Differential Patterns of Interaction between HIV Type 1 and HTLV Type I in Monocyte-Derived Macrophages Cultured in Vitro : Implications for in Vivo Coinfection with HIV Type 1 and HTLV Type I

1999 ◽  
Vol 15 (18) ◽  
pp. 1653-1666 ◽  
Author(s):  
Judit Szabo ◽  
Zoltan Beck ◽  
Eva Csoman ◽  
Xiangdong Liu ◽  
Istvan Andirko ◽  
...  
Keyword(s):  
Type I ◽  
Hiv Type 1 ◽  
Patterns Of Interaction

scholarly journals Evaluation In Vivo and In Vitro of the Antioxidant, Antinociceptive, and Anti-Inflammatory Activities of Biflavonoids From Ouratea hexasperma and O. ferruginea

2019 ◽  
Vol 14 (6) ◽  
pp. 1934578X1985680 ◽  
Author(s):  
Poliana de Araujo Oliveira ◽  
Queli Cristina Fidelis ◽  
Thayane Ferreira da Costa Fernandes ◽  
Milene Conceição de Souza ◽  
Dayane Magalhães Coutinho ◽  
...  
Keyword(s):  
Type I Collagen ◽  
In Vivo Model ◽  
Type I ◽  
Anti Inflammatory ◽  
Vitro Model ◽  
Factor Α ◽  
Necrosis Factor

Ouratea species are used for the treatment of inflammation-related diseases such as rheumatism and arthritic disorders. The Ouratea genus is a rich source of flavonoids and bioflavonoids and for this reason we evaluated the effects of the biflavonoid fractions from the leaves of O. hexasperma (OHME) and O. ferruginea (OFME) in the in vivo model of complete Freund’s adjuvant (CFA)-induced arthritis and in the in vitro model of oxidative stress and cellular viability. The CFA-induced arthritis model in rats was followed by paw volume, articular incapacitation and Randall-selitto models, as well as quantification of cytokines and serum C-terminal telopeptide of type I collagen levels. OHME and OFME demonstrated antinociceptive and anti-inflammatory activities, as well as improvement in articular incapacity and reduction in levels of interleukin 1β (IL-1β), IL-6, tumor necrosis factor α, and type 1 collagen, and increased cell viability. No adverse effects were observed. The results suggest that OHME and OFME can reduce inflammation and bone resorption besides their antioxidant action.

scholarly journals Lentiviral Nef Proteins Utilize PAK2-Mediated Deregulation of Cofilin as a General Strategy To Interfere with Actin Remodeling

2010 ◽  
Vol 84 (8) ◽  
pp. 3935-3948 ◽  
Author(s):  
Bettina Stolp ◽  
Libin Abraham ◽  
Jochen M. Rudolph ◽  
Oliver T. Fackler
Keyword(s):  
Host Cells ◽  
General Strategy ◽  
Actin Remodeling ◽  
Mechanistic Analysis ◽  
Immunodeficiency Virus ◽  
Hiv Type 1 ◽  
Hiv 1

ABSTRACT Nef is an accessory protein and pathogenicity factor of human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) which elevates virus replication in vivo. We recently described for HIV type 1SF2 (HIV-1SF2) the potent interference of Nef with T-lymphocyte chemotaxis via its association with the cellular kinase PAK2. Mechanistic analysis revealed that this interaction results in deregulation of the actin-severing factor cofilin and thus blocks the chemokine-mediated actin remodeling required for cell motility. However, the efficiency of PAK2 association is highly variable among Nef proteins from different lentiviruses, prompting us to evaluate the conservation of this actin-remodeling/cofilin-deregulating mechanism. Based on the analysis of a total of 17 HIV-1, HIV-2, and SIV Nef proteins, we report here that inhibition of chemokine-induced actin remodeling as well as inactivation of cofilin are strongly conserved activities of lentiviral Nef proteins. Of note, even for Nef variants that display only marginal PAK2 association in vitro, these activities require the integrity of a PAK2 recruitment motif and the presence of endogenous PAK2. Thus, reduced in vitro affinity to PAK2 does not indicate limited functionality of Nef-PAK2 complexes in intact HIV-1 host cells. These results establish hijacking of PAK2 for deregulation of cofilin and inhibition of triggered actin remodeling as a highly conserved function of lentiviral Nef proteins, supporting the notion that PAK2 association may be critical for Nef's activity in vivo.

scholarly journals HIV Type 1 Infection Up-Regulates TLR2 and TLR4 Expression and Function in Vivo and in Vitro

2012 ◽  
Vol 28 (10) ◽  
pp. 1313-1328 ◽  
Author(s):  
Juan C. Hernández ◽  
Mario Stevenson ◽  
Eicke Latz ◽  
Silvio Urcuqui-Inchima
Keyword(s):  
Tlr4 Expression ◽  
Hiv Type 1 ◽  
And Function

scholarly journals In Vitro Antiviral Interaction of Lopinavir with Other Protease Inhibitors

2002 ◽  
Vol 46 (7) ◽  
pp. 2249-2253 ◽  
Author(s):  
Akhteruzzaman Molla ◽  
Hongmei Mo ◽  
Sudthida Vasavanonda ◽  
Lixin Han ◽  
C. Thomas Lin ◽  
...  
Keyword(s):  
Protease Inhibitors ◽  
Drug Combination ◽  
Wild Type ◽  
Synergistic Inhibition ◽  
Drug Concentrations ◽  
Immunodeficiency Virus ◽  
Hiv Type 1

ABSTRACT The in vitro inhibition of wild-type human immunodeficiency virus (HIV) by combinations of lopinavir and six other protease inhibitors over a range of two-drug combination ratios was evaluated. Combinations of lopinavir with indinavir, nelfinavir, amprenavir, tipranavir, and BMS-232632 generally displayed an additive relationship. In contrast, a consistent, statistically significant synergistic inhibition of HIV type 1 replication with combinations of lopinavir and saquinavir was observed. Analysis of the combination indices indicated that lopinavir with saquinavir was synergistic over the entire range of drug combination ratios tested and at all levels of inhibition in excess of 40%. Cellular toxicity was not observed at the highest drug concentrations tested. These results suggest that administration of combinations of the appropriate dose of lopinavir with other protease inhibitors in vivo may result in enhanced antiviral activity with no associated increase in cellular cytotoxicity. More importantly, the observed in vitro synergy between lopinavir and saquinavir provides a theoretical basis for the clinical exploration of a novel regimen of lopinavir-ritonavir and saquinavir.

scholarly journals Innate lymphoid cells in the upper airways: importance of CD117 and IL-1RI expression

2018 ◽  
Vol 52 (6) ◽  
pp. 1800742 ◽  
Author(s):  
Koen Van Crombruggen ◽  
Sylvie Taveirne ◽  
Gabriele Holtappels ◽  
Georges Leclercq ◽  
Claus Bachert
Keyword(s):  
Nasal Polyps ◽  
Upper Airway ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Type I ◽  
Upper Airways ◽  
Airway Mucosa

Although type 1, 2 and 3 innate lymphoid cells (ILC1s, ILC2s and ILC3s, respectively) are emerging as important cell populations regulating tissue homeostasis, remodelling and inflammation, a vast majority of our knowledge stems from in vitro and murine experiments, and requires thorough confirmation in human diseases.Relative levels of ILCs were evaluated by means of flow cytometry in freshly resected human upper airways mucosa of patients with chronic rhinosinusitis without nasal polyps (CRSsNP) and with nasal polyps (CRSwNP), taking into account the patient's clinical parameters and disease comorbidities.We report that the CD117 and interleukin-receptor type I (IL-1RI) expression status of human ILC2s depends on the local tissue environment. Only CD117+ IL-1RI+ ILC2s, exclusively present in CRSwNP, possess an interrelationship with type 2 T-helper cell cytokine and eosinophil levels in human upper airway mucosa. In CRSsNP, mainly CD117−IL-1RI− ILC2s are increased, yielding lower eosinophilia in this disease despite the high levels of ILC2s.These data unveil that the CD117− and CD117+ fractions within the native human ILC2 population are not a random phenomenon, in contrast to what could be concluded from in vitro data, and that the IL-1RI expression is not ubiquitous in ILC2s in vivo in humans, which cannot be assessed via in vitro and murine experiments.

In Vivo Expansion Coincident with Excessive in Vitro Cell Death within the Memory Subset of CD8+ T Cells in HIV Type 1 Infection

1999 ◽  
Vol 15 (3) ◽  
pp. 265-272 ◽  
Author(s):  
Emiliano N. Mugnaini ◽  
Lise L. Haaheim ◽  
Mette Sannes ◽  
Jan E. Brinchmann
Keyword(s):  
T Cells ◽  
Cell Death ◽  
Cd8 T Cells ◽  
Hiv Type 1 ◽  
Memory Subset

scholarly journals Human Immunodeficiency Virus Viremia Induces Plasmacytoid Dendritic Cell Activation In Vivo and Diminished Alpha Interferon Production In Vitro

2008 ◽  
Vol 82 (8) ◽  
pp. 3997-4006 ◽  
Author(s):  
John C. Tilton ◽  
Maura M. Manion ◽  
Marlise R. Luskin ◽  
Alison J. Johnson ◽  
Andy A. Patamawenu ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
De Novo ◽  
Type I Interferons ◽  
Type I ◽  
Interferon Production ◽  
Immunodeficiency Virus ◽  
Hiv 1

ABSTRACT Human immunodeficiency virus type 1 (HIV-1) infection has been associated with perturbations of plasmacytoid dendritic cells (PDC), including diminished frequencies in the peripheral blood and reduced production of type I interferons (IFNs) in response to in vitro stimulation. However, recent data suggest a paradoxical increase in production of type 1 interferons in vivo in HIV-infected patients compared to uninfected controls. Using a flow cytometric assay to detect IFN-α-producing cells within unseparated peripheral blood mononuclear cells, we observed that short-term interruptions of antiretroviral therapy are sufficient to result in significantly reduced IFN-α production by PDC in vitro in response to CpG A ligands or inactivated HIV particles. The primary cause of diminished IFN-α production was reduced responsiveness of PDC to de novo stimulation, not diminished per cell IFN-α production or migration of cells to lymphoid organs. Real-time PCR analysis of purified PDC from patients prior to and during treatment interruptions revealed that active HIV-1 replication is associated with upregulation of type I IFN-stimulated gene expression. Treatment of hepatitis C virus-infected patients with IFN-α2b and ribavirin for hepatitis C virus infection resulted in a profound suppression of de novo IFN-α production in response to CpG A or inactivated HIV particles, similar to the response observed in HIV-infected patients. Together, these results suggest that diminished production of type I interferons in vitro by PDC from HIV-1-infected patients may not represent diminished interferon production in vivo. Rather, diminished function in vitro is likely a consequence of prior activation via type I interferons or HIV virions in vivo.

Peculiarities of the course of type I allergic reactions in patients with blood diseases

2020 ◽  
pp. 40-50
Author(s):  
A. Nikitina
Keyword(s):  
Search Engines ◽  
Anaphylactic Shock ◽  
Type I ◽  
Allergic Reactions ◽  
Common Cause ◽  
Blood Diseases ◽  
Treatment Regimens ◽  
Modern Methods

Analysis of literature data presented in search engines — Elibrary, PubMed, Cochrane — concerning the risk of developing type I allergic reactions in patients with blood diseases is presented. It is shown that the most common cause of type I allergic reactions is drugs included in the treatment regimens of this category of patients. The article presents statistics on the increase in the number of drug allergies leading to cases of anaphylactic shock in patients with blood diseases. Modern methods for the diagnosis of type I allergic reactions in vivo and in vitro are considered.

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