scholarly journals Cyclosporine A Inhibits Viral Infection and Release as Well as Cytokine Production in Lung Cells by Three SARS-CoV-2 Variants

2022 ◽  
Author(s):  
Claudio Fenizia ◽  
Silvia Galbiati ◽  
Claudia Vanetti ◽  
Riccardo Vago ◽  
Mario Clerici ◽  
...  
Keyword(s):  
Viral Infection ◽  
Cyclosporine A ◽  
Cytokine Production ◽  
Lung Cells ◽  
Antibody Neutralization ◽  
Rapid Diffusion

SARS-CoV-2 is the most recently identified member of the betacoronavirus genus responsible for the COVID-19 pandemic. Repurposing of available drugs has been a “quick and dirty” approach to try to reduce mortality and severe symptoms in affected patients initially, and can still represent an undeniable and valuable approach to face COVID-19 as the continuous appearance and rapid diffusion of more “aggressive”/transmissible variants, capable of eluding antibody neutralization, challenges the effectiveness of some anti-SARS-CoV-2 vaccines.

Cytokine Production in Viral Infection

Cytokines ◽  
2011 ◽  
pp. 107-121
Author(s):  
Monica Tomaszewsik ◽  
Frank Jenkins
Keyword(s):  
Viral Infection ◽  
Cytokine Production

scholarly journals Cyclosporine A Regulates Pro-Inflammatory Cytokine Production in Ulcerative Colitis

2014 ◽  
Vol 63 (1) ◽  
pp. 53-63 ◽  
Author(s):  
Stefanie Steiner ◽  
Carolin Daniel ◽  
Anika Fischer ◽  
Imke Atreya ◽  
Simon Hirschmann ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Cyclosporine A ◽  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Inflammatory Cytokine Production

scholarly journals Tissue-Resident Innate and Innate-Like Lymphocyte Responses to Viral Infection

Viruses ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 272
Author(s):  
Andrew Hildreth ◽  
Timothy O’Sullivan
Keyword(s):  
Viral Infection ◽  
Cytokine Production ◽  
Lymphocyte Subsets ◽  
Current Knowledge ◽  
Critical Role ◽  
Lymphoid Cells ◽  
T Cell Subsets ◽  
Antiviral Responses ◽  
Host Protection ◽  
Lymphocyte Responses

Infection is restrained by the concerted activation of tissue-resident and circulating immune cells. Recent discoveries have demonstrated that tissue-resident lymphocyte subsets, comprised of innate lymphoid cells (ILCs) and unconventional T cells, have vital roles in the initiation of primary antiviral responses. Via direct and indirect mechanisms, ILCs and unconventional T cell subsets play a critical role in the ability of the immune system to mount an effective antiviral response through potent early cytokine production. In this review, we will summarize the current knowledge of tissue-resident lymphocytes during initial viral infection and evaluate their redundant or nonredundant contributions to host protection or virus-induced pathology.

scholarly journals KRAB-Zinc Finger Protein ZNF268a Deficiency Attenuates the Virus-Induced Pro-Inflammatory Response by Preventing IKK Complex Assembly

Cells ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 1604 ◽  
Author(s):  
Yi Liu ◽  
Wei Yin ◽  
Jingwen Wang ◽  
Yucong Lei ◽  
Guihong Sun ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Viral Infection ◽  
Zinc Finger ◽  
Cytokine Production ◽  
Zinc Finger Protein ◽  
Nuclear Translocation ◽  
Sendai Virus ◽  
Positive Role ◽  
Finger Protein ◽  
Ikk Complex

Despite progress in understanding how virus-induced, NF-κB-dependent pro-inflammatory cytokines are regulated, there are still factors and mechanisms that remain to be explored. We aimed to uncover the relationship between KRAB-zinc finger protein ZNF268a and NF-κB-mediated cytokine production in response to viral infection. To this end, we established a ZNF268a-knockout cell line using a pair of sgRNAs that simultaneously target exon 3 in the coding sequence of the ZNF268 gene in HEK293T. HEK293T cells lacking ZNF268a showed less cytokine expression at the transcription and protein levels in response to Sendai virus/vesicular stomatitis virus (SeV/VSV) infection than wild-type cells. Consistent with HEK293T, knock-down of ZNF268a by siRNAs in THP-1 cells significantly dampened the inflammatory response. Mechanistically, ZNF268a facilitated NF-κB activation by targeting IKKα, helping to maintain the IKK signaling complex and thus enabling proper p65 phosphorylation and nuclear translocation. Taken together, our data suggest that ZNF268a plays a positive role in the regulation of virus-induced pro-inflammatory cytokine production. By interacting with IKKα, ZNF268a promotes NF-κB signal transduction upon viral infection by helping to maintain the association between IKK complex subunits.

scholarly journals Effect of NMSO3 treatment in a murine model of human metapneumovirus infection

2008 ◽  
Vol 89 (11) ◽  
pp. 2709-2712 ◽  
Author(s):  
Leanne Spetch ◽  
Terry L. Bowlin ◽  
Antonella Casola
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Viral Infection ◽  
Murine Model ◽  
Cytokine Production ◽  
Antiviral Treatment ◽  
Pulmonary Inflammation ◽  
Body Weight Loss ◽  
Human Metapneumovirus ◽  
Time Of Infection

BALB/c mice infected with human metapneumovirus (hMPV) were treated with the sulfated sialyl lipid NMSO3 (one dose of 50 mg kg−1) given at the time of infection. NMSO3 significantly reduced viral replication in the lungs, as well as hMPV-induced body weight loss, pulmonary inflammation and cytokine production, suggesting that antiviral treatment initiated at the beginning of viral infection can modify hMPV-induced disease.

INHIBITION OF CYTOKINE PRODUCTION BY CYCLOSPORINE A AND G

1989 ◽  
Vol 47 (2) ◽  
pp. 343-347 ◽  
Author(s):  
RACHEL MARY MCKENNA ◽  
KATHLEEN SZTURM ◽  
JOHN ROGER JEFFERY ◽  
DAVID NICHOLAS RUSH
Keyword(s):  
Cyclosporine A ◽  
Cytokine Production

scholarly journals Excessive Innate Immunity Steers Pathogenic Adaptive Immunity in the Development of Theiler’s Virus-Induced Demyelinating Disease

2021 ◽  
Vol 22 (10) ◽  
pp. 5254
Author(s):  
Byung S. Kim
Keyword(s):  
B Cells ◽  
Viral Infection ◽  
Cytokine Production ◽  
Viral Infections ◽  
Demyelinating Disease ◽  
Demyelinating Diseases ◽  
Viral Loads ◽  
Underlying Mechanisms ◽  
The Many ◽  
Antigen Presenting

Several virus-induced models were used to study the underlying mechanisms of multiple sclerosis (MS). The infection of susceptible mice with Theiler’s murine encephalomyelitis virus (TMEV) establishes persistent viral infections and induces chronic inflammatory demyelinating disease. In this review, the innate and adaptive immune responses to TMEV are discussed to better understand the pathogenic mechanisms of viral infections. Professional (dendritic cells (DCs), macrophages, and B cells) and non-professional (microglia, astrocytes, and oligodendrocytes) antigen-presenting cells (APCs) are the major cell populations permissive to viral infection and involved in cytokine production. The levels of viral loads and cytokine production in the APCs correspond to the degrees of susceptibility of the mice to the TMEV-induced demyelinating diseases. TMEV infection leads to the activation of cytokine production via TLRs and MDA-5 coupled with NF-κB activation, which is required for TMEV replication. These activation signals further amplify the cytokine production and viral loads, promote the differentiation of pathogenic Th17 responses, and prevent cellular apoptosis, enabling viral persistence. Among the many chemokines and cytokines induced after viral infection, IFN α/β plays an essential role in the downstream expression of costimulatory molecules in APCs. The excessive levels of cytokine production after viral infection facilitate the pathogenesis of TMEV-induced demyelinating disease. In particular, IL-6 and IL-1β play critical roles in the development of pathogenic Th17 responses to viral antigens and autoantigens. These cytokines, together with TLR2, may preferentially generate deficient FoxP3+CD25- regulatory cells converting to Th17. These cytokines also inhibit the apoptosis of TMEV-infected cells and cytolytic function of CD8+ T lymphocytes (CTLs) and prolong the survival of B cells reactive to viral and self-antigens, which preferentially stimulate Th17 responses.

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