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  1. AU="Lanbo Shi"
  2. AU="Gregg, R J"
  3. AU="Zou, Peiyuan"
  4. AU="Sasha Stevenson"
  5. AU="Boncompagni, Alessandra"
  6. AU="Lewis, Annisa L"
  7. AU="Daniel Freilich"
  8. AU="Glascock, Abigail L"
  9. AU="Gordon Bernard"
  10. AU="Lv, Mengwen"
  11. AU="Rottman Pietrzak, Kathleen A"
  12. AU=Panczak Radoslaw
  13. AU="Hosseini, Seyed Mohammad Hadi"
  14. AU="Noda, Haruna"
  15. AU="Raoul, Cédric"
  16. AU=Wissing Silke AU=Wissing Silke
  17. AU="Chun-Lin Yang"
  18. AU="Romine, Kyle A"
  19. AU="Cunsolo, Vincenzo"
  20. AU="Ba, Aboubacar"
  21. AU="Prisca, Mirandolina"
  22. AU="Perez, Tate"
  23. AU="Bakkaloglu, Sevan"
  24. AU="Guernieri, Rebecca L"
  25. AU="Xing, Z Y"
  26. AU="Yu-Heng Cheng"
  27. AU=Freeman Richard B Jr
  28. AU="Wang, Qi-En"
  29. AU="Mallamaci, M"
  30. AU="Turk, Yael R"
  31. AU="Tinto, Monica"
  32. AU="Selvendiran, Karuppaiyah" AU="Selvendiran, Karuppaiyah"
  33. AU="Enns, Murray W"
  34. AU="Yaohua Yang" AU="Yaohua Yang"

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  1. Artikel ; Online: Diabetes as a potential compounding factor in COVID-19-mediated male subfertility

    Qingkui Jiang / Thomas Linn / Karl Drlica / Lanbo Shi

    Cell & Bioscience, Vol 12, Iss 1, Pp 1-

    2022  Band 10

    Abstract: Abstract Recent work indicates that male fertility is compromised by SARS-CoV-2 infection. Direct effects derive from the presence of viral entry receptors (ACE2 and/or CD147) on the surface of testicular cells, such as spermatocytes, Sertoli cells, and ... ...

    Abstract Abstract Recent work indicates that male fertility is compromised by SARS-CoV-2 infection. Direct effects derive from the presence of viral entry receptors (ACE2 and/or CD147) on the surface of testicular cells, such as spermatocytes, Sertoli cells, and Leydig cells. Indirect effects on testis and concentrations of male reproductive hormones derive from (1) virus-stimulated inflammation; (2) viral-induced diabetes, and (3) an interaction between diabetes and inflammation that exacerbates the deleterious effect of each perturbation. Reproductive hormones affected include testosterone, luteinizing hormone, and follicle-stimulating hormone. Reduction of male fertility is also observed with other viral infections, but the global pandemic of COVID-19 makes demographic and public health implications of reduced male fertility of major concern, especially if it occurs in the absence of serious symptoms that would otherwise encourage vaccination. Clinical documentation of COVID-19-associated male subfertility is now warranted to obtain quantitative relationships between infection severity and subfertility; mechanistic studies using animal models may reveal ways to mitigate the problem. In the meantime, the possibility of subfertility due to COVID-19 should enter considerations of vaccine hesitancy by reproductive-age males.
    Schlagwörter SARS-CoV-2 ; Inflammation ; Diabetes ; Spermatogenesis ; Male reproductive hormones ; Male subfertility ; Biotechnology ; TP248.13-248.65 ; Biology (General) ; QH301-705.5 ; Biochemistry ; QD415-436
    Thema/Rubrik (Code) 590
    Sprache Englisch
    Erscheinungsdatum 2022-03-01T00:00:00Z
    Verlag BMC
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  2. Artikel ; Online: Immunometabolism of Phagocytes During Mycobacterium tuberculosis Infection

    Ranjeet Kumar / Pooja Singh / Afsal Kolloli / Lanbo Shi / Yuri Bushkin / Sanjay Tyagi / Selvakumar Subbian

    Frontiers in Molecular Biosciences, Vol

    2019  Band 6

    Abstract: Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb) remains as a leading killer among infectious diseases worldwide. The nature of the host immune response dictates whether the initial Mtb infection is cleared or progresses toward active ... ...

    Abstract Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb) remains as a leading killer among infectious diseases worldwide. The nature of the host immune response dictates whether the initial Mtb infection is cleared or progresses toward active disease, and is ultimately determined by intricate host-pathogen interactions that are yet to be fully understood. The early immune response to infection is mediated by innate immune cells, including macrophages and neutrophils that can phagocytose Mtb and mount an antimicrobial response. However, Mtb can exploit these innate immune cells for its survival and dissemination. Recently, it has become clear that the immune response and metabolic remodeling are interconnected, which is highlighted by the rapid evolution of the interdisciplinary field of immunometabolism. It has been proposed that the net outcome to Mtb infection—clearance or chronic disease—is likely a result of combined immunologic and metabolic activities of the immune cells. Indeed, host cells activated by Mtb infection have strikingly different metabolic requirements than naïve/non-infected cells. Macrophages activated by Mtb-derived molecules or upon phagocytosis acquire a phenotype similar to M1 with elevated production of pro-inflammatory molecules and rely on glycolysis and pentose phosphate pathway to meet their bioenergetic and metabolic requirements. In these macrophages, oxidative phosphorylation and fatty acid oxidation are dampened. However, the non-infected/naive, M2-type macrophages are anti-inflammatory and derive their energy from oxidative phosphorylation and fatty acid oxidation. Similar metabolic adaptations also occur in other phagocytes, including dendritic cells, neutrophils upon Mtb infection. This metabolic reprogramming of innate immune cells during Mtb infection can differentially regulate their effector functions, such as the production of cytokines and chemokines, and antimicrobial response, all of which can ultimately determine the outcome of Mtb-host interactions within the ...
    Schlagwörter tuberculosis ; Mycobacteria ; innate immunity ; immunometabolism ; immune cells ; epigenetics ; Biology (General) ; QH301-705.5
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2019-10-01T00:00:00Z
    Verlag Frontiers Media S.A.
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel ; Online: Development of a novel human CD147 knock-in NSG mouse model to test SARS-CoV-2 viral infection

    Saiaditya Badeti / Qingkui Jiang / Alireza Naghizadeh / Hsiang-chi Tseng / Yuri Bushkin / Salvatore A. E. Marras / Annuurun Nisa / Sanjay Tyagi / Fei Chen / Peter Romanienko / Ghassan Yehia / Deborah Evans / Moises Lopez-Gonzalez / David Alland / Riccardo Russo / William Gause / Lanbo Shi / Dongfang Liu

    Cell & Bioscience, Vol 12, Iss 1, Pp 1-

    2022  Band 19

    Abstract: Abstract Background An animal model that can mimic the SARS-CoV-2 infection in humans is critical to understanding the rapidly evolving SARS-CoV-2 virus and for development of prophylactic and therapeutic strategies to combat emerging mutants. Studies ... ...

    Abstract Abstract Background An animal model that can mimic the SARS-CoV-2 infection in humans is critical to understanding the rapidly evolving SARS-CoV-2 virus and for development of prophylactic and therapeutic strategies to combat emerging mutants. Studies show that the spike proteins of SARS-CoV and SARS-CoV-2 bind to human angiotensin-converting enzyme 2 (hACE2, a well-recognized, functional receptor for SARS-CoV and SARS-CoV-2) to mediate viral entry. Several hACE2 transgenic (hACE2Tg) mouse models are being widely used, which are clearly invaluable. However, the hACE2Tg mouse model cannot fully explain: (1) low expression of ACE2 observed in human lung and heart, but lung or heart failure occurs frequently in severe COVID-19 patients; (2) low expression of ACE2 on immune cells, but lymphocytopenia occurs frequently in COVID-19 patients; and (3) hACE2Tg mice do not mimic the natural course of SARS-CoV-2 infection in humans. Moreover, one of most outstanding features of coronavirus infection is the diversity of receptor usage, which includes the newly proposed human CD147 (hCD147) as a possible co-receptor for SARS-CoV-2 entry. It is still debatable whether CD147 can serve as a functional receptor for SARS-CoV-2 infection or entry. Results Here we successfully generated a hCD147 knock-in mouse model (hCD147KI) in the NOD-scid IL2Rgammanull (NSG) background. In this hCD147KI-NSG mouse model, the hCD147 genetic sequence was placed downstream of the endogenous mouse promoter for mouse CD147 (mCD147), which creates an in vivo model that may better recapitulate physiological expression of hCD147 proteins at the molecular level compared to the existing and well-studied K18-hACE2-B6 (JAX) model. In addition, the hCD147KI-NSG mouse model allows further study of SARS-CoV-2 in the immunodeficiency condition which may assist our understanding of this virus in the context of high-risk populations in immunosuppressed states. Our data show (1) the human CD147 protein is expressed in various organs (including bronchiolar ...
    Schlagwörter CD147 ; Basigin ; BSG ; hCD147KI ; NSG ; SARS-CoV-2 ; Biotechnology ; TP248.13-248.65 ; Biology (General) ; QH301-705.5 ; Biochemistry ; QD415-436
    Thema/Rubrik (Code) 616
    Sprache Englisch
    Erscheinungsdatum 2022-06-01T00:00:00Z
    Verlag BMC
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  4. Artikel ; Online: Role of Alanine Dehydrogenase of Mycobacterium tuberculosis during Recovery from Hypoxic Nonreplicating Persistence.

    Michelle M Giffin / Lanbo Shi / Maria L Gennaro / Charles D Sohaskey

    PLoS ONE, Vol 11, Iss 5, p e

    2016  Band 0155522

    Abstract: Mycobacterium tuberculosis can maintain a nonreplicating persistent state in the host for decades, but must maintain the ability to efficiently reactivate and produce active disease to survive and spread in a population. Among the enzymes expressed ... ...

    Abstract Mycobacterium tuberculosis can maintain a nonreplicating persistent state in the host for decades, but must maintain the ability to efficiently reactivate and produce active disease to survive and spread in a population. Among the enzymes expressed during this dormancy is alanine dehydrogenase, which converts pyruvate to alanine, and glyoxylate to glycine concurrent with the oxidation of NADH to NAD. It is involved in the metabolic remodeling of M. tuberculosis through its possible interactions with both the glyoxylate and methylcitrate cycle. Both mRNA levels and enzymatic activities of isocitrate lyase, the first enzyme of the glyoxylate cycle, and alanine dehydrogenase increased during entry into nonreplicating persistence, while the gene and activity for the second enzyme of the glyoxylate cycle, malate synthase were not. This could suggest a shift in carbon flow away from the glyoxylate cycle and instead through alanine dehydrogenase. Expression of ald was also induced in vitro by other persistence-inducing stresses such as nitric oxide, and was expressed at high levels in vivo during the initial lung infection in mice. Enzyme activity was maintained during extended hypoxia even after transcription levels decreased. An ald knockout mutant of M. tuberculosis showed no reduction in anaerobic survival in vitro, but resulted in a significant lag in the resumption of growth after reoxygenation. During reactivation the ald mutant had an altered NADH/NAD ratio, and alanine dehydrogenase is proposed to maintain the optimal NADH/NAD ratio during anaerobiosis in preparation of eventual regrowth, and during the initial response during reoxygenation.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 572
    Sprache Englisch
    Erscheinungsdatum 2016-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  5. Artikel ; Online: Elevated CCL2 causes Leydig cell malfunction in metabolic syndrome

    Qingkui Jiang / Constanze C. Maresch / Sebastian Friedrich Petry / Agnieszka Paradowska-Dogan / Sudhanshu Bhushan / Yongsheng Chang / Christine Wrenzycki / Hans-Christian Schuppe / Petr Houska / Michaela F. Hartmann / Stefan A. Wudy / Lanbo Shi / Thomas Linn

    JCI Insight, Vol 5, Iss

    2020  Band 21

    Abstract: Metabolic syndrome (MetS), which is associated with chronic inflammation, predisposes males to hypogonadism and subfertility. The underlying mechanism of these pathologies remains poorly understood. Homozygous leptin-resistant obese db/db mice are ... ...

    Abstract Metabolic syndrome (MetS), which is associated with chronic inflammation, predisposes males to hypogonadism and subfertility. The underlying mechanism of these pathologies remains poorly understood. Homozygous leptin-resistant obese db/db mice are characterized by small testes, low testicular testosterone, and a reduced number of Leydig cells. Here we report that IL-1β, CCL2 (also known as MCP-1), and corticosterone concentrations were increased in the testes of db/db mice relative to those in WT controls. Cultured murine and human Leydig cells responded to cytokine stress with increased CCL2 release and apoptotic signals. Chemical inhibition of CCL2 rescued Leydig cell function in vitro and in db/db mice. Consistently, we found that Ccl2-deficient mice fed with a high-energy diet were protected from testicular dysfunction compared with similarly fed WT mice. Finally, a cohort of infertile men with a history of MetS showed that reduction of CCL2 plasma levels could be achieved by weight loss and was clearly associated with recovery from hypogonadism. Taken together, we conclude that CCL2-mediated chronic inflammation is, to a large extent, responsible for the subfertility in MetS by causing damage to Leydig cells.
    Schlagwörter Endocrinology ; Reproductive biology ; Medicine ; R
    Sprache Englisch
    Erscheinungsdatum 2020-11-01T00:00:00Z
    Verlag American Society for Clinical investigation
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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