Persons who inject drugs (PWID) retain functional NK cells, dendritic cell stimulation, and adaptive immune recall responses despite prolonged opioid use

Previous literature suggests that acute opioid use results in the functional impairment of the immune response, thereby decreasing resistance to viral infection. Here, we assessed if innate and adaptive immune responses are compromised ex vivo in persons who inject drugs (PWID) and whether long‐term...

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Published inJournal of leukocyte biology Vol. 110; no. 2; pp. 385 - 396
Main Authors Tomescu, Costin, Colon, Krystal, Smith, Peter, Taylor, Mack, Azzoni, Livio, Metzger, David S., Montaner, Luis J.
Format Journal Article
LanguageEnglish
Published England Oxford University Press 01.08.2021
Subjects
activation
CD28 antigen
CD3 antigen
CD38 antigen
CD4 antigen
CD69 antigen
CD8 antigen
Crosstalk
CXCR4 protein
Cytotoxicity
Dendritic cells
Dendritic structure
Drugs
HIV
HIV infection
Human immunodeficiency virus
Immune response
Immune system
Immunosuppressive agents
Infections
Infectivity
Leukocytes
Lymphocytes
Lymphocytes T
memory response
Narcotics
Natural killer cells
Opioids
people who inject drugs (PWID)
Peptides
Plasma levels
Staphylococcal enterotoxin B
memory response
HIV
people who inject drugs (PWID)
activation
HIV infection
opioids
Online AccessGet full text
ISSN0741-5400
1938-3673
1938-3673
DOI10.1002/JLB.5A0920-604R

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Abstract Previous literature suggests that acute opioid use results in the functional impairment of the immune response, thereby decreasing resistance to viral infection. Here, we assessed if innate and adaptive immune responses are compromised ex vivo in persons who inject drugs (PWID) and whether long‐term injection drug use may impact host susceptibility to in vitro HIV infection. We measured the frequency, activation state, and functional profile of NK cells, dendritic cells, and CD4+ and CD8+ T cells in low‐risk PWID who do not share needles, high‐risk needle‐sharing PWID, and control donors who did not inject drugs. We also assessed plasma levels of inflammatory markers and CD4+ T cell susceptibility to HIV infection. We observed a significant increase in the amount of sCD14 (P = 0.0023, n = 16) and sCD163 (P = 0.0001, n = 16) in the plasma of PWID compared to controls. Evidence of constitutive activation was noted in PWID as compared to controls with increased CD69 expression in CD56dim NK cells (P = 0.0103, n = 26) and increased CD38 and HLA‐DR expression in CD4+ T cells (P = 0.0355, n = 23). However, no innate or adaptive functional differences were detected between PWID and controls, including: NK cell direct or antibody‐dependent cellular cytotoxicity poly‐functional response, TLR‐stimulated dendritic cell/NK crosstalk, CD8+ T cell response to Staphylococcal enterotoxin B or CMV/EBV/FLU peptides, or constitutive or anti‐CD3/CD28‐stimulated CD4+ T cell infectivity with CCR5‐tropic or CXCR4‐tropic HIV‐1 isolates. Our data indicate that PWID who utilize opioids over as prolonged time frame can retain a functional ex vivo immune response without a measurable increase in CD4+ T cell infectivity suggesting that leukocytes from PWID are not intrinsically more susceptibility to infection with HIV than non‐PWID controls. Graphical Long‐term opioid drug users have evidence of increased immune activation but no detectable immune dysfunction in NK, DC, and T cell responses measured ex vivo, nor increased susceptibility to in vitro HIV infection.
AbstractList Previous literature suggests that acute opioid use results in the functional impairment of the immune response, thereby decreasing resistance to viral infection. Here, we assessed if innate and adaptive immune responses are compromised ex vivo in persons who inject drugs (PWID) and whether long-term injection drug use may impact host susceptibility to in vitro HIV infection. We measured the frequency, activation state, and functional profile of NK cells, dendritic cells, CD4+ and CD8+ T cells in low-risk PWID who do not share needles, high-risk needle-sharing PWID, and control donors who did not inject drugs. We also assessed plasma levels of inflammatory markers and CD4+ T cell susceptibility to HIV infection. We observed a significant increase in the amount of sCD14 (p=0.0023, n=16) and sCD163 (p=0.0001, n=16) in the plasma of PWID compared to controls. Evidence of constitutive activation was noted in PWID as compared to controls with increased CD69 expression in CD56dim NK cells (p=0.0103, n=26) and increased CD38 and HLA-DR expression in CD4+ T cells (p=0.0355, n=23). However, no innate or adaptive functional differences were detected between PWID and controls including: NK cell direct or ADCC poly-functional response, TLR-stimulated dendritic cell/NK cross-talk, CD8+ T cell response to SEB or CMV/EBV/FLU peptides, or constitutive or anti-CD3/CD28 stimulated CD4+ T cell infectivity with CCR5-tropic or CXCR4-tropic HIV-1 isolates. Our data indicate that PWID who utilize opioids over as prolonged time frame can retain a functional ex vivo immune response without a measurable increase in CD4+ T cell infectivity suggesting that leukocytes from PWID are not intrinsically more susceptibility to infection with HIV than non-PWID controls. Long-term opioid injection-drug users have evidence of increased immune activation, but no detectable immune dysfunction in NK, DC and T cell nor increased susceptibility to in vitro HIV infection.
Previous literature suggests that acute opioid use results in the functional impairment of the immune response, thereby decreasing resistance to viral infection. Here, we assessed if innate and adaptive immune responses are compromised ex vivo in persons who inject drugs (PWID) and whether long-term injection drug use may impact host susceptibility to in vitro HIV infection. We measured the frequency, activation state, and functional profile of NK cells, dendritic cells, and CD4+ and CD8+ T cells in low-risk PWID who do not share needles, high-risk needle-sharing PWID, and control donors who did not inject drugs. We also assessed plasma levels of inflammatory markers and CD4+ T cell susceptibility to HIV infection. We observed a significant increase in the amount of sCD14 (P = 0.0023, n = 16) and sCD163 (P = 0.0001, n = 16) in the plasma of PWID compared to controls. Evidence of constitutive activation was noted in PWID as compared to controls with increased CD69 expression in CD56dim NK cells (P = 0.0103, n = 26) and increased CD38 and HLA-DR expression in CD4+ T cells (P = 0.0355, n = 23). However, no innate or adaptive functional differences were detected between PWID and controls, including: NK cell direct or antibody-dependent cellular cytotoxicity poly-functional response, TLR-stimulated dendritic cell/NK crosstalk, CD8+ T cell response to Staphylococcal enterotoxin B or CMV/EBV/FLU peptides, or constitutive or anti-CD3/CD28-stimulated CD4+ T cell infectivity with CCR5-tropic or CXCR4-tropic HIV-1 isolates. Our data indicate that PWID who utilize opioids over as prolonged time frame can retain a functional ex vivo immune response without a measurable increase in CD4+ T cell infectivity suggesting that leukocytes from PWID are not intrinsically more susceptibility to infection with HIV than non-PWID controls.
Previous literature suggests that acute opioid use results in the functional impairment of the immune response, thereby decreasing resistance to viral infection. Here, we assessed if innate and adaptive immune responses are compromised ex vivo in persons who inject drugs (PWID) and whether long-term injection drug use may impact host susceptibility to in vitro HIV infection. We measured the frequency, activation state, and functional profile of NK cells, dendritic cells, and CD4+ and CD8+ T cells in low-risk PWID who do not share needles, high-risk needle-sharing PWID, and control donors who did not inject drugs. We also assessed plasma levels of inflammatory markers and CD4+ T cell susceptibility to HIV infection. We observed a significant increase in the amount of sCD14 (P = 0.0023, n = 16) and sCD163 (P = 0.0001, n = 16) in the plasma of PWID compared to controls. Evidence of constitutive activation was noted in PWID as compared to controls with increased CD69 expression in CD56dim NK cells (P = 0.0103, n = 26) and increased CD38 and HLA-DR expression in CD4+ T cells (P = 0.0355, n = 23). However, no innate or adaptive functional differences were detected between PWID and controls, including: NK cell direct or antibody-dependent cellular cytotoxicity poly-functional response, TLR-stimulated dendritic cell/NK crosstalk, CD8+ T cell response to Staphylococcal enterotoxin B or CMV/EBV/FLU peptides, or constitutive or anti-CD3/CD28-stimulated CD4+ T cell infectivity with CCR5-tropic or CXCR4-tropic HIV-1 isolates. Our data indicate that PWID who utilize opioids over as prolonged time frame can retain a functional ex vivo immune response without a measurable increase in CD4+ T cell infectivity suggesting that leukocytes from PWID are not intrinsically more susceptibility to infection with HIV than non-PWID controls.
Previous literature suggests that acute opioid use results in the functional impairment of the immune response, thereby decreasing resistance to viral infection. Here, we assessed if innate and adaptive immune responses are compromised ex vivo in persons who inject drugs (PWID) and whether long-term injection drug use may impact host susceptibility to in vitro HIV infection. We measured the frequency, activation state, and functional profile of NK cells, dendritic cells, and CD4 and CD8 T cells in low-risk PWID who do not share needles, high-risk needle-sharing PWID, and control donors who did not inject drugs. We also assessed plasma levels of inflammatory markers and CD4 T cell susceptibility to HIV infection. We observed a significant increase in the amount of sCD14 (P = 0.0023, n = 16) and sCD163 (P = 0.0001, n = 16) in the plasma of PWID compared to controls. Evidence of constitutive activation was noted in PWID as compared to controls with increased CD69 expression in CD56 NK cells (P = 0.0103, n = 26) and increased CD38 and HLA-DR expression in CD4 T cells (P = 0.0355, n = 23). However, no innate or adaptive functional differences were detected between PWID and controls, including: NK cell direct or antibody-dependent cellular cytotoxicity poly-functional response, TLR-stimulated dendritic cell/NK crosstalk, CD8 T cell response to Staphylococcal enterotoxin B or CMV/EBV/FLU peptides, or constitutive or anti-CD3/CD28-stimulated CD4 T cell infectivity with CCR5-tropic or CXCR4-tropic HIV-1 isolates. Our data indicate that PWID who utilize opioids over as prolonged time frame can retain a functional ex vivo immune response without a measurable increase in CD4 T cell infectivity suggesting that leukocytes from PWID are not intrinsically more susceptibility to infection with HIV than non-PWID controls.
Previous literature suggests that acute opioid use results in the functional impairment of the immune response, thereby decreasing resistance to viral infection. Here, we assessed if innate and adaptive immune responses are compromised ex vivo in persons who inject drugs (PWID) and whether long-term injection drug use may impact host susceptibility to in vitro HIV infection. We measured the frequency, activation state, and functional profile of NK cells, dendritic cells, and CD4+ and CD8+ T cells in low-risk PWID who do not share needles, high-risk needle-sharing PWID, and control donors who did not inject drugs. We also assessed plasma levels of inflammatory markers and CD4+ T cell susceptibility to HIV infection. We observed a significant increase in the amount of sCD14 (P = 0.0023, n = 16) and sCD163 (P = 0.0001, n = 16) in the plasma of PWID compared to controls. Evidence of constitutive activation was noted in PWID as compared to controls with increased CD69 expression in CD56dim NK cells (P = 0.0103, n = 26) and increased CD38 and HLA-DR expression in CD4+ T cells (P = 0.0355, n = 23). However, no innate or adaptive functional differences were detected between PWID and controls, including: NK cell direct or antibody-dependent cellular cytotoxicity poly-functional response, TLR-stimulated dendritic cell/NK crosstalk, CD8+ T cell response to Staphylococcal enterotoxin B or CMV/EBV/FLU peptides, or constitutive or anti-CD3/CD28-stimulated CD4+ T cell infectivity with CCR5-tropic or CXCR4-tropic HIV-1 isolates. Our data indicate that PWID who utilize opioids over as prolonged time frame can retain a functional ex vivo immune response without a measurable increase in CD4+ T cell infectivity suggesting that leukocytes from PWID are not intrinsically more susceptibility to infection with HIV than non-PWID controls.Previous literature suggests that acute opioid use results in the functional impairment of the immune response, thereby decreasing resistance to viral infection. Here, we assessed if innate and adaptive immune responses are compromised ex vivo in persons who inject drugs (PWID) and whether long-term injection drug use may impact host susceptibility to in vitro HIV infection. We measured the frequency, activation state, and functional profile of NK cells, dendritic cells, and CD4+ and CD8+ T cells in low-risk PWID who do not share needles, high-risk needle-sharing PWID, and control donors who did not inject drugs. We also assessed plasma levels of inflammatory markers and CD4+ T cell susceptibility to HIV infection. We observed a significant increase in the amount of sCD14 (P = 0.0023, n = 16) and sCD163 (P = 0.0001, n = 16) in the plasma of PWID compared to controls. Evidence of constitutive activation was noted in PWID as compared to controls with increased CD69 expression in CD56dim NK cells (P = 0.0103, n = 26) and increased CD38 and HLA-DR expression in CD4+ T cells (P = 0.0355, n = 23). However, no innate or adaptive functional differences were detected between PWID and controls, including: NK cell direct or antibody-dependent cellular cytotoxicity poly-functional response, TLR-stimulated dendritic cell/NK crosstalk, CD8+ T cell response to Staphylococcal enterotoxin B or CMV/EBV/FLU peptides, or constitutive or anti-CD3/CD28-stimulated CD4+ T cell infectivity with CCR5-tropic or CXCR4-tropic HIV-1 isolates. Our data indicate that PWID who utilize opioids over as prolonged time frame can retain a functional ex vivo immune response without a measurable increase in CD4+ T cell infectivity suggesting that leukocytes from PWID are not intrinsically more susceptibility to infection with HIV than non-PWID controls.
Previous literature suggests that acute opioid use results in the functional impairment of the immune response, thereby decreasing resistance to viral infection. Here, we assessed if innate and adaptive immune responses are compromised ex vivo in persons who inject drugs (PWID) and whether long‐term injection drug use may impact host susceptibility to in vitro HIV infection. We measured the frequency, activation state, and functional profile of NK cells, dendritic cells, and CD4+ and CD8+ T cells in low‐risk PWID who do not share needles, high‐risk needle‐sharing PWID, and control donors who did not inject drugs. We also assessed plasma levels of inflammatory markers and CD4+ T cell susceptibility to HIV infection. We observed a significant increase in the amount of sCD14 (P = 0.0023, n = 16) and sCD163 (P = 0.0001, n = 16) in the plasma of PWID compared to controls. Evidence of constitutive activation was noted in PWID as compared to controls with increased CD69 expression in CD56dim NK cells (P = 0.0103, n = 26) and increased CD38 and HLA‐DR expression in CD4+ T cells (P = 0.0355, n = 23). However, no innate or adaptive functional differences were detected between PWID and controls, including: NK cell direct or antibody‐dependent cellular cytotoxicity poly‐functional response, TLR‐stimulated dendritic cell/NK crosstalk, CD8+ T cell response to Staphylococcal enterotoxin B or CMV/EBV/FLU peptides, or constitutive or anti‐CD3/CD28‐stimulated CD4+ T cell infectivity with CCR5‐tropic or CXCR4‐tropic HIV‐1 isolates. Our data indicate that PWID who utilize opioids over as prolonged time frame can retain a functional ex vivo immune response without a measurable increase in CD4+ T cell infectivity suggesting that leukocytes from PWID are not intrinsically more susceptibility to infection with HIV than non‐PWID controls. Graphical Long‐term opioid drug users have evidence of increased immune activation but no detectable immune dysfunction in NK, DC, and T cell responses measured ex vivo, nor increased susceptibility to in vitro HIV infection.
Author Azzoni, Livio
Colon, Krystal
Metzger, David S.
Montaner, Luis J.
Tomescu, Costin
Smith, Peter
Taylor, Mack
AuthorAffiliation 1 The Wistar Institute, HIV Immunopathogenesis Laboratory, Philadelphia, PA 19104
2 The University of Pennsylvania, Department of Psychiatry, HIV Prevention Division, Philadelphia, PA, 19104
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/33289158$$D View this record in MEDLINE/PubMed
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Issue 2
Keywords memory response
HIV
people who inject drugs (PWID)
activation
HIV infection
opioids
Language English
License https://academic.oup.com/pages/standard-publication-reuse-rights
2020 Society for Leukocyte Biology.
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content type line 14
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Costin Tomescu (Performed dendritic cell phenotypic and functional assays, performed CD8 T cell phenotypic and functional assays, co-wrote the manuscript, oversaw the study, performed statistical analysis), Krystal Colon (Performed NK phenotypic and functional assays, performed CD4+ T cell phenotypic assays and HIV infections, edited the manuscript), Peter Smith and Mack Taylor (Coordinated subject recruitment, analyzed subject behavioral data), Livio Azzoni (Coordinated plasma analysis, provided statistical support, edited the manuscript), David S. Metzger (Coordinated PWID cohort, analyzed subject behavioral data, edited the manuscript), Luis J. Montaner (Coordinated the study, analyzed all of the functional data, co-wrote the manuscript).
Authorship.
ORCID 0000-0001-5799-6759
OpenAccessLink https://proxy.k.utb.cz/login?url=https://www.ncbi.nlm.nih.gov/pmc/articles/8244827
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PublicationDate August 2021
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  text: August 2021
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PublicationTitle Journal of leukocyte biology
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Snippet Previous literature suggests that acute opioid use results in the functional impairment of the immune response, thereby decreasing resistance to viral...
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StartPage 385
SubjectTerms activation
CD28 antigen
CD3 antigen
CD38 antigen
CD4 antigen
CD69 antigen
CD8 antigen
Crosstalk
CXCR4 protein
Cytotoxicity
Dendritic cells
Dendritic structure
Drugs
HIV
HIV infection
Human immunodeficiency virus
Immune response
Immune system
Immunosuppressive agents
Infections
Infectivity
Leukocytes
Lymphocytes
Lymphocytes T
memory response
Narcotics
Natural killer cells
Opioids
people who inject drugs (PWID)
Peptides
Plasma levels
Staphylococcal enterotoxin B
Title Persons who inject drugs (PWID) retain functional NK cells, dendritic cell stimulation, and adaptive immune recall responses despite prolonged opioid use
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2FJLB.5A0920-604R
https://www.ncbi.nlm.nih.gov/pubmed/33289158
https://www.proquest.com/docview/3248801593
https://www.proquest.com/docview/2468329994
https://pubmed.ncbi.nlm.nih.gov/PMC8244827
https://www.ncbi.nlm.nih.gov/pmc/articles/8244827
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