Activation of the P2X7 receptor triggers the elimination of Toxoplasma gondii tachyzoites from infected macrophages

Corrêa, Gladys; Silva, Camila Marques da; Moreira-Souza, Aline Cristina Abreu; Vommaro, Rossiane C.; Coutinho‐Silva, Robson

doi:10.1016/j.micinf.2010.03.004

Cited by 90 publications

(97 citation statements)

References 29 publications

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“…P2X7-induced ROS formation has been previously observed in myeloid cells [6][7][8][9][10][11][12]35], glomerular mesangial cells [36] and submandibular gland cells [30,31], but to the best of our knowledge, the current study is the first to demonstrate that P2X7 activation causes ROS formation in erythroid cells. It will be of future importance to determine if P2X7 induces ROS formation in primary erythroid cells.…”

Section: Discussionmentioning

confidence: 46%

“…The various biological roles attributed to P2X7 are the result of various signalling events downstream of P2X7 activation including reactive oxygen species (ROS) formation [5]. P2X7 activation induces ROS generation in a variety of cell types resulting in transcription factor activation [6], pro-inflammatory cytokine release [7,8], microbial killing [9], cell death [10,11] and autophagy [12]. However, it remains unknown if P2X7 activation can induce ROS formation in erythroid cells.…”

Section: Introductionmentioning

confidence: 99%

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P2X7 receptor activation induces reactive oxygen species formation in erythroid cells

Wang

Sluyter

2012

Purinergic Signalling

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The presence of P2X7 on erythroid cells is well established, but its physiological role remains unclear. The current study aimed to determine if P2X7 activation induces reactive oxygen species (ROS) formation in murine erythroleukaemia (MEL) cells, a commonly used erythroid cell line. ATP induced ROS formation in a time-and concentrationdependent fashion. The most potent P2X7 agonist, 2′(3′)-O-(4-benzoylbenzoyl)ATP, but not UTP or ADP, also induced ROS formation. The P2X7 antagonist, A-438079, impaired ATP-induced ROS formation. The ROS scavenger, N-acetyl-L-cysteine, and the ROS inhibitor, diphenyleneiodonium, also impaired P2X7-induced ROS formation, but use of enzymespecific ROS inhibitors failed to identify the intracellular source of P2X7-induced ROS formation. P2X7-induced ROS formation was impaired partly by physiological concentrations of Ca 2+ and Mg 2+ and almost completely in cells in N-methyl-D-glucamine chloride medium. The p38 MAPK inhibitors SB202190 and SB203580, and the caspase inhibitor Z-VAD-FMK, but not N-acetyl-L-cysteine, impaired P2X7-induced MEL cell apoptosis. ATP also stimulated p38 MAPK and caspase activation, both of which could be impaired by A-438079. In conclusion, these findings indicate that P2X7 activation induces ROS formation in MEL cells and that this process may be involved in events downstream of P2X7 activation, other than apoptosis, in erythroid cells.

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Section: Discussionmentioning

confidence: 46%

Section: Introductionmentioning

confidence: 99%

P2X7 receptor activation induces reactive oxygen species formation in erythroid cells

Wang

Sluyter

2012

Purinergic Signalling

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“…[17] In this study, SOD activity in pregnant women of the case group was higher, suggesting that elevation of these antioxidant enzyme provides mainly protection against ROS-induced tissue injury also neutrophils and macrophages release ROS as part of the oxidative burst during T. gondii infection. [18] ROS generation is controlled by the cellular antioxidant enzymes such as SOD which detoxifies superoxide to hydrogen peroxide (H2O2). 18 this result agree with [19,20] ,although others pointed there was no changes in serum SOD activity in infected women with T.…”

Section: Discussionmentioning

confidence: 99%

“…[18] ROS generation is controlled by the cellular antioxidant enzymes such as SOD which detoxifies superoxide to hydrogen peroxide (H2O2). 18 this result agree with [19,20] ,although others pointed there was no changes in serum SOD activity in infected women with T. gondii., that related to increasing the severity of parasitemia and oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Oxidative Stress during Toxoplasmosis in Pregnant Women

Abdulrahman¹,

Mahmood²,

Abdul-Aziz³

2015

International Conference on Chemical, Agricultural and Biological Sciences (CABS-2015) Sept. 4-5, 2015 Istanbul (Turkey)

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“…Specifically, in Mycobacteria [111,112] and Chlamydia [50,73,113] infections, P2X7R activation mediates inhibition of the infection through fusion of vacuoles with lysosomes, promoting vacuole acidification, a process that requires the activation of host-cell phospholipases [50,113,114]. In macrophages infected with T. gondii, ATP mediates parasite elimination through acidification of the parasitophorous vacuole [115], which suggests a role for PLD in this infection (Fig. 3).…”

Section: The Lipid Pathway and P2x7 Receptors In Infectionmentioning

confidence: 99%

Lipid metabolism modulation by the P2X7 receptor in the immune system and during the course of infection: new insights into the old view

Costa-Junior

Marques-da-Silva

Vieira

et al. 2011

Purinergic Signalling

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For decades, scientists have described numerous protein pathways and functions. Much of a protein's function depends on its interactions with different partners, and those partners can change depending on the cell type or system. The P2X7 receptor (P2X7R) is one such multifunctional protein that is related to multiple partners and signaling pathways. The relationship between P2X7R and different enzymes involved in lipid metabolism represents a relatively new field in P2X7R research. This field of research began in epithelial cells and currently includes immune and nervous cells. The P2X7R-lipid metabolism pathway is related to many biological functions of P2X7R, such as cell death and pathogen clearance, and this signaling pathway may be involved in many functions that are dependent on bioactive lipids. In the present review, we will attempt to summarize data related to the P2X7R-lipid metabolism pathway, focusing on signaling pathways and their biological relevance to the immune system and infection.

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Activation of the P2X7 receptor triggers the elimination of Toxoplasma gondii tachyzoites from infected macrophages

Cited by 90 publications

References 29 publications

P2X7 receptor activation induces reactive oxygen species formation in erythroid cells

P2X7 receptor activation induces reactive oxygen species formation in erythroid cells

Evaluation of Oxidative Stress during Toxoplasmosis in Pregnant Women

Lipid metabolism modulation by the P2X7 receptor in the immune system and during the course of infection: new insights into the old view

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