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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]