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Table 1 Involvement of purinergic in infectious processes

From: Putative roles of purinergic signaling in human immunodeficiency virus-1 infection

Microorganism Receptor Cell type Involvement Reference
Bacteria
M. tuberculosis ND monocyte ATP induced apoptosis of infected monocyte and reduced viability of intracellular bacilli [97]
BCG P2X7 Human macrophage Treatment with exogenous ATP caused cell death and killing of intracellular mycobacteria within BCG infected macrophages [98]
M. tuberculosis P2X7 Human macrophage Treatment with ATP reduced viability of three virulent strains of mycobacteria within human macrophages, what was associated with stimulation of phospholipase D activity [99]
BCG P2X7 and P2Y Human macrophage Apoptosis of infected cells and killing of intracellular bacilli [100]
M.bovis P2X7 Bovine macrophage ATP induced killing Mycobacterium bovis in bovine macrophages in a mechanism P2X7R-dependent [101]
BCG P2X7 Murine bone-marrow derived macrophages and murine macrophage cell line P2X7R stimulation with ATP induced rapid fusion of BCG-containing phagosomes with lysosomes, resulting in formation of multibacillary vacuoles. Also, P2X7R resulted in progressive acidification of BCG-containing phagosomes in infected macrophages [102]
BCG P2X7 Human macrophage Loss-of-function polymorphism 1513A → C abolished apoptosis of infected macrophages and mycobacterial killing [103]
BCG P2X7 Human macrophage The 1513C allele was associated to increased susceptibility to extracellular TB and ATP-mediated killing of mycobacteria in macrophages was absent in homozygous subjects and impaired in heterozygous subjects [104]
BCG P2X7 Human macrophage Loss-of-function polymorphism 1096C → G (change Thr(357) to Ser (T357S)) associated to reduced or near to absent ATP-induced killing of intracellular mycobacteria [105]
M. tuberculosis P2X7 Human PBMC PBMC from TB patients presented different pattern of gene expression in response to ATP when compared to healthy contacts [106]
M. tuberculosis P2X7 Human monocyte/macrophages Mycobacterial infection induced an increase of P2X7 expression, higher release of ATP and an increment of intracellular ATP accumulation [107]
BCG P2X7 THP-1 and monocyte-derived macrophage ATP treatment activated autophagy pathway via a Ca2 + -dependent process. This effect was associated with a phago-lysosomal fusion and of mycobacteria-containing phagosomes, resulting in reduction in intracellular BCG viability [108]
C. psittaci P2X7 Murine macrophage cell line ATP but no other nucleotides was able to induce reduction in viability of intracellular bacteria and chlamydial infection prevented ATP-mediated apoptosis [109]
C. trachomatis P2X7 Murine peritoneal macrophage cells and macrophage cell line Chlamydial killing upon ATP treatment of infected cells required phospholipase D activation, which is mediated by P2X7R stimulation that leads to lysosome fusion with mature Chlamydia vacuoles [110]
C. muridarum, P2X7 Human cervical adenocarcinoma cell line Extracellular ATP or other P2X7R agonists induced a decrease in chlamydial viability in epithelial cells, which was dependent on phospholipase D activity and blocked by treatment with P2X7R antagonists and butan-1-ol (PLD inhibitor). Also, vaginal infection was more efficient in P2X7R-deficient mice, what was correlated to higher level of acute inflammation [111]
Protozoan
L. amazonensis P2X7 Murine macrophage cell line Native and recombinant Leishmania nucleoside diphosphate kinase (NdK) prevented ATP-induced cell death [112]
L. amazonensis P2X7 Murine peritoneal macrophage Leishmania infection leads to increased expression of P2X7R and higher responsiveness to ATP treatment. Also, incubation with ATP reduced the parasite load, which was reverted by pre-treatment with oxidized ATP and was not not dependent of cell lysis or NO production [113]
L. amazonensis P2X7 Murine peritoneal macrophage Macrophages infected with L. amazonensis exhibit higher apoptosis rate and parasite degradation upon ATP treatment and presented differential modulation of the uptake of cationic and anionic dyes [114]
L. amazonensis P2Y Murine peritoneal macrophage Uridine nucleotides reduced parasite load and induced morphological damage of intracellular parasites and infected cells. They also induced significant levels of apoptosis, ROI and RNI in infected cells. [115]
T. gondii P2X7 Murine peritoneal cell and macrophage cell line ATP or BzATP treatment reduced parasite load. Parasite load was not reduced in P2X7R-deficient mouse. Furthermore, ATP treatment caused ultrastructural changes in tachyzoite inside macrophages, increased lysosome fusion with parasitophorous vacuole and ROS production [116]
T. gondii P2X7 Human macrophage and murine bone marrow-derived macrophage and macrophage-like cell line Infected macrophages obtained from homozygous individuals for loss-of-function polymorphism 1513A → C had no significant alteration in parasite load after ATP treatment. Similarly, macrophages from P2X7R knockout mice were not able to kill T. gondii upon ATP treatment [117]
T. gondii P2X7 Human Peripheral blood cells SNP 1068T→C was found positively associated with resistance to both congenital and ocular toxoplasmosis [118]
T. gondii P2X7 Murine peritoneal cell In vivo infection of P2X7-deficient mouse resulted in a more severe acute infection, higher parasite burdens and pronounced liver pathology [119]