic Lung Inflammation and Airway Hyperreactivity in Mice

2005 ◽  
Vol 125 (5) ◽  
pp. 962-968 ◽  
Author(s):  
Maili Lehto ◽  
Rita Haapakoski ◽  
Henrik Wolff ◽  
Marja-Leena Majuri ◽  
Mika J. Mäkelä ◽  
...  
Keyword(s):  
Lung Inflammation ◽  
Airway Hyperreactivity ◽  
Allergic Lung Inflammation

scholarly journals A Guinea Pig Model of Airway Smooth Muscle Hyperreactivity Induced by Chronic Allergic Lung Inflammation: Contribution of Epithelium and Oxidative Stress

2019 ◽  
Vol 9 ◽  
Author(s):  
Luiz Henrique César Vasconcelos ◽  
Maria da Conceição Correia Silva ◽  
Alana Cristina Costa ◽  
Giuliana Amanda de Oliveira ◽  
Iara Leão Luna de Souza ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Smooth Muscle ◽  
Guinea Pig ◽  
Airway Smooth Muscle ◽  
Lung Inflammation ◽  
Pig Model ◽  
Allergic Lung Inflammation ◽  
Guinea Pig Model ◽  
And Oxidative Stress

Aerobic conditioning and allergic pulmonary inflammation in mice. II. Effects on lung vascular and parenchymal inflammation and remodeling

2008 ◽  
Vol 295 (4) ◽  
pp. L670-L679 ◽  
Author(s):  
Rodolfo P. Vieira ◽  
Vanessa F. de Andrade ◽  
Anna Cecília S. Duarte ◽  
Ângela B. G. dos Santos ◽  
Thaís Mauad ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Lung Inflammation ◽  
Aerobic Training ◽  
Mononuclear Cells ◽  
Muscle Thickness ◽  
Pulmonary Vessel ◽  
Pulmonary Vessels ◽  
Allergic Lung Inflammation ◽  
Aerobic Conditioning ◽  
Igf I

Recent evidence suggests that asthma leads to inflammation and remodeling not only in the airways but also in pulmonary vessels and parenchyma. In addition, some studies demonstrated that aerobic training decreases chronic allergic inflammation in the airways; however, its effects on the pulmonary vessels and parenchyma have not been previously evaluated. Our objective was to test the hypothesis that aerobic conditioning reduces inflammation and remodeling in pulmonary vessels and parenchyma in a model of chronic allergic lung inflammation. Balb/c mice were sensitized at days 0, 14, 28, and 42 and challenged with ovalbumin (OVA) from day 21 to day 50. Aerobic training started on day 21 and continued until day 50. Pulmonary vessel and parenchyma inflammation and remodeling were evaluated by quantitative analysis of eosinophils and mononuclear cells and by collagen and elastin contents and smooth muscle thickness. Immunohistochemistry was performed to quantify the density of positive cells to interleukin (IL)-2, IL-4, IL-5, interferon-γ, IL-10, monocyte chemotatic protein (MCP)-1, nuclear factor (NF)-κB p65, and insulin-like growth factor (IGF)-I. OVA exposure induced pulmonary blood vessels and parenchyma inflammation as well as increased expression of IL-4, IL-5, MCP-1, NF-κB p65, and IGF-I by inflammatory cells were reduced by aerobic conditioning. OVA exposure also induced an increase in smooth muscle thickness and elastic and collagen contents in pulmonary vessels, which were reduced by aerobic conditioning. Aerobic conditioning increased the expression of IL-10 in sensitized mice. We conclude that aerobic conditioning decreases pulmonary vascular and parenchymal inflammation and remodeling in this experimental model of chronic allergic lung inflammation in mice.

Hyperoxic exposure enhances airway reactivity of newborn guinea pigs

1993 ◽  
Vol 74 (6) ◽  
pp. 2649-2654 ◽  
Author(s):  
C. F. Uyehara ◽  
B. E. Pichoff ◽  
H. H. Sim ◽  
H. S. Uemura ◽  
K. T. Nakamura
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Guinea Pigs ◽  
Airway Hyperreactivity ◽  
Muscle Contractility ◽  
Airway Reactivity ◽  
Smooth Muscle Contractility ◽  
Contractile Responses ◽  
Hyperoxic Exposure

To determine whether altered airway smooth muscle contractility contributes to airway hyperreactivity resulting from hyperoxic exposure, in vitro contractile responses of airways to two physiological constrictors, acetylcholine (10(-9) to 10(-4) M) and histamine (10(-8) to 10(-4) M), were examined. Extrathoracic trachea, intrathoracic trachea, and bronchus from 1- to 2-day-old (newborn) guinea pigs exposed to 85% oxygen for 84 h were compared with tissues obtained from newborns reared in room air. Responses in the presence and absence of aspirin (ASA; 10(-3) M) were compared. Hyperoxic exposure did not affect the histology of the airway epithelia. Contractile responses to acetylcholine and histamine were similar. Without ASA, maximal tensions generated were higher in both extrathoracic and intrathoracic trachea obtained from hyperoxia-exposed neonates than in trachea from newborns reared in room air. ASA caused maximal tensions of trachea from newborns reared in room air to increase but did not affect the already increased contractility of trachea from hyperoxia-exposed animals; the tensions achieved in hyperoxic tissues with and without ASA were similar to the hyperactive responses induced by ASA in tissues from animals reared in room air. Bronchi showed responses similar to those seen in tracheal segments. Thus, despite no apparent histological effect on the airway epithelium, hyperoxic exposure seems to increase airway smooth muscle contractility, is nonspecific for different constricting agents, and shows no regional differences in airway reactivity.

Neutralization of either IL-17A or IL-17F is sufficient to inhibit house dust mite induced allergic asthma in mice

2017 ◽  
Vol 131 (20) ◽  
pp. 2533-2548 ◽  
Author(s):  
Pauline Chenuet ◽  
Louis Fauconnier ◽  
Fahima Madouri ◽  
Tiffany Marchiol ◽  
Nathalie Rouxel ◽  
...  
Keyword(s):  
Allergic Asthma ◽  
House Dust ◽  
House Dust Mite ◽  
Lung Inflammation ◽  
Adaptor Protein ◽  
Airway Hyperreactivity ◽  
Cell Hyperplasia ◽  
Chemokine Production ◽  
Allergic Lung Inflammation ◽  
Dust Mite

T helper (Th)17 immune response participates in allergic lung inflammation and asthma is reduced in the absence of interleukin (IL)-17 in mice. Since IL-17A and IL-17F are induced and bind the shared receptor IL-17RA, we asked whether both IL-17A and IL-17F contribute to house dust mite (HDM) induced asthma. We report that allergic lung inflammation is attenuated in absence of either IL-17A or IL-17F with reduced airway hyperreactivity, eosinophilic inflammation, goblet cell hyperplasia, cytokine and chemokine production as found in absence of IL-17RA. Furthermore, specific antibody neutralization of either IL-17A or IL-17F given during the sensitization phase attenuated allergic lung inflammation and airway hyperreactivity. In vitro activation by HDM of primary dendritic cells revealed a comparable induction of CXCL1 and IL-6 expression and the response to IL-17A and IL-17F relied on IL-17RA signaling via the adaptor protein act1 in fibroblasts. Therefore, HDM-induced allergic respiratory response depends on IL-17RA via act1 signaling and inactivation of either IL-17A or IL-17F is sufficient to attenuate allergic asthma in mice.

scholarly journals AMD3100, a CxCR4 Antagonist, Attenuates Allergic Lung Inflammation and Airway Hyperreactivity

2002 ◽  
Vol 160 (4) ◽  
pp. 1353-1360 ◽  
Author(s):  
Nicholas W. Lukacs ◽  
Aaron Berlin ◽  
Dominique Schols ◽  
Renato T. Skerlj ◽  
Gary J. Bridger
Keyword(s):  
Lung Inflammation ◽  
Airway Hyperreactivity ◽  
Cxcr4 Antagonist ◽  
Allergic Lung Inflammation

PENGARUH VIRGIN COCONUT OIL (VCO) TERHADAP KARAKTERISTIK DAN UMUR SIMPAN ROTI MANIS

2020 ◽  
Vol 5 (1) ◽  
Author(s):  
Aulia Alfi
Keyword(s):  
Moisture Content ◽  
Shelf Life ◽  
Coconut Oil ◽  
Temperature Treatment ◽  
Ash Content ◽  
Virgin Coconut Oil ◽  
Food Ingredients ◽  
Life Analysis ◽  
Antibacterial And Antifungal ◽  
Physical And Chemical

Virgin Coconut Oil (VCO) adalah bahan alami yang memiliki sifat antimikroba (antivirus, antibakteri, dan antijamur). Sehingga VCO dapat memberikan efek pengawet pada bahan makanan, salah satunya adalah roti manis. Penelitian ini dilakukan untuk mengevaluasi pengaruh VCO terhadap karakteristik (fisik dan kimia) dan umur simpan roti manis. Roti manis dianalisis secara fisik (tekstur dan porositas) dan kimia (kadar air, kadar abu, kadar lemak, kadar protein, dan kandungan karbohidrat), dan analisis umur simpan dengan FFA, uji organoleptik dan jamur setiap dua hari selama delapan hari penyimpanan di suhu ruang. Variasi perlakuan roti manis adalah dari rasio konsentrasi VCO: margarin: mentega, K (0%: 8%: 8%); A (4%: 6%: 6%); B (8%: 4%: 4%), C (12%: 2%: 2%); D (16%: 0%: 0%). Hasil penelitian menunjukkan bahwa VCO tidak memiliki pengaruh yang signifikan terhadap karakteristik fisik dan karakteristik kimia roti manis. Namun, VCO berpengaruh signifikan terhadap kadar air roti manis yang dihasilkan, roti manis K memiliki kadar air tertinggi (22,36%) dan berbeda dengan sampel roti manis lainnya. VCO secara efektif menghambat pertumbuhan jamur di roti manis pada konsentrasi 8%, 12%, dan 16%. Roti manis K dan A memiliki masa simpan 4 hari, sedangkan roti manis B, C, dan D memiliki masa simpan 6 hari.Kata kunci: VCO, roti manis, karakteristik, umur simpanABSTRACTVirgin Coconut Oil (VCO) is a natural ingredient that has antimicrobial (antiviral, antibacterial, and antifungal) properties. So that VCO can provide a preservative effect on food ingredients, one of which is sweet bread. This research was conducted to evaluate the effect of VCO on characteristics (physical and chemical) and shelf life of sweet bread. Sweet bread was analyzed physically (texture and porosity) and chemistry (moisture content, ash content, fat content, protein content, and carbohydrate content), and shelf life analysis with FFA, organoleptic and mold tests every two days for eight days of storage at ambient temperature. Treatment variations of sweet breads is from the ratio of the concentration of VCO: margarine: butter, K (0%: 8%: 8%); A (4%: 6%: 6%); B (8%: 4%: 4%), C (12%: 2%: 2%); D (16%: 0%: 0%). The results showed that VCO did not have a significant effect on the physical characteristics and chemical characteristics of sweet bread. However, the VCO has a significant effect on the water content of the sweet bread produced, sweet bread K has the highest moisture content (22,36%) and it is different from other sweet bread samples. VCO effectively inhibits the growth of sweet bread mold at concentrations of 8%, 12%, and 16%. K and A sweet bread has a shelf life of 4 days, while sweet breads B, C, and D have a shelf life of 6 days.Keywords: VCO, sweet bread, characteristics, shelf life

Effects of Virgin Coconut Oil as Adjunct Therapy in the Treatment of Allergic Rhinitis

2016 ◽  
Vol 1 (1) ◽  
pp. 22
Author(s):  
Nazli Zainuddin ◽  
Nurul Azira Mohd Shah ◽  
Rosdan Salim
Keyword(s):  
Allergic Rhinitis ◽  
Side Effects ◽  
Coconut Oil ◽  
Test Group ◽  
Nasal Symptom ◽  
Control Group ◽  
Virgin Coconut Oil ◽  
Control Groups ◽  
Significant Difference ◽  
And Control

Introduction: The role of virgin coconut oil in the treatment of allergic rhinitis is controversial. Thus, the aim of the present study is to determine the effects of virgin coconut oil ingestion, in addition to standard medications, on allergic rhinitis. We also studied the side effects of consumption of virgin coconut oil. Methods: Fifty two subjects were equally divided into test and control groups. All subjects received a daily dose of 10mg of loratadine for 28 days. The test group was given 10ml of virgin coconut oil three times a day in addition to loratadine. The symptoms of allergic rhinitis were scored at the beginning and end of the study. Results:, the symptom score were divided into nasal and non-nasal symptom scores. Sneezing score showed a significant difference, however the score was more in control group than test group, indicating that improvement in symptom was more in control group. The rest of the nasal symptom and non-nasal symptom score showed no significant difference between test and control groups. Approximately 58% of the test subjects developed side effects from consumption of virgin coconut oil, mainly gastrointestinal side effects. Conclusion: In the present study, ingestion of virgin coconut oil does not improve the overall and individual symptoms of allergic rhinitis, furthermore it has side effects.

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