دورية أكاديمية

Trypanosoma cruzi Needs a Signal Provided by Reactive Oxygen Species to Infect Macrophages.

التفاصيل البيبلوغرافية
العنوان: Trypanosoma cruzi Needs a Signal Provided by Reactive Oxygen Species to Infect Macrophages.
المؤلفون: Goes GR; Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil., Rocha PS; Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil., Diniz AR; Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil., Aguiar PH; Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil., Machado CR; Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil., Vieira LQ; Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
المصدر: PLoS neglected tropical diseases [PLoS Negl Trop Dis] 2016 Apr 01; Vol. 10 (4), pp. e0004555. Date of Electronic Publication: 2016 Apr 01 (Print Publication: 2016).
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Public Library of Science Country of Publication: United States NLM ID: 101291488 Publication Model: eCollection Cited Medium: Internet ISSN: 1935-2735 (Electronic) Linking ISSN: 19352727 NLM ISO Abbreviation: PLoS Negl Trop Dis Subsets: MEDLINE
أسماء مطبوعة: Original Publication: San Francisco, CA : Public Library of Science
مواضيع طبية MeSH: Macrophages, Peritoneal/*parasitology , Reactive Oxygen Species/*metabolism , Trypanosoma cruzi/*physiology, Animals ; Cells, Cultured ; Chagas Disease/parasitology ; Deoxyguanine Nucleotides/metabolism ; Disease Models, Animal ; Host-Parasite Interactions ; Hydrogen Peroxide/pharmacology ; Macrophages, Peritoneal/drug effects ; Membrane Glycoproteins/genetics ; Membrane Glycoproteins/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; NADPH Oxidase 2 ; NADPH Oxidases/genetics ; NADPH Oxidases/metabolism ; Oxidative Stress ; Rhodamines/metabolism ; Trypanosoma cruzi/drug effects ; Trypanosoma cruzi/genetics ; Trypanosoma cruzi/growth & development
مستخلص: Background: During Trypanosoma cruzi infection, macrophages produce reactive oxygen species (ROS) in a process called respiratory burst. Several works have aimed to elucidate the role of ROS during T. cruzi infection and the results obtained are sometimes contradictory. T. cruzi has a highly efficiently regulated antioxidant machinery to deal with the oxidative burst, but the parasite macromolecules, particularly DNA, may still suffer oxidative damage. Guanine (G) is the most vulnerable base and its oxidation results in formation of 8-oxoG, a cellular marker of oxidative stress.
Methodology/principal Findings: In order to investigate the contribution of ROS in T. cruzi survival and infection, we utilized mice deficient in the gp91phox (Phox KO) subunit of NADPH oxidase and parasites that overexpress the enzyme EcMutT (from Escherichia coli) or TcMTH (from T. cruzi), which is responsible for removing 8-oxo-dGTP from the nucleotide pool. The modified parasites presented enhanced replication inside murine inflammatory macrophages from C57BL/6 WT mice when compared with control parasites. Interestingly, when Phox KO macrophages were infected with these parasites, we observed a decreased number of all parasites when compared with macrophages from C57BL/6 WT. Scavengers for ROS also decreased parasite growth in WT macrophages. In addition, treatment of macrophages or parasites with hydrogen peroxide increased parasite replication in Phox KO mice and in vivo.
Conclusions: Our results indicate a paradoxical role for ROS since modified parasites multiply better inside macrophages, but proliferation is significantly reduced when ROS is removed from the host cell. Our findings suggest that ROS can work like a signaling molecule, contributing to T. cruzi growth inside the cells.
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المشرفين على المادة: 0 (Deoxyguanine Nucleotides)
0 (Membrane Glycoproteins)
0 (Reactive Oxygen Species)
0 (Rhodamines)
109244-58-8 (dihydrorhodamine 123)
139307-94-1 (8-oxodeoxyguanosine triphosphate)
BBX060AN9V (Hydrogen Peroxide)
EC 1.6.3.- (Cybb protein, mouse)
EC 1.6.3.- (NADPH Oxidase 2)
EC 1.6.3.- (NADPH Oxidases)
تواريخ الأحداث: Date Created: 20160402 Date Completed: 20160811 Latest Revision: 20190202
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC4818108
DOI: 10.1371/journal.pntd.0004555
PMID: 27035573
قاعدة البيانات: MEDLINE
الوصف
تدمد:1935-2735
DOI:10.1371/journal.pntd.0004555