The Ecto-5′nucleotidase/CD73 Mediates Leishmania amazonensis Survival in Macrophages
Endogenous nucleotides produced by various group of cells under inflammatory conditions act as potential danger signals in vivo. Extracellularly released nucleotides such as ATP are rapidly hydrolyzed to adenosine by the coordinated ectonucleotidase activities of CD39 and CD73. Leishmania is an obli...
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| creator | Bajracharya, Bijay Shrestha, Deena Talvani, André Gonçalves, Ricardo Afonso, Luís Carlos Crocco |
| description | Endogenous nucleotides produced by various group of cells under inflammatory conditions act as potential danger signals in vivo. Extracellularly released nucleotides such as ATP are rapidly hydrolyzed to adenosine by the coordinated ectonucleotidase activities of CD39 and CD73. Leishmania is an obligate intracellular parasite of macrophages and capable of modulating host immune response in order to survive and multiply within host cells. In this study, the activity of CD73 induced by Leishmania amazonensis in infected macrophages has been investigated and correlated with parasite survival and infection in vitro. For this, the expression of CD39 and CD73, by flow cytometry, in murine peritoneal macrophages infected with metacyclic promastigotes of L. amazonensis has been analyzed. Our results showed that L. amazonensis-infected macrophages, unlike LPS-treated macrophages, increased CD73 expression. It was also noted that when CD73 enzymatic activity was blocked by α, β-methyleneadenosine 5′-diphosphate sodium salt (APCP), macrophage parasitism was significantly decreased. Interestingly, these effects were not associated with the production of TNF-α, IL-10, or nitric oxide (NO). Together, these data demonstrate that L. amazonensis induces a regulatory phenotype in macrophages, which by activating the CD39/CD73 pathway allows parasite survival through the action of immunomodulatory adenosine receptors. |
| doi_str_mv | 10.1155/2022/9928362 |
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Extracellularly released nucleotides such as ATP are rapidly hydrolyzed to adenosine by the coordinated ectonucleotidase activities of CD39 and CD73. Leishmania is an obligate intracellular parasite of macrophages and capable of modulating host immune response in order to survive and multiply within host cells. In this study, the activity of CD73 induced by Leishmania amazonensis in infected macrophages has been investigated and correlated with parasite survival and infection in vitro. For this, the expression of CD39 and CD73, by flow cytometry, in murine peritoneal macrophages infected with metacyclic promastigotes of L. amazonensis has been analyzed. Our results showed that L. amazonensis-infected macrophages, unlike LPS-treated macrophages, increased CD73 expression. It was also noted that when CD73 enzymatic activity was blocked by α, β-methyleneadenosine 5′-diphosphate sodium salt (APCP), macrophage parasitism was significantly decreased. Interestingly, these effects were not associated with the production of TNF-α, IL-10, or nitric oxide (NO). Together, these data demonstrate that L. amazonensis induces a regulatory phenotype in macrophages, which by activating the CD39/CD73 pathway allows parasite survival through the action of immunomodulatory adenosine receptors.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2022/9928362</identifier><identifier>PMID: 35187176</identifier><language>eng</language><publisher>New York: Hindawi</publisher><subject>Adenosine ; Adenosine receptors ; Adenosine triphosphate ; Antibodies ; CD73 antigen ; Cell culture ; Cytokines ; Dendritic cells ; Development and progression ; Ectonucleotidase ; Enzymatic activity ; Flow cytometry ; Health aspects ; Immune response ; Immune system ; Immunomodulation ; Infections ; Inflammation ; Interleukin 10 ; Laboratory animals ; Leishmania ; Leishmania amazonensis ; Leishmaniasis ; Lipopolysaccharides ; Macrophages ; Nitric oxide ; Nucleotidase ; Nucleotidases ; Nucleotides ; Parasites ; Parasitic diseases ; Parasitism ; Phenotypes ; Physiological aspects ; Population ; Promastigotes ; Sodium salts ; Survival ; Tumor necrosis factor-α ; Variance analysis</subject><ispartof>BioMed research international, 2022, Vol.2022 (1)</ispartof><rights>Copyright © 2022 Bijay Bajracharya et al.</rights><rights>COPYRIGHT 2022 John Wiley & Sons, Inc.</rights><rights>Copyright © 2022 Bijay Bajracharya et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2022 Bijay Bajracharya et al. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3352-a89473a30436a959ca368d39da671105f13cfee82883a4915015e56dab4e714a3</citedby><cites>FETCH-LOGICAL-c3352-a89473a30436a959ca368d39da671105f13cfee82883a4915015e56dab4e714a3</cites><orcidid>0000-0002-1127-4483 ; 0000-0002-6685-6229 ; 0000-0003-1281-5330 ; 0000-0003-2498-4086 ; 0000-0003-2476-821X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8856795/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8856795/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,4022,27922,27923,27924,53790,53792</link.rule.ids></links><search><contributor>D Amelio, Stefano</contributor><contributor>Stefano D Amelio</contributor><creatorcontrib>Bajracharya, Bijay</creatorcontrib><creatorcontrib>Shrestha, Deena</creatorcontrib><creatorcontrib>Talvani, André</creatorcontrib><creatorcontrib>Gonçalves, Ricardo</creatorcontrib><creatorcontrib>Afonso, Luís Carlos Crocco</creatorcontrib><title>The Ecto-5′nucleotidase/CD73 Mediates Leishmania amazonensis Survival in Macrophages</title><title>BioMed research international</title><description>Endogenous nucleotides produced by various group of cells under inflammatory conditions act as potential danger signals in vivo. Extracellularly released nucleotides such as ATP are rapidly hydrolyzed to adenosine by the coordinated ectonucleotidase activities of CD39 and CD73. Leishmania is an obligate intracellular parasite of macrophages and capable of modulating host immune response in order to survive and multiply within host cells. In this study, the activity of CD73 induced by Leishmania amazonensis in infected macrophages has been investigated and correlated with parasite survival and infection in vitro. For this, the expression of CD39 and CD73, by flow cytometry, in murine peritoneal macrophages infected with metacyclic promastigotes of L. amazonensis has been analyzed. Our results showed that L. amazonensis-infected macrophages, unlike LPS-treated macrophages, increased CD73 expression. It was also noted that when CD73 enzymatic activity was blocked by α, β-methyleneadenosine 5′-diphosphate sodium salt (APCP), macrophage parasitism was significantly decreased. Interestingly, these effects were not associated with the production of TNF-α, IL-10, or nitric oxide (NO). Together, these data demonstrate that L. amazonensis induces a regulatory phenotype in macrophages, which by activating the CD39/CD73 pathway allows parasite survival through the action of immunomodulatory adenosine receptors.</description><subject>Adenosine</subject><subject>Adenosine receptors</subject><subject>Adenosine triphosphate</subject><subject>Antibodies</subject><subject>CD73 antigen</subject><subject>Cell culture</subject><subject>Cytokines</subject><subject>Dendritic cells</subject><subject>Development and progression</subject><subject>Ectonucleotidase</subject><subject>Enzymatic activity</subject><subject>Flow cytometry</subject><subject>Health aspects</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Immunomodulation</subject><subject>Infections</subject><subject>Inflammation</subject><subject>Interleukin 10</subject><subject>Laboratory animals</subject><subject>Leishmania</subject><subject>Leishmania amazonensis</subject><subject>Leishmaniasis</subject><subject>Lipopolysaccharides</subject><subject>Macrophages</subject><subject>Nitric oxide</subject><subject>Nucleotidase</subject><subject>Nucleotidases</subject><subject>Nucleotides</subject><subject>Parasites</subject><subject>Parasitic diseases</subject><subject>Parasitism</subject><subject>Phenotypes</subject><subject>Physiological aspects</subject><subject>Population</subject><subject>Promastigotes</subject><subject>Sodium salts</subject><subject>Survival</subject><subject>Tumor necrosis factor-α</subject><subject>Variance 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Ecto-5′nucleotidase/CD73 Mediates Leishmania amazonensis Survival in Macrophages</title><author>Bajracharya, Bijay ; Shrestha, Deena ; Talvani, André ; Gonçalves, Ricardo ; Afonso, Luís Carlos Crocco</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3352-a89473a30436a959ca368d39da671105f13cfee82883a4915015e56dab4e714a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Adenosine</topic><topic>Adenosine receptors</topic><topic>Adenosine triphosphate</topic><topic>Antibodies</topic><topic>CD73 antigen</topic><topic>Cell culture</topic><topic>Cytokines</topic><topic>Dendritic cells</topic><topic>Development and progression</topic><topic>Ectonucleotidase</topic><topic>Enzymatic activity</topic><topic>Flow cytometry</topic><topic>Health aspects</topic><topic>Immune response</topic><topic>Immune system</topic><topic>Immunomodulation</topic><topic>Infections</topic><topic>Inflammation</topic><topic>Interleukin 10</topic><topic>Laboratory animals</topic><topic>Leishmania</topic><topic>Leishmania amazonensis</topic><topic>Leishmaniasis</topic><topic>Lipopolysaccharides</topic><topic>Macrophages</topic><topic>Nitric oxide</topic><topic>Nucleotidase</topic><topic>Nucleotidases</topic><topic>Nucleotides</topic><topic>Parasites</topic><topic>Parasitic diseases</topic><topic>Parasitism</topic><topic>Phenotypes</topic><topic>Physiological aspects</topic><topic>Population</topic><topic>Promastigotes</topic><topic>Sodium salts</topic><topic>Survival</topic><topic>Tumor necrosis factor-α</topic><topic>Variance analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bajracharya, Bijay</creatorcontrib><creatorcontrib>Shrestha, Deena</creatorcontrib><creatorcontrib>Talvani, André</creatorcontrib><creatorcontrib>Gonçalves, 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various group of cells under inflammatory conditions act as potential danger signals in vivo. Extracellularly released nucleotides such as ATP are rapidly hydrolyzed to adenosine by the coordinated ectonucleotidase activities of CD39 and CD73. Leishmania is an obligate intracellular parasite of macrophages and capable of modulating host immune response in order to survive and multiply within host cells. In this study, the activity of CD73 induced by Leishmania amazonensis in infected macrophages has been investigated and correlated with parasite survival and infection in vitro. For this, the expression of CD39 and CD73, by flow cytometry, in murine peritoneal macrophages infected with metacyclic promastigotes of L. amazonensis has been analyzed. Our results showed that L. amazonensis-infected macrophages, unlike LPS-treated macrophages, increased CD73 expression. It was also noted that when CD73 enzymatic activity was blocked by α, β-methyleneadenosine 5′-diphosphate sodium salt (APCP), macrophage parasitism was significantly decreased. Interestingly, these effects were not associated with the production of TNF-α, IL-10, or nitric oxide (NO). Together, these data demonstrate that L. amazonensis induces a regulatory phenotype in macrophages, which by activating the CD39/CD73 pathway allows parasite survival through the action of immunomodulatory adenosine receptors.</abstract><cop>New York</cop><pub>Hindawi</pub><pmid>35187176</pmid><doi>10.1155/2022/9928362</doi><orcidid>https://orcid.org/0000-0002-1127-4483</orcidid><orcidid>https://orcid.org/0000-0002-6685-6229</orcidid><orcidid>https://orcid.org/0000-0003-1281-5330</orcidid><orcidid>https://orcid.org/0000-0003-2498-4086</orcidid><orcidid>https://orcid.org/0000-0003-2476-821X</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adenosine Adenosine receptors Adenosine triphosphate Antibodies CD73 antigen Cell culture Cytokines Dendritic cells Development and progression Ectonucleotidase Enzymatic activity Flow cytometry Health aspects Immune response Immune system Immunomodulation Infections Inflammation Interleukin 10 Laboratory animals Leishmania Leishmania amazonensis Leishmaniasis Lipopolysaccharides Macrophages Nitric oxide Nucleotidase Nucleotidases Nucleotides Parasites Parasitic diseases Parasitism Phenotypes Physiological aspects Population Promastigotes Sodium salts Survival Tumor necrosis factor-α Variance analysis |
| title | The Ecto-5′nucleotidase/CD73 Mediates Leishmania amazonensis Survival in Macrophages |
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