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Article ; Online: Beneficial effects of acetylsalicylic acid (aspirin) on the actions of extracellular vesicles shed by Trypanosoma cruzi in macrophages.

Dos Santos, Lucas Felipe / Rodrigues, Gabriella Ferreira / Malvezi, Aparecida Donizette / de Souza, Mariana / Nakama, Raquel Pires / Lovo-Martins, Maria Isabel / Pinge-Filho, Phileno

Parasitology international

2022 Volume 92, Page(s) 102697

Abstract: Trypomastigote forms of Trypanosoma cruzi, the causative agent of Chagas disease, shed extracellular vesicles (EVs) that promote the susceptibility of host cells to infection. During T. cruzi infection, the immune response of the host is important for ... ...

Abstract	Trypomastigote forms of Trypanosoma cruzi, the causative agent of Chagas disease, shed extracellular vesicles (EVs) that promote the susceptibility of host cells to infection. During T. cruzi infection, the immune response of the host is important for controlling parasitism, which is necessary for survival. Macrophages produce inflammatory mediators, such as eicosanoids and nitric oxide (NO), with trypanocidal effects that control the parasite load in the early stages of the disease. In this study, we evaluated the contribution of host cyclooxygenase (COX) to the actions of EVs shed by T. cruzi strain Y (EVs-Y) in infected macrophages. RAW 264.7 macrophages exposed to EVs-Y and then infected with trypomastigote forms of T. cruzi produced less NO, and an increased number of trypomastigote forms were internalized in the cell compared to the controls, indicating that the effects exerted by EVs-Y favor the parasite. Interestingly, when macrophages were pretreated with acetylsalicylic acid, a dual COX inhibitor, before exposure to EVs-Y and subsequent infection with trypomastigote forms, there was an increase in NO production and a decrease in trypomastigote uptake compared to the controls. These results suggest that EVs-Y modulates the macrophage response in favor of T. cruzi and indicate a role for COX in the effects of EVs.
MeSH term(s)	Humans ; Trypanosoma cruzi ; Aspirin/pharmacology ; Chagas Disease ; Extracellular Vesicles ; Macrophages ; Cyclooxygenase 2 ; Nitric Oxide
Chemical Substances	Aspirin (R16CO5Y76E) ; Cyclooxygenase 2 (EC 1.14.99.1) ; Nitric Oxide (31C4KY9ESH)
Language	English
Publishing date	2022-11-01
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1363151-2
ISSN	1873-0329 ; 1383-5769
ISSN (online)	1873-0329
ISSN	1383-5769
DOI	10.1016/j.parint.2022.102697
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Article: Antiprotozoal Activity of Benzoylthiourea Derivatives against

Pereira, Patrícia Morais Lopes / Fernandes, Bruna Terci / Dos Santos, Vitória Ribeiro / Cabral, Weslei Roberto Correia / Lovo-Martins, Maria Isabel / Alonso, Lais / Lancheros, César Armando Contreras / de Paula, Jéssica Carreira / Camargo, Priscila Goes / Suzukawa, Helena Tiemi / Alonso, Antônio / Macedo, Fernando / Nakamura, Celso Vataru / Tavares, Eliandro Reis / de Lima Ferreira Bispo, Marcelle / Yamauchi, Lucy Megumi / Pinge-Filho, Phileno / Yamada-Ogatta, Sueli Fumie

Pathogens (Basel, Switzerland)

2023 Volume 12, Issue 8

Abstract: For decades, only two nitroheterocyclic drugs have been used as therapeutic agents for Chagas disease. However, these drugs present limited effectiveness during the chronic phase, possess unfavorable pharmacokinetic properties, and induce severe adverse ... ...

Abstract	For decades, only two nitroheterocyclic drugs have been used as therapeutic agents for Chagas disease. However, these drugs present limited effectiveness during the chronic phase, possess unfavorable pharmacokinetic properties, and induce severe adverse effects, resulting in low treatment adherence. A previous study reported that
Language	English
Publishing date	2023-08-03
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2695572-6
ISSN	2076-0817
ISSN	2076-0817
DOI	10.3390/pathogens12081012
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Article ; Online: Metabolic syndrome improves cardiovascular dysfunction and survival during cecal ligation and puncture-induced mild sepsis in mice.

Nakama, Raquel Pires / Malvezi, Aparecida Donizette / Lovo-Martins, Maria Isabel / Dos Santos, Lucas Felipe / Canizares Cardoso, Ana Paula / Scacco, Gustavo / de Freitas, Andressa Mendes Dionísio / Martins-Pinge, Marli Cardoso / Pinge-Filho, Phileno

Life sciences

2021 Volume 286, Page(s) 120033

Abstract: Aims: Sepsis is a potentially fatal systemic inflammatory response and its underlying pathophysiology is still poorly understood. Studies suggest that obesity, a component of metabolic syndrome (MS), is associated with sepsis survival. Therefore, this ... ...

Abstract	Aims: Sepsis is a potentially fatal systemic inflammatory response and its underlying pathophysiology is still poorly understood. Studies suggest that obesity, a component of metabolic syndrome (MS), is associated with sepsis survival. Therefore, this study focused on investigating the influence of MS on mortality and cardiovascular dysfunction induced by sublethal cecal ligation and puncture (SL-CLP). Main methods: Newborn Swiss mice received monosodium glutamate (MSG) (4 mg kg Key findings: MS improved the survival of septic mice, preventing impairment to hematological and cardiovascular parameters. In addition, MS attenuated plasmatic NO increase, which is a typical feature of sepsis. Significance: These findings provide new insights into the relationship between obesity and mild sepsis in mice, thus revealing an approach in favor of the "obesity paradox."
MeSH term(s)	Animals ; Cardiovascular System/physiopathology ; Cecum/pathology ; Disease Models, Animal ; Ligation ; Metabolic Syndrome/physiopathology ; Mice ; Nitric Oxide/metabolism ; Punctures ; Sepsis/etiology ; Survival Analysis
Chemical Substances	Nitric Oxide (31C4KY9ESH)
Language	English
Publishing date	2021-10-08
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2021.120033
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Article ; Online: Concanavalin-A stimulates IL-17 and nitric oxide production and induces macrophage polarization and resistance to Trypanosoma cruzi infection.

Zanluqui, Nágela Ghabdan / Lovo-Martins, Maria Isabel / Malvezi, Aparecida Donizette / Panis, Carolina / da Silva, Rosiane Valeriano / Tatakihara, Vera Lucia Hideko / Felipe, Ionice / Martins-Pinge, Marli Cardoso / Wowk, Pryscilla Fanini / Pinge-Filho, Phileno

Life sciences

2020 Volume 258, Page(s) 118137

Abstract: Aims: Chagas disease is a neglected tropical disease. The ability of Trypanosoma cruzi to survive within phagocytes is likely a critical factor for T. cruzi dissemination in the host. For control of the parasite load and host survival, macrophage action ...

Abstract	Aims: Chagas disease is a neglected tropical disease. The ability of Trypanosoma cruzi to survive within phagocytes is likely a critical factor for T. cruzi dissemination in the host. For control of the parasite load and host survival, macrophage action is required. Concanavalin-A (Con-A) presents properties that modulate immune functions and protect hosts from several experimental infectious diseases. Here, we evaluated the effects of Con-A on peritoneal macrophages as well as on the course of experimental infection by T. cruzi. Main methods: BALB/c mice, a susceptible model for T. cruzi infection, were treated with Con-A via the intraperitoneal route and 3 days later infected with T. cruzi. We quantified parasitemia, cytokines and nitric oxide (NO). Peritoneal exudate and macrophages were collected for macrophage phenotyping and cell viability, NO and cytokine detection, as well as for T. cruzi internalization and release index determination. Key findings: Con-A treatment induced IL-17a and NO production by cells from the peritoneal cavity, and M1 marker expression predominated on peritoneal macrophages. These cells are also more prone to producing TNF-α, IL-6 and NO when infected by T. cruzi and show high trypanocidal capacity. Due to a hostile peritoneal microenvironment caused by Con-A, which induces macrophage cNOS and iNOS expression, infected BALB/c mice showed reduced parasitemia and an increased survival rate. Significance: We conclude that Con-A can induce peritoneal M1 macrophage polarization to increase trypanocidal activity, resulting in ameliorated systemic infection in a susceptible experimental model.
MeSH term(s)	Animals ; Cell Polarity/drug effects ; Chagas Disease/metabolism ; Chagas Disease/pathology ; Concanavalin A/pharmacology ; Female ; Interleukin-17/metabolism ; Macrophages, Peritoneal/drug effects ; Macrophages, Peritoneal/parasitology ; Macrophages, Peritoneal/pathology ; Mice, Inbred BALB C ; Nitric Oxide/metabolism ; Nitric Oxide Synthase Type II/metabolism ; Parasitemia/metabolism ; Parasitemia/pathology ; Trypanosoma cruzi/drug effects ; Trypanosoma cruzi/physiology
Chemical Substances	Interleukin-17 ; Concanavalin A (11028-71-0) ; Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase Type II (EC 1.14.13.39)
Language	English
Publishing date	2020-07-24
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2020.118137
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Article ; Online: Patterns of cell death induced by metformin in human MCF-7 breast cancer cells.

Dias Lopes, Natália Medeiros / Marinello, Poliana Camila / Sanches, Larissa Juliani / da Silva Brito, Walison Augusto / Lovo-Martins, Maria Isabel / Pinge-Filho, Phileno / Luiz, Rodrigo Cabral / Cecchini, Rubens / Cecchini, Alessandra Lourenço

Pathology, research and practice

2020 Volume 216, Issue 11, Page(s) 153199

Abstract: The ability to evade apoptosis is an important mechanism of drug resistance and tumor progression in breast cancer. The induction of different pathways of cell death could be an important strategy to limit tumor progression. Metformin, a drug used to ... ...

Abstract	The ability to evade apoptosis is an important mechanism of drug resistance and tumor progression in breast cancer. The induction of different pathways of cell death could be an important strategy to limit tumor progression. Metformin, a drug used to treat type two diabetes, has demonstrated promising results in breast cancer experiments. However, little is known about the patterns of cell death induced by this drug. We analyzed the involvement of apoptosis, necroptosis and ferroptosis in the toxicity of metformin in MCF-7 cells, evaluating proliferation, viability and oxidative stress. It was used different inhibitors of cell death: Z-VAD, a pan-caspase inhibitor that blocks apoptosis; Necrostatin-1, which inhibits RIPK1 activity and blocks necroptosis; and the iron chelator, deferoxamine, that chelates iron and prevents ferroptosis. The participation of oxidative stress was analyzed through the evaluation of total thiols, reduced glutathione (GSH) and malondialdehyde (MDA). Our results showed that metformin increased cell death, reduced proliferation, thiol and GSH and increased MDA in cells. After the association between metformin and Z-VAD or Necrostatin-1, the drug toxicity was abolished. Ferroptosis did not significantly enrolled in metformin action against MCF-7 cells. The preservation of cellular antioxidants was found in all situations that cell death was blocked. Together, these results reveals that metformin induces necroptosis and apoptosis in MCF-7 cells and oxidative stress generation play a role in these two pathways of cell death. This information could help future studies to improve strategies to breast cancer treatment.
MeSH term(s)	Apoptosis/drug effects ; Ferroptosis/drug effects ; Glutathione/metabolism ; Humans ; Hypoglycemic Agents/pharmacology ; MCF-7 Cells ; Malondialdehyde/metabolism ; Metformin/pharmacology ; Necroptosis/drug effects ; Oligopeptides/pharmacology ; Oxidative Stress/drug effects ; Reactive Oxygen Species/metabolism ; Sulfhydryl Compounds/metabolism
Chemical Substances	Hypoglycemic Agents ; Oligopeptides ; Reactive Oxygen Species ; Sulfhydryl Compounds ; benzyloxycarbonyl-valyl-alanyl-aspartic acid ; Malondialdehyde (4Y8F71G49Q) ; Metformin (9100L32L2N) ; Glutathione (GAN16C9B8O)
Language	English
Publishing date	2020-09-06
Publishing country	Germany
Document type	Journal Article
ZDB-ID	391889-0
ISSN	1618-0631 ; 0344-0338
ISSN (online)	1618-0631
ISSN	0344-0338
DOI	10.1016/j.prp.2020.153199
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Article ; Online: Combination Therapy Using Benznidazole and Aspirin during the Acute Phase of Experimental Chagas Disease Prevents Cardiovascular Dysfunction and Decreases Typical Cardiac Lesions in the Chronic Phase.

Pereira, Rito Santo / Malvezi, Aparecida Donizette / Lovo-Martins, Maria Isabel / Lucchetti, Bruno Fernando Cruz / Santos, Jussevania Pereira / Tavares, Eliandro Reis / Verri, Waldiceu Aparecido / de Almeida Araújo, Eduardo José / Yamauchi, Lucy Megumi / Yamada-Ogatta, Sueli Fumie / Martins-Pinge, Marli Cardoso / Pinge-Filho, Phileno

Antimicrobial agents and chemotherapy

2020 Volume 64, Issue 7

Abstract: Chagas disease, caused by the ... ...

Abstract	Chagas disease, caused by the protozoan
MeSH term(s)	Animals ; Aspirin/therapeutic use ; Chagas Disease/drug therapy ; Drug Combinations ; Humans ; Mice ; Nitroimidazoles/pharmacology ; Nitroimidazoles/therapeutic use ; Trypanocidal Agents/therapeutic use ; Trypanosoma cruzi
Chemical Substances	Drug Combinations ; Nitroimidazoles ; Trypanocidal Agents ; Aspirin (R16CO5Y76E) ; benzonidazole (YC42NRJ1ZD)
Language	English
Publishing date	2020-06-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	217602-6
ISSN	1098-6596 ; 0066-4804
ISSN (online)	1098-6596
ISSN	0066-4804
DOI	10.1128/AAC.00069-20
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Article: Metabolic syndrome improves cardiovascular dysfunction and survival during cecal ligation and puncture-induced mild sepsis in mice

Nakama, Raquel Pires / Malvezi, Aparecida Donizette / Lovo-Martins, Maria Isabel / dos Santos, Lucas Felipe / Canizares Cardoso, Ana Paula / Scacco, Gustavo / de Freitas, Andressa Mendes Dionísio / Martins-Pinge, Marli Cardoso / Pinge-Filho, Phileno

Life sciences. 2021 Dec. 01, v. 286

2021

Abstract: Sepsis is a potentially fatal systemic inflammatory response and its underlying pathophysiology is still poorly understood. Studies suggest that obesity, a component of metabolic syndrome (MS), is associated with sepsis survival. Therefore, this study ... ...

Abstract	Sepsis is a potentially fatal systemic inflammatory response and its underlying pathophysiology is still poorly understood. Studies suggest that obesity, a component of metabolic syndrome (MS), is associated with sepsis survival. Therefore, this study focused on investigating the influence of MS on mortality and cardiovascular dysfunction induced by sublethal cecal ligation and puncture (SL-CLP).Newborn Swiss mice received monosodium glutamate (MSG) (4 mg kg⁻¹ day⁻¹, s.c.) during the first 5 d of life for MS induction, while the control pups received equimolar saline solution. On the 75th day, SL-CLP was used to induce mild sepsis (M-CLP) in the MS (MS-M-CLP) and control (SAL-M-CLP) mice. The effect of MS on sepsis in mice was assessed by determining the survival rate and quantification of nitric oxide (NO) in the plasma, and associating this data with hematological and cardiovascular parameters.MS improved the survival of septic mice, preventing impairment to hematological and cardiovascular parameters. In addition, MS attenuated plasmatic NO increase, which is a typical feature of sepsis.These findings provide new insights into the relationship between obesity and mild sepsis in mice, thus revealing an approach in favor of the “obesity paradox.”
Keywords	inflammation ; metabolic syndrome ; monosodium glutamate ; nitric oxide ; obesity ; pathophysiology ; sodium chloride ; survival rate
Language	English
Dates of publication	2021-1201
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2021.120033
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Article: Extracellular Vesicles Shed By

Lovo-Martins, Maria Isabel / Malvezi, Aparecida Donizette / Zanluqui, Nágela Ghabdan / Lucchetti, Bruno Fernando Cruz / Tatakihara, Vera Lúcia Hideko / Mörking, Patricia Alves / de Oliveira, Admilton Gonçalves / Goldenberg, Samuel / Wowk, Pryscilla Fanini / Pinge-Filho, Phileno

Frontiers in immunology

2018 Volume 9, Page(s) 896

Abstract: During the onset ... ...

Abstract	During the onset of
MeSH term(s)	Animals ; Cercopithecus aethiops ; Chagas Disease/immunology ; Chagas Disease/parasitology ; Dinoprostone/immunology ; Dinoprostone/metabolism ; Disease Models, Animal ; Extracellular Vesicles/immunology ; Host-Parasite Interactions/immunology ; Humans ; Immune Evasion ; Lipid Droplets/immunology ; Lipid Droplets/metabolism ; Macrophage Activation/immunology ; Macrophages, Peritoneal/immunology ; Macrophages, Peritoneal/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Spleen/cytology ; Spleen/immunology ; Trypanosoma cruzi/immunology ; Trypanosoma cruzi/metabolism ; Vero Cells
Chemical Substances	Dinoprostone (K7Q1JQR04M)
Language	English
Publishing date	2018-04-27
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2018.00896
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Article ; Online: Metabolic syndrome agravates cardiovascular, oxidative and inflammatory dysfunction during the acute phase of Trypanosoma cruzi infection in mice.

Lucchetti, Bruno Fernando Cruz / Boaretto, Natalia / Lopes, Fernanda Novi Cortegoso / Malvezi, Aparecida Donizette / Lovo-Martins, Maria Isabel / Tatakihara, Vera Lúcia Hideko / Fattori, Victor / Pereira, Rito Santo / Verri, Waldiceu Aparecido / de Almeida Araujo, Eduardo Jose / Pinge-Filho, Phileno / Martins-Pinge, Marli Cardoso

Scientific reports

2019 Volume 9, Issue 1, Page(s) 18885

Abstract: We evaluated the influence of metabolic syndrome (MS) on acute Trypanosoma cruzi infection. Obese Swiss mice, 70 days of age, were subjected to intraperitoneal infection with 5 × ... ...

Abstract	We evaluated the influence of metabolic syndrome (MS) on acute Trypanosoma cruzi infection. Obese Swiss mice, 70 days of age, were subjected to intraperitoneal infection with 5 × 10
MeSH term(s)	Adipose Tissue/metabolism ; Adipose Tissue/pathology ; Animals ; Chagas Disease/complications ; Chagas Disease/metabolism ; Chagas Disease/pathology ; Cytokines/blood ; Disease Models, Animal ; Fatty Liver/metabolism ; Fatty Liver/pathology ; Inflammation/complications ; Inflammation/metabolism ; Inflammation/pathology ; Insulin Resistance/physiology ; Liver/metabolism ; Liver/pathology ; Male ; Metabolic Syndrome/complications ; Metabolic Syndrome/metabolism ; Metabolic Syndrome/pathology ; Mice ; Myocardium/metabolism ; Myocardium/pathology ; Oxidative Stress/physiology ; Trypanosoma cruzi
Chemical Substances	Cytokines
Language	English
Publishing date	2019-12-11
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/s41598-019-55363-9
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Article: Concanavalin-A stimulates IL-17 and nitric oxide production and induces macrophage polarization and resistance to Trypanosoma cruzi infection

Life sciences. 2020 Oct. 01, v. 258

2020

Abstract: Chagas disease is a neglected tropical disease. The ability of Trypanosoma cruzi to survive within phagocytes is likely a critical factor for T. cruzi dissemination in the host. For control of the parasite load and host survival, macrophage action is ... ...

Abstract	Chagas disease is a neglected tropical disease. The ability of Trypanosoma cruzi to survive within phagocytes is likely a critical factor for T. cruzi dissemination in the host. For control of the parasite load and host survival, macrophage action is required. Concanavalin-A (Con-A) presents properties that modulate immune functions and protect hosts from several experimental infectious diseases. Here, we evaluated the effects of Con-A on peritoneal macrophages as well as on the course of experimental infection by T. cruzi.BALB/c mice, a susceptible model for T. cruzi infection, were treated with Con-A via the intraperitoneal route and 3 days later infected with T. cruzi. We quantified parasitemia, cytokines and nitric oxide (NO). Peritoneal exudate and macrophages were collected for macrophage phenotyping and cell viability, NO and cytokine detection, as well as for T. cruzi internalization and release index determination.Con-A treatment induced IL-17a and NO production by cells from the peritoneal cavity, and M1 marker expression predominated on peritoneal macrophages. These cells are also more prone to producing TNF-α, IL-6 and NO when infected by T. cruzi and show high trypanocidal capacity. Due to a hostile peritoneal microenvironment caused by Con-A, which induces macrophage cNOS and iNOS expression, infected BALB/c mice showed reduced parasitemia and an increased survival rate.We conclude that Con-A can induce peritoneal M1 macrophage polarization to increase trypanocidal activity, resulting in ameliorated systemic infection in a susceptible experimental model.
Keywords	Chagas disease ; Trypanosoma cruzi ; cell viability ; concanavalin A ; interleukin-17 ; interleukin-6 ; macrophages ; models ; nitric oxide ; parasite load ; parasitemia ; phenotype ; tropical diseases
Language	English
Dates of publication	2020-1001
Publishing place	Elsevier Inc.
Document type	Article
Note	NAL-light
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2020.118137
Database	NAL-Catalogue (AGRICOLA)

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