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  1. Article ; Online: Characterization of the novel HLA-DPA1*01:144 allele by next generation sequencing.

    Liacini, Abdelhamid / Peters, Lindsey / Mancini, Shannon / Persidsky, Yuri / Geier, Steven

    HLA

    2023  Volume 102, Issue 2, Page(s) 264–266

    Abstract: HLA-DPA1*01:144 differs from HLA-DPA*01:03:01:04 by one nucleotide substitution at position 44, codon-17 located in exon 1. ...

    Abstract HLA-DPA1*01:144 differs from HLA-DPA*01:03:01:04 by one nucleotide substitution at position 44, codon-17 located in exon 1.
    MeSH term(s) Humans ; Alleles ; High-Throughput Nucleotide Sequencing ; Histocompatibility Testing ; Codon
    Chemical Substances HLA-DPA1 antigen ; Codon
    Language English
    Publishing date 2023-04-03
    Publishing country England
    Document type Journal Article
    ZDB-ID 2845111-9
    ISSN 2059-2310 ; 2059-2302
    ISSN (online) 2059-2310
    ISSN 2059-2302
    DOI 10.1111/tan.15054
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Characterization of the novel HLA-A*32:172 allele by next generation sequencing.

    Liacini, Abdelhamid / Peters, Lindsey / Mancini, Shannon / Persidsky, Yuri / Geier, Steven

    HLA

    2023  Volume 102, Issue 2, Page(s) 223–224

    Abstract: HLA-A*32:172 differs from HLA-A*32:01:01:01 by one nucleotide substitution at position 1013, codon 314 located in exon 6. ...

    Abstract HLA-A*32:172 differs from HLA-A*32:01:01:01 by one nucleotide substitution at position 1013, codon 314 located in exon 6.
    MeSH term(s) Humans ; High-Throughput Nucleotide Sequencing ; Alleles ; Exons/genetics ; Nucleotides ; HLA-A Antigens/genetics
    Chemical Substances Nucleotides ; HLA-A Antigens
    Language English
    Publishing date 2023-05-08
    Publishing country England
    Document type Journal Article
    ZDB-ID 2845111-9
    ISSN 2059-2310 ; 2059-2302
    ISSN (online) 2059-2310
    ISSN 2059-2302
    DOI 10.1111/tan.15079
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Alcohol and e-cigarette damage alveolar-epithelial barrier by activation of P2X7r and provoke brain endothelial injury via extracellular vesicles.

    Mekala, Naveen / Trivedi, Jayshil / Bhoj, Priyanka / Togre, Namdev / Rom, Slava / Sriram, Uma / Persidsky, Yuri

    Cell communication and signaling : CCS

    2024  Volume 22, Issue 1, Page(s) 39

    Abstract: Background: Use of nicotine containing products like electronic cigarettes (e-Cig) and alcohol are associated with mitochondrial membrane depolarization, resulting in the extracellular release of ATP, and mitochondrial DNA (mtDNA), mediating ... ...

    Abstract Background: Use of nicotine containing products like electronic cigarettes (e-Cig) and alcohol are associated with mitochondrial membrane depolarization, resulting in the extracellular release of ATP, and mitochondrial DNA (mtDNA), mediating inflammatory responses. While nicotine effects on lungs is well-known, chronic alcohol (ETH) exposure also weakens lung immune responses and cause inflammation. Extracellular ATP (eATP) released by inflammatory/stressed cells stimulate purinergic P2X7 receptors (P2X7r) activation in adjacent cells. We hypothesized that injury caused by alcohol and e-Cig to pulmonary alveolar epithelial cells (hPAEpiC) promote the release of eATP, mtDNA and P2X7r in circulation. This induces a paracrine signaling communication either directly or via EVs to affect brain cells (human brain endothelial cells - hBMVEC).
    Methods: We used a model of primary human pulmonary alveolar epithelial cells (hPAEpiC) and exposed the cells to 100 mM ethanol (ETH), 100 µM acetaldehyde (ALD), or e-Cig (1.75 µg/mL of 1.8% or 0% nicotine) conditioned media, and measured the mitochondrial efficiency using Agilent Seahorse machine. Gene expression was measured by Taqman RT-qPCR and digital PCR. hPAEpiC-EVs were extracted from culture supernatant and characterized by flow cytometric analysis. Calcium (Ca
    Results: ETH, ALD, or e-Cig (1.8% nicotine) stimulation depleted the mitochondrial spare respiration capacity in hPAEpiC. We observed increased expression of P2X7r and TRPV1 genes (3-6-fold) and increased intracellular Ca
    Conclusion: Abusive drugs like ETH and e-Cig promote mitochondrial and endoplasmic reticulum stress in hPAEpiC and disrupts the cell functions via P2X7 receptor signaling. EVs released by lung epithelial cells against ETH/e-cig insults, carry a cargo of secondary messengers that stimulate brain cells via paracrine signals.
    MeSH term(s) Humans ; Electronic Nicotine Delivery Systems ; Receptors, Purinergic P2X7 ; Nicotine/pharmacology ; Culture Media, Conditioned ; Endothelial Cells ; Ethanol/pharmacology ; Brain ; Extracellular Vesicles ; Adenosine Triphosphate ; DNA, Mitochondrial
    Chemical Substances Receptors, Purinergic P2X7 ; Nicotine (6M3C89ZY6R) ; Culture Media, Conditioned ; Ethanol (3K9958V90M) ; Adenosine Triphosphate (8L70Q75FXE) ; DNA, Mitochondrial
    Language English
    Publishing date 2024-01-15
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2126315-2
    ISSN 1478-811X ; 1478-811X
    ISSN (online) 1478-811X
    ISSN 1478-811X
    DOI 10.1186/s12964-023-01461-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Insights into end-organ injury in HIV infection: dynamics of monocyte trafficking to the brain in SIV encephalitis.

    Persidsky, Yuri

    The American journal of pathology

    2015  Volume 185, Issue 6, Page(s) 1548–1551

    Abstract: This commentary highlights the article by Nowlin et al, which explores the dynamic roles of macrophages in early and late central nervous system lentiviral disease. ...

    Abstract This commentary highlights the article by Nowlin et al, which explores the dynamic roles of macrophages in early and late central nervous system lentiviral disease.
    MeSH term(s) Animals ; Brain/pathology ; Encephalitis/pathology ; Macrophages/pathology ; Male ; Simian Acquired Immunodeficiency Syndrome/pathology ; Simian Immunodeficiency Virus
    Language English
    Publishing date 2015-06
    Publishing country United States
    Document type Comment ; Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2943-9
    ISSN 1525-2191 ; 0002-9440
    ISSN (online) 1525-2191
    ISSN 0002-9440
    DOI 10.1016/j.ajpath.2015.03.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Characterization of the novel HLA-C*05:01:72 allele by next generation sequencing.

    Peters, Lindsey / Mancini, Shannon / Gravante, Christopher / Persidsky, Yuri / Liacini, Abdelhamid

    HLA

    2022  Volume 101, Issue 2, Page(s) 179–181

    Abstract: Full-length sequence of HLA-C*05:01:72 covers the 5'-untranslated region (UTR), all introns and exons and the 3' UTR. ...

    Abstract Full-length sequence of HLA-C*05:01:72 covers the 5'-untranslated region (UTR), all introns and exons and the 3' UTR.
    MeSH term(s) Humans ; HLA-C Antigens/genetics ; Base Sequence ; Alleles ; High-Throughput Nucleotide Sequencing ; Exons/genetics ; Introns ; Sequence Analysis, DNA
    Chemical Substances HLA-C Antigens
    Language English
    Publishing date 2022-11-15
    Publishing country England
    Document type Journal Article
    ZDB-ID 2845111-9
    ISSN 2059-2310 ; 2059-2302
    ISSN (online) 2059-2310
    ISSN 2059-2302
    DOI 10.1111/tan.14875
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Characterization of the novel HLA-DPA1*02:72 allele by next generation sequencing.

    Liacini, Abdelhamid / Peters, Lindsey / Mancini, Shannon / Persidsky, Yuri / Geier, Steven

    HLA

    2022  Volume 100, Issue 6, Page(s) 671–672

    Abstract: HLA-DPA1*02:72 differs from HLA-DPA1*02:02:02:01 by one nucleotide substitution at position 4273, codon 86 located in exon 3. ...

    Abstract HLA-DPA1*02:72 differs from HLA-DPA1*02:02:02:01 by one nucleotide substitution at position 4273, codon 86 located in exon 3.
    MeSH term(s) Humans ; Alleles ; High-Throughput Nucleotide Sequencing ; Histocompatibility Testing ; Sequence Alignment
    Chemical Substances HLA-DPA1 antigen
    Language English
    Publishing date 2022-08-30
    Publishing country England
    Document type Journal Article
    ZDB-ID 2845111-9
    ISSN 2059-2310 ; 2059-2302
    ISSN (online) 2059-2310
    ISSN 2059-2302
    DOI 10.1111/tan.14776
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: Alcohol and e-cigarette damage alveolar-epithelial barrier by activation of P2X7r and provoke brain endothelial injury via extracellular vesicles.

    Mekala, Naveen / Trivedi, Jayshil / Bhoj, Priyanka / Togre, Namdev / Rom, Slava / Sriram, Uma / Persidsky, Yuri

    Research square

    2023  

    Abstract: Background: Use of nicotine containing products like electronic cigarettes (e-Cig) and alcohol are associated with mitochondrial membrane depolarization, resulting in the extracellular release of ATP, and mitochondrial DNA (mtDNA), mediating ... ...

    Abstract Background: Use of nicotine containing products like electronic cigarettes (e-Cig) and alcohol are associated with mitochondrial membrane depolarization, resulting in the extracellular release of ATP, and mitochondrial DNA (mtDNA), mediating inflammatory responses. While nicotine effects on lungs is well-known, chronic alcohol (ETH) exposure also weakens lung immune responses and cause inflammation. Extracellular ATP (eATP) released by inflammatory/stressed cells stimulate purinergic P2X7 receptors (P2X7r) activation in adjacent cells. We hypothesized that injury caused by alcohol and e-Cig to pulmonary alveolar epithelial cells (hPAEpiC) promote the release of eATP, mtDNA and P2X7r in circulation. This induces a paracrine signaling communication either directly or via EVs to affect brain cells (human brain endothelial cells - hBMVEC).
    Methods: We used a model of primary human pulmonary alveolar epithelial cells (hPAEpiC) and exposed the cells to 100 mM ethanol (ETH), 100 μM acetaldehyde (ALD), or e-Cig (1.75μg/mL of 1.8% or 0% nicotine) conditioned media, and measured the mitochondrial efficiency using Agilent Seahorse machine. Gene expression was measured by Taqman RT-qPCR and digital PCR. hPAEpiC-EVs were extracted from culture supernatant and characterized by flow cytometric analysis. Calcium (Ca
    Results: ETH, ALD, or e-Cig (1.8% nicotine) stimulation depleted the mitochondrial spare respiration capacity in hPAEpiC. We observed increased expression of P2X7r and TRPV1 genes (3-6-fold) and increased intracellular Ca
    Conclusion: Abusive drugs like ETH and e-Cig promote mitochondrial and endoplasmic reticulum stress in hPAEpiC and disrupts the cell functions via P2X7 receptor signaling. EVs released by lung epithelial cells against ETH/e-cig insults, carry a cargo of secondary messengers that stimulate brain cells via paracrine signals.
    Language English
    Publishing date 2023-11-14
    Publishing country United States
    Document type Preprint
    DOI 10.21203/rs.3.rs-3552555/v1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: Blocking of P2X7r Reduces Mitochondrial Stress Induced by Alcohol and Electronic Cigarette Exposure in Brain Microvascular Endothelial Cells.

    Mekala, Naveen / Gheewala, Nishi / Rom, Slava / Sriram, Uma / Persidsky, Yuri

    Antioxidants (Basel, Switzerland)

    2022  Volume 11, Issue 7

    Abstract: Studies in both humans and animal models demonstrated that chronic alcohol/e-cigarette (e-Cig) exposure affects mitochondrial function and impairs barrier function in brain microvascular endothelial cells (BMVECs). Identification of the signaling ... ...

    Abstract Studies in both humans and animal models demonstrated that chronic alcohol/e-cigarette (e-Cig) exposure affects mitochondrial function and impairs barrier function in brain microvascular endothelial cells (BMVECs). Identification of the signaling pathways by which chronic alcohol/e-Cig exposure induces mitochondrial damage in BMVEC is vital for protection of the blood-brain barrier (BBB). To address the issue, we treated human BMVEC [hBMVECs (D3 cell-line)] with ethanol (ETH) [100 mM], acetaldehyde (ALD) [100 μM], or e-cigarette (e-Cig) [35 ng/mL of 1.8% or 0% nicotine] conditioned medium and showed reduced mitochondrial oxidative phosphorylation (OXPHOS) measured by a Seahorse analyzer. Seahorse data were further complemented with the expression of mitochondrial OXPHOS proteins detected by Western blots. We also observed cytosolic escape of ATP and its extracellular release due to the disruption of mitochondrial membrane potential caused by ETH, ALD, or 1.8% e-Cig exposure. Moreover ETH, ALD, or 1.8% e-Cig treatment resulted in elevated purinergic P2X7r and TRPV1 channel gene expression, measured using qPCR. We also demonstrated the protective role of P2X7r antagonist A804598 (10 μM) in restoring mitochondrial oxidative phosphorylation levels and preventing extracellular ATP release. In a BBB functional assay using trans-endothelial electrical resistance, we showed that blocking the P2X7r channel enhanced barrier function. In summary, we identified the potential common pathways of mitochondrial injury caused by ETH, ALD, and 1.8% e-Cig which allow new protective interventions. We are further investigating the potential link between P2X7 regulatory pathways and mitochondrial health.
    Language English
    Publishing date 2022-07-06
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2704216-9
    ISSN 2076-3921
    ISSN 2076-3921
    DOI 10.3390/antiox11071328
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Full genomic sequence of the HLA-DRB3*02:32 allele by Single Molecule Real-time Sequencing Technology.

    Liacini, Abdelhamid / 't Hart, Daan C / Peters, Lindsey / Persidsky, Yuri / Geier, Steven

    HLA

    2022  Volume 101, Issue 2, Page(s) 188–190

    Abstract: Full-length sequence covers the 5'-untranslated region (UTR), all introns and exons and the 3' UTR. ...

    Abstract Full-length sequence covers the 5'-untranslated region (UTR), all introns and exons and the 3' UTR.
    MeSH term(s) Humans ; 3' Untranslated Regions ; 5' Untranslated Regions ; Alleles ; Base Sequence ; Genomics ; HLA-DRB3 Chains/genetics ; Sequence Analysis, DNA
    Chemical Substances 3' Untranslated Regions ; 5' Untranslated Regions ; HLA-DRB3 Chains
    Language English
    Publishing date 2022-11-13
    Publishing country England
    Document type Journal Article
    ZDB-ID 2845111-9
    ISSN 2059-2310 ; 2059-2302
    ISSN (online) 2059-2310
    ISSN 2059-2302
    DOI 10.1111/tan.14867
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Effects of Electronic Nicotine Delivery Systems and Cigarettes on Systemic Circulation and Blood-Brain Barrier: Implications for Cognitive Decline.

    Heldt, Nathan A / Reichenbach, Nancy / McGary, Hannah M / Persidsky, Yuri

    The American journal of pathology

    2020  Volume 191, Issue 2, Page(s) 243–255

    Abstract: Electronic nicotine delivery systems (often known as e-cigarettes) are a novel tobacco product with growing popularity, particularly among younger demographics. The implications for public health are twofold, as these products may represent a novel ... ...

    Abstract Electronic nicotine delivery systems (often known as e-cigarettes) are a novel tobacco product with growing popularity, particularly among younger demographics. The implications for public health are twofold, as these products may represent a novel source of tobacco-associated disease but may also provide a harm reduction strategy for current tobacco users. There is increasing recognition that e-cigarettes impact vascular function across multiple organ systems. Herein, we provide a comparison of evidence regarding the role of e-cigarettes versus combustible tobacco in vascular disease and implications for blood-brain barrier dysfunction and cognitive decline. Multiple non-nicotinic components of tobacco smoke have been identified in e-cigarette aerosol, and their involvement in vascular disease is discussed. In addition, nicotine and nicotinic signaling may modulate peripheral immune and endothelial cell populations in a highly context-dependent manner. Direct preclinical evidence for electronic nicotine delivery system-associated neurovascular impairment is provided, and a model is proposed in which non-nicotinic elements exert a proinflammatory effect that is functionally antagonized by the presence of nicotine.
    MeSH term(s) Animals ; Blood-Brain Barrier/drug effects ; Cerebrovascular Circulation/drug effects ; Cognitive Dysfunction/chemically induced ; Electronic Nicotine Delivery Systems ; Humans ; Nicotine/adverse effects ; Nicotinic Agonists/adverse effects ; Tobacco Products/adverse effects ; Vaping/adverse effects
    Chemical Substances Nicotinic Agonists ; Nicotine (6M3C89ZY6R)
    Language English
    Publishing date 2020-12-04
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2943-9
    ISSN 1525-2191 ; 0002-9440
    ISSN (online) 1525-2191
    ISSN 0002-9440
    DOI 10.1016/j.ajpath.2020.11.007
    Database MEDical Literature Analysis and Retrieval System OnLINE

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