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Article ; Online: Alpha-7 Nicotinic Receptor Agonist Protects Mice Against Pulmonary Emphysema Induced by Elastase.

Banzato, Rosana / Pinheiro-Menegasso, Nathalia M / Novelli, Fernanda Paula Roncon Santana / Olivo, Clarice R / Taguchi, Laura / de Oliveira Santos, Stheffany / Fukuzaki, Silvia / Teodoro, Walcy Paganelli Rosolia / Lopes, Fernanda D T Q S / Tibério, Iolanda F L C / de Toledo-Arruda, Alessandra Choqueta / Prado, Marco Antônio M / Prado, Vânia F / Prado, Carla M

Inflammation

2024

Abstract: Pulmonary emphysema is a primary component of chronic obstructive pulmonary disease (COPD), a life-threatening disorder characterized by lung inflammation and restricted airflow, primarily resulting from the destruction of small airways and alveolar ... ...

Abstract	Pulmonary emphysema is a primary component of chronic obstructive pulmonary disease (COPD), a life-threatening disorder characterized by lung inflammation and restricted airflow, primarily resulting from the destruction of small airways and alveolar walls. Cumulative evidence suggests that nicotinic receptors, especially the α7 subtype (α7nAChR), is required for anti-inflammatory cholinergic responses. We postulated that the stimulation of α7nAChR could offer therapeutic benefits in the context of pulmonary emphysema. To investigate this, we assessed the potential protective effects of PNU-282987, a selective α7nAChR agonist, using an experimental emphysema model. Male mice (C57BL/6) were submitted to a nasal instillation of porcine pancreatic elastase (PPE) (50 µl, 0.667 IU) to induce emphysema. Treatment with PNU-282987 (2.0 mg/kg, ip) was performed pre and post-emphysema induction by measuring anti-inflammatory effects (inflammatory cells, cytokines) as well as anti-remodeling and anti-oxidant effects. Elastase-induced emphysema led to an increase in the number of α7nAChR-positive cells in the lungs. Notably, both groups treated with PNU-282987 (prior to and following emphysema induction) exhibited a significant decrease in the number of α7nAChR-positive cells. Furthermore, both groups treated with PNU-282987 demonstrated decreased levels of macrophages, IL-6, IL-1β, collagen, and elastic fiber deposition. Additionally, both groups exhibited reduced STAT3 phosphorylation and lower levels of SOCS3. Of particular note, in the post-treated group, PNU-282987 successfully attenuated alveolar enlargement, decreased IL-17 and TNF-α levels, and reduced the recruitment of polymorphonuclear cells to the lung parenchyma. Significantly, it is worth noting that MLA, an antagonist of α7nAChR, counteracted the protective effects of PNU-282987 in relation to certain crucial inflammatory parameters. In summary, these findings unequivocally demonstrate the protective abilities of α7nAChR against elastase-induced emphysema, strongly supporting α7nAChR as a pivotal therapeutic target for ameliorating pulmonary emphysema.
Language	English
Publishing date	2024-01-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	434408-x
ISSN	1573-2576 ; 0360-3997
ISSN (online)	1573-2576
ISSN	0360-3997
DOI	10.1007/s10753-023-01953-9
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Article ; Online: Modulating asthma-COPD overlap responses with IL-17 inhibition.

Camargo, Leandro do Nascimento / Righetti, Renato Fraga / de Almeida, Francine Maria / Dos Santos, Tabata Maruyama / Fukuzaki, Silvia / Martins, Nilo Arthur Bezerra / Barbeiro, Miguel Cantadori / Saraiva-Romanholo, Beatriz Mangueira / Lopes, Fernanda Degobbi Tenorio Quirino Dos Santos / Leick, Edna Aparecida / Prado, Carla Máximo / Tibério, Iolanda de Fátima Lopes Calvo

Frontiers in immunology

2023 Volume 14, Page(s) 1271342

Abstract: Background: IL-17 is a modulator of the inflammatory response and is implicated in lung remodeling in both asthma and chronic obstructive pulmonary disease (COPD). Well as and probably in patients with asthma-COPD overlap (ACO).: Methods: In this ... ...

Abstract	Background: IL-17 is a modulator of the inflammatory response and is implicated in lung remodeling in both asthma and chronic obstructive pulmonary disease (COPD). Well as and probably in patients with asthma-COPD overlap (ACO). Methods: In this study, we evaluated the response of the airways and alveolar septa to anti-IL-17 treatment in an ACO model. Fifty-six male BALB/c mice were sensitized with ovalbumin (OVA group), received porcine pancreatic elastase (PPE group), or both (ACO group). Mice were then treated with either anti-IL-17 monoclonal antibody or saline. We evaluated hyperresponsiveness, bronchoalveolar lavage fluid (BALF) cell counts, and mean alveolar diameter. We quantified inflammatory, response, extracellular matrix remodeling, oxidative stress markers, and signaling pathway markers. Results: Anti-IL-17 treatment in the ACO anti-IL-17 group reduced the maximum response of respiratory system Rrs, Ers, Raw, Gtis, this when compared to the ACO group (p<0.05). There was a reduction in the total number of inflammatory cells, neutrophils, and macrophages in the BALF in the ACO anti-IL-17 group compared to the ACO group (p<0.05). There was attenuated dendritic cells, CD4+, CD8+, FOXP3, IL-1β, IL-2, IL-6, IL-13, IL-17, IL-33 in ACO anti-IL-17 group in airway and alveolar septum compared to the ACO group (p<0.05). We observed a reduction of MMP-9, MMP-12, TIMP-1, TGF-β, collagen type I in ACO anti-IL-17 group in airway and alveolar septum compared to the ACO group (p < 0.05). We also observed a reduction of iNOS and 8-iso-PGF2α in the airways and in the alveolar septum was reduced in the ACO anti-IL-17group compared to the ACO group (p < 0.05). Regarding the signaling pathways, NF-kB, ROCK-1, and ROCK-2 in the airway and alveolar septum were attenuated in the ACO anti-IL-17 group when compared to the ACO group (p<0.05). Conclusions: Our results suggest that inhibiting IL-17 modulates cell-associated cytokine production in lung tissue, extracellular matrix remodeling, and oxidative stress in ACO through the modulation of NF-kB and FOXP3.
MeSH term(s)	Animals ; Male ; Mice ; Asthma ; Forkhead Transcription Factors ; Interleukin-17 ; NF-kappa B ; Pulmonary Disease, Chronic Obstructive/drug therapy ; Swine
Chemical Substances	Forkhead Transcription Factors ; Interleukin-17 ; NF-kappa B
Language	English
Publishing date	2023-10-27
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1271342
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Article ; Online: Investigating the Effects of a New Peptide, Derived from the

Barbosa, Jéssica Anastácia Silva / da Silva, Luana Laura Sales / João, Juliana Morelli Lopes Gonçalves / de Campos, Elaine Cristina / Fukuzaki, Silvia / Camargo, Leandro do Nascimento / Dos Santos, Tabata Maruyama / Dos Santos, Henrique Tibucheski / Bezerra, Suellen Karoline Moreira / Saraiva-Romanholo, Beatriz Mangueira / Lopes, Fernanda Degobbi Tenório Quirino Dos Santos / Bonturi, Camila Ramalho / Oliva, Maria Luiza Vilela / Leick, Edna Aparecida / Righetti, Renato Fraga / Tibério, Iolanda de Fátima Lopes Calvo

International journal of molecular sciences

2023 Volume 24, Issue 19

Abstract: The synthesized peptide derived ... ...

Abstract	The synthesized peptide derived from
MeSH term(s)	Animals ; Mice ; Interleukin-10/metabolism ; Interleukin-17/metabolism ; Ovalbumin/metabolism ; Interleukin-13/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Nitric Oxide/metabolism ; Interleukin-6/metabolism ; Matrix Metalloproteinase 12/metabolism ; Asthma/metabolism ; Pulmonary Disease, Chronic Obstructive/metabolism ; Lung/pathology ; Inflammation/metabolism ; Protease Inhibitors/pharmacology ; Bronchoalveolar Lavage Fluid ; Oxidative Stress ; Collagen/metabolism ; Pancreatic Elastase/metabolism ; Transforming Growth Factor beta/metabolism ; Dexamethasone/pharmacology ; Mice, Inbred BALB C ; Disease Models, Animal
Chemical Substances	Interleukin-10 (130068-27-8) ; Interleukin-17 ; Ovalbumin (9006-59-1) ; Interleukin-13 ; Tumor Necrosis Factor-alpha ; Nitric Oxide (31C4KY9ESH) ; Interleukin-6 ; Matrix Metalloproteinase 12 (EC 3.4.24.65) ; Protease Inhibitors ; Collagen (9007-34-5) ; Pancreatic Elastase (EC 3.4.21.36) ; Transforming Growth Factor beta ; Dexamethasone (7S5I7G3JQL)
Language	English
Publishing date	2023-09-28
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms241914710
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Article ; Online: Effects of a Peptide Derived from the Primary Sequence of a Kallikrein Inhibitor Isolated from

Silva, Luana Laura Sales da / Barbosa, Jéssica Anastácia Silva / João, Juliana Morelli Lopes Gonçalves / Fukuzaki, Silvia / Camargo, Leandro do Nascimento / Dos Santos, Tabata Maruyama / Campos, Elaine Cristina de / Costa, Arthur Silva / Saraiva-Romanholo, Beatriz Mangueira / Bezerra, Suellen Karoline Moreira / Lopes, Fernanda Tenório Quirino Dos Santos / Bonturi, Camila Ramalho / Oliva, Maria Luiza Vilela / Leick, Edna Aparecida / Righetti, Renato Fraga / Tibério, Iolanda de Fátima Lopes Calvo

International journal of molecular sciences

2023 Volume 24, Issue 14

Abstract: 1) There are several patients with asthma-COPD overlap (ACO). A peptide derived from the primary sequence of a kallikrein inhibitor isolated ... ...

Abstract	(1) There are several patients with asthma-COPD overlap (ACO). A peptide derived from the primary sequence of a kallikrein inhibitor isolated from
MeSH term(s)	Animals ; Mice ; Bauhinia ; Interleukin-10 ; Interleukin-17 ; Ovalbumin ; Interleukin-13 ; Interleukin-5 ; Interleukin-6 ; Matrix Metalloproteinase 12 ; Tumor Necrosis Factor-alpha ; Plant Proteins/pharmacology ; Peptides/pharmacology ; Bronchoalveolar Lavage Fluid ; Asthma/drug therapy ; Kallikreins ; Pancreatic Elastase ; Dexamethasone ; Collagen ; Pulmonary Disease, Chronic Obstructive/drug therapy ; Disease Models, Animal ; Mice, Inbred BALB C
Chemical Substances	Interleukin-10 (130068-27-8) ; Interleukin-17 ; Ovalbumin (9006-59-1) ; Interleukin-13 ; Interleukin-5 ; Interleukin-6 ; Matrix Metalloproteinase 12 (EC 3.4.24.65) ; Tumor Necrosis Factor-alpha ; Plant Proteins ; Peptides ; Kallikreins (EC 3.4.21.-) ; Pancreatic Elastase (EC 3.4.21.36) ; Dexamethasone (7S5I7G3JQL) ; Collagen (9007-34-5)
Language	English
Publishing date	2023-07-09
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms241411261
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Article ; Online: Effects of environmental exposure to iron powder on healthy and elastase-exposed mice.

Galli, Thiago Tafarel / de Campos, Elaine Cristina / do Nascimento Camargo, Leandro / Fukuzaki, Silvia / Dos Santos, Tabata Marayama / Hamaguchi, Sara Sumie Sobral / Bezerra, Suellen Karoline Moreira / Silva, Fabio José Alencar / Rezende, Bianca Goulart / Dos Santos Lopes, Fernanda Tenório Quirino / Olivo, Clarice Rosa / Saraiva-Romanholo, Beatriz Mangueira / Prado, Carla Máximo / Leick, Edna Aparecida / Bourotte, Christine Laure Marie / Benseñor, Isabela Judith Martins / Lotufo, Paulo Andrade / Righetti, Renato Fraga / Tibério, Iolanda Fátima Lopes Calvo

Scientific reports

2024 Volume 14, Issue 1, Page(s) 9134

Abstract: Prolonged exposure to iron powder and other mineral dusts can threaten the health of individuals, especially those with COPD. The goal of this study was to determine how environmental exposure to metal dust from two different mining centers in Brazil ... ...

Abstract	Prolonged exposure to iron powder and other mineral dusts can threaten the health of individuals, especially those with COPD. The goal of this study was to determine how environmental exposure to metal dust from two different mining centers in Brazil affects lung mechanics, inflammation, remodeling and oxidative stress responses in healthy and elastase-exposed mice. This study divided 72 male C57Bl/6 mice into two groups, the summer group and the winter group. These groups were further divided into six groups: control, nonexposed (SAL); nonexposed, given elastase (ELA); exposed to metal powder at a mining company (SAL-L1 and ELA-L1); and exposed to a location three miles away from the mining company (SAL-L2 and ELA-L2) for four weeks. On the 29th day of the protocol, the researchers assessed lung mechanics, bronchoalveolar lavage fluid (BALF), inflammation, remodeling, oxidative stress, macrophage iron and alveolar wall alterations (mean linear intercept-Lm). The Lm was increased in the ELA, ELA-L1 and ELA-L2 groups compared to the SAL group (p < 0.05). There was an increase in the total number of cells and macrophages in the ELA-L1 and ELA-L2 groups compared to the other groups (p < 0.05). Compared to the ELA and SAL groups, the exposed groups (ELA-L1, ELA-L2, SAL-L1, and SAL-L2) exhibited increased expression of IL-1β, IL-6, IL-10, IL-17, TNF-α, neutrophil elastase, TIMP-1, MMP-9, MMP-12, TGF-β, collagen fibers, MUC5AC, iNOS, Gp91phox, NFkB and iron positive macrophages (p < 0.05). Although we did not find differences in lung mechanics across all groups, there were low to moderate correlations between inflammation remodeling, oxidative stress and NFkB with elastance, resistance of lung tissue and iron positive macrophages (p < 0.05). Environmental exposure to iron, confirmed by evaluation of iron in alveolar macrophages and in air, exacerbated inflammation, initiated remodeling, and induced oxidative stress responses in exposed mice with and without emphysema. Activation of the iNOS, Gp91phox and NFkB pathways play a role in these changes.
MeSH term(s)	Animals ; Male ; Mice ; Bronchoalveolar Lavage Fluid/chemistry ; Environmental Exposure/adverse effects ; Inflammation/metabolism ; Inflammation/chemically induced ; Iron/toxicity ; Lung/drug effects ; Lung/metabolism ; Lung/pathology ; Mice, Inbred C57BL ; Oxidative Stress/drug effects ; Pancreatic Elastase/metabolism ; Pancreatic Elastase/pharmacology ; Powders/toxicity
Chemical Substances	Iron (E1UOL152H7) ; Pancreatic Elastase (EC 3.4.21.36) ; Powders
Language	English
Publishing date	2024-04-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-024-59573-8
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Article ; Online: Effect of anti-IL17 and/or Rho-kinase inhibitor treatments on vascular remodeling induced by chronic allergic pulmonary inflammation.

Dos Santos, Tabata M / Righetti, Renato F / Rezende, Bianca G / Campos, Elaine C / Camargo, Leandro do N / Saraiva-Romanholo, Beatriz M / Fukuzaki, Silvia / Prado, Carla M / Leick, Edna A / Martins, Milton A / Tibério, Iolanda F L C

Therapeutic advances in respiratory disease

2020 Volume 14, Page(s) 1753466620962665

Abstract: Background and aims: Expansion and morphological dysregulation of the bronchial vascular network occurs in asthmatic airways. Interleukin (IL) -17 and Rho-kinase (ROCK) are known to act in inflammation control and remodeling. Modulation of Rho-kinase ... ...

Abstract	Background and aims: Expansion and morphological dysregulation of the bronchial vascular network occurs in asthmatic airways. Interleukin (IL) -17 and Rho-kinase (ROCK) are known to act in inflammation control and remodeling. Modulation of Rho-kinase proteins and IL-17 may be a promising approach for the treatment of asthma through the control of angiogenesis. Our objective was to analyze the effects of treatment with anti-IL17 and/or Rho-kinase inhibitor on vascular changes in mice with chronic allergic pulmonary inflammation. Methods: Sixty-four BALB/c mice, with pulmonary inflammation induced by ovalbumin were treated with anti-IL17A (7.5/µg per dose, intraperitoneal) and/or Rho-kinase inhibitor (Y-27632-10 mg/kg, intranasal), 1 h before each ovalbumin challenge (22, 24, 26, and 28/days). Control animals were made to inhale saline. At the end of the protocol, lungs were removed, and morphometric analysis was performed to quantify vascular inflammatory, remodeling, and oxidative stress responses. Results: Anti-IL17 or Rho-kinase inhibitor reduced the number of CD4 Conclusion: We observed no difference in angiogenesis after treatment with Rho-kinase inhibitor and anti-IL17. Although the treatments did not show differences in angiogenesis, they showed differences in the markers involved in the angiogenesis process contributing to inflammation control and vascular remodeling.
MeSH term(s)	Amides/pharmacology ; Animals ; Asthma/physiopathology ; Biomarkers/metabolism ; Cytokines/metabolism ; Enzyme Inhibitors/pharmacology ; Interleukin-17/antagonists & inhibitors ; Isoprostanes/metabolism ; Mice, Inbred BALB C ; Nitric Oxide Synthase/metabolism ; Pneumonia/physiopathology ; Pyridines/pharmacology ; Vascular Remodeling/drug effects ; Vascular Remodeling/physiology ; rho-Associated Kinases/antagonists & inhibitors ; rho-Associated Kinases/metabolism
Chemical Substances	Amides ; Biomarkers ; Cytokines ; Enzyme Inhibitors ; IL17A protein, human ; Interleukin-17 ; Isoprostanes ; Pyridines ; Y 27632 (138381-45-0) ; Nitric Oxide Synthase (EC 1.14.13.39) ; Rock1 protein, mouse (EC 2.7.11.1) ; Rock2 protein, mouse (EC 2.7.11.1) ; rho-Associated Kinases (EC 2.7.11.1)
Language	English
Publishing date	2020-12-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2476459-0
ISSN	1753-4666 ; 1753-4658
ISSN (online)	1753-4666
ISSN	1753-4658
DOI	10.1177/1753466620962665
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Article: Bronchial Vascular Remodeling Is Attenuated by Anti-IL-17 in Asthmatic Responses Exacerbated by LPS.

Camargo, Leandro do Nascimento / Dos Santos, Tabata Maruyama / de Andrade, Felipp Costa Pinto / Fukuzaki, Silvia / Dos Santos Lopes, Fernanda Degobbi Tenorio Quirino / de Arruda Martins, Milton / Prado, Carla Máximo / Leick, Edna Aparecida / Righetti, Renato Fraga / Tibério, Iolanda de Fátima Lopes Calvo

Frontiers in pharmacology

2020 Volume 11, Page(s) 1269

Abstract: Introduction: Although the major alterations associated with asthma are related to the airways, there is also evidence of the importance of peribronchial vascular inflammation and remodeling in its pathophysiology.: Objectives: To determine the ... ...

Abstract	Introduction: Although the major alterations associated with asthma are related to the airways, there is also evidence of the importance of peribronchial vascular inflammation and remodeling in its pathophysiology. Objectives: To determine the effects of anti-IL-17 therapy on peribronchial vessels of an asthma model exacerbated by lipopolysaccharide. Methods: We evaluated several factors, including lung function, inflammation, oxidative stress, vascular remodeling, and signaling pathways present in the peribronchial vessels of 66 male BALB/c mice exposed to ovalbumin and treated (or not) treated with anti-IL-17. Twenty-four hours before the end of the experimental protocol, groups of sensitized animals (OVA-LPS and OVA-LPS anti-IL-17) also received LPS. Results: The OVA-LPS-anti-IL-17 group presented a decrease in several factors [airway resistance and elastance, bronchoalveolar lavage fluid (BALF) cell counts, inflammatory response, eosinophils, TSLP, IL-33, TARC, TNF-α, CD4+, CD8+, IL-4, IL-6, IL-10, IL-17, and VEGF positive cells/10 Conclusions: In this model of LPS-induced asthma exacerbation, IL-17 inhibition represents a promising therapeutic strategy, indicating the potential of bronchial vascular control of Th2 and Th17 responses and the activation of the remodeling and oxidative stress pathways, associated with the control of signaling pathways.
Language	English
Publishing date	2020-09-04
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2020.01269
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Article ; Online: Preventive and therapeutic effect of anti-IL-17 in an experimental model of elastase-induced lung injury in C57Bl6 mice.

Fukuzaki, Silvia / Righetti, Renato Fraga / Santos, Tabata Maruyama Dos / Camargo, Leandro do Nascimento / Aristóteles, Luciana R C R B / Souza, Flavia C R / Garrido, Aurelio C / Saraiva-Romanholo, Beatriz Mangueira / Leick, Edna Aparecida / Prado, Carla Máximo / Martins, Mílton de Arruda / Tibério, Iolanda de Fátima Lopes Calvo

American journal of physiology. Cell physiology

2020 Volume 320, Issue 3, Page(s) C341–C354

Abstract: Chronic obstructive pulmonary disease (COPD) is an important health care issue, and IL-17 can modulate inflammatory responses. We evaluated preventive and therapeutic effect of anti-interleukin (IL)-17 in a model of lung injury induced by elastase, using ...

Abstract	Chronic obstructive pulmonary disease (COPD) is an important health care issue, and IL-17 can modulate inflammatory responses. We evaluated preventive and therapeutic effect of anti-interleukin (IL)-17 in a model of lung injury induced by elastase, using 32 male C57Bl6 mice, divided into 4 groups: SAL, ELASTASE CONTROL (EC), ELASTASE + PREVENTIVE ANTI-IL-17 (EP), and ELASTASE + THERAPEUTIC ANTI-IL-17 (ET). On the 29th day, animals were anesthetized with thiopental, tracheotomized, and placed on a ventilator to evaluate lung mechanical, exhaled nitric oxide (eNO), and total cells of bronchoalveolar lavage fluid was collected. We performed histological techniques, and linear mean intercept (Lm) was analyzed. Both treatments with anti-IL-17 decreased respiratory resistance and elastance, airway resistance, elastance of pulmonary parenchyma, eNO, and Lm compared with EC. There was reduction in total cells and macrophages in ET compared with EC. Both treatments decreased nuclear factor-кB, inducible nitric oxide synthase, matrix metalloproteinase (MMP)-9, MMP-12, transforming growth factor-β, tumor necrosis factor-α, neutrophils, IL-1β, isoprostane, and IL-17 in airways and alveolar septa; collagen fibers, decorin and lumican in airways; and elastic fibers and fibronectin in alveolar septa compared with EC. There was reduction of collagen fibers in alveolar septa and biglycan in airways in EP and a reduction of eNO synthase in airways in ET. In conclusion, both treatments with anti-IL-17 contributed to improve most of parameters evaluated in inflammation and extracellular matrix remodeling in this model of lung injury.
MeSH term(s)	Animals ; Bronchoalveolar Lavage Fluid ; Disease Models, Animal ; Inflammation/metabolism ; Interleukin-17/metabolism ; Lung/metabolism ; Lung Injury/metabolism ; Macrophages/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Neutrophils/metabolism ; Nitric Oxide Synthase Type II/metabolism ; Pancreatic Elastase/metabolism ; Pulmonary Disease, Chronic Obstructive/metabolism
Chemical Substances	Il17a protein, mouse ; Interleukin-17 ; Nitric Oxide Synthase Type II (EC 1.14.13.39) ; Pancreatic Elastase (EC 3.4.21.36)
Language	English
Publishing date	2020-12-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00017.2020
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Article: Effect of Anti-IL17 Antibody Treatment Alone and in Combination With Rho-Kinase Inhibitor in a Murine Model of Asthma.

Dos Santos, Tabata M / Righetti, Renato F / Camargo, Leandro do N / Saraiva-Romanholo, Beatriz M / Aristoteles, Luciana R C R B / de Souza, Flávia C R / Fukuzaki, Silvia / Alonso-Vale, Maria I C / Cruz, Maysa M / Prado, Carla M / Leick, Edna A / Martins, Milton A / Tibério, Iolanda F L C

Frontiers in physiology

2018 Volume 9, Page(s) 1183

Abstract: Background: ...

Abstract	Background:
Language	English
Publishing date	2018-09-05
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2018.01183
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Article: Effects of Anti-IL-17 on Inflammation, Remodeling, and Oxidative Stress in an Experimental Model of Asthma Exacerbated by LPS.

Camargo, Leandro do Nascimento / Righetti, Renato Fraga / Aristóteles, Luciana Ritha de Cássia Rolim Barbosa / Dos Santos, Tabata Maruyama / de Souza, Flávia Castro Ribas / Fukuzaki, Silvia / Cruz, Maysa Mariana / Alonso-Vale, Maria Isabel Cardoso / Saraiva-Romanholo, Beatriz Mangueira / Prado, Carla Máximo / Martins, Mílton de Arruda / Leick, Edna Aparecida / Tibério, Iolanda de Fátima Lopes Calvo

Frontiers in immunology

2017 Volume 8, Page(s) 1835

Abstract: Inflammation plays a central role in the development of asthma, which is considered an allergic disease with a classic Th2 inflammatory profile. However, cytokine IL-17 has been examined to better understand the pathophysiology of this disease. Severe ... ...

Abstract	Inflammation plays a central role in the development of asthma, which is considered an allergic disease with a classic Th2 inflammatory profile. However, cytokine IL-17 has been examined to better understand the pathophysiology of this disease. Severe asthmatic patients experience frequent exacerbations, leading to infection, and subsequently show altered levels of inflammation that are unlikely to be due to the Th2 immune response alone. This study estimates the effects of anti-IL-17 therapy in the pulmonary parenchyma in a murine asthma model exacerbated by LPS. BALB/c mice were sensitized with intraperitoneal ovalbumin and repeatedly exposed to inhalation with ovalbumin, followed by treatment with or without anti-IL-17. Twenty-four hours prior to the end of the 29-day experimental protocol, the two groups received LPS (0.1 mg/ml intratracheal OVA-LPS and OVA-LPS IL-17). We subsequently evaluated bronchoalveolar lavage fluid, performed a lung tissue morphometric analysis, and measured IL-6 gene expression. OVA-LPS-treated animals treated with anti-IL-17 showed decreased pulmonary inflammation, edema, oxidative stress, and extracellular matrix remodeling compared to the non-treated OVA and OVA-LPS groups (
Language	English
Publishing date	2017
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2017.01835
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In stock of ZB MED Cologne/Königswinter

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Order via subito