scholarly journals Piscirickettsia salmonis Imbalances the Innate Immune Response to Succeed in a Productive Infection in a Salmonid Cell Line Model

PLoS ONE ◽  
2016 ◽  
Vol 11 (10) ◽  
pp. e0163943 ◽  
Author(s):  
Claudio A. Álvarez ◽  
Fernando A. Gomez ◽  
Luis Mercado ◽  
Ramón Ramírez ◽  
Sergio H. Marshall
Keyword(s):  
Immune Response ◽  
Cell Line ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Productive Infection ◽  
Line Model ◽  
Cell Line Model ◽  
Piscirickettsia Salmonis

scholarly journals Induction of an Embryonic Mouse Innate Immune Response following Inoculation In Utero with Minute Virus of Mice

2014 ◽  
Vol 89 (4) ◽  
pp. 2182-2191 ◽  
Author(s):  
Irina Rostovsky ◽  
Claytus Davis
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
In Utero ◽  
Innate Immune ◽  
Productive Infection ◽  
Interferon Response ◽  
Minute Virus Of Mice ◽  
Embryonic Mouse ◽  
Minute Virus ◽  
Ifn Γ

ABSTRACTWe used an embryonic-infection model system to show that MVMp, the prototypic minute virus of mice (MVM) serotype and a member of the genusProtoparvovirus, triggers a comprehensive innate immune response in the developing mouse embryo. Direct inoculation of the midtrimester embryoin uterowith MVMp results in a widespread, productive infection. During a 96-h infection course, embryonic beta interferon (IFN-β) and IFN-γ transcription were induced 90- and 60-fold, respectively. IFN-β levels correlated with the embryo viral burden, while IFN-γ levels first increased and then decreased. Production of proinflammatory cytokines, interleukin 1β (IL-1β) and tumor necrosis factor alpha (TNF-α), also increased, but by smaller amounts, approximately 7-fold each. We observed increased levels of downstream antiviral effector molecules, PKR and phosphorylated STAT2. Finally, we showed that there is an immune cell response to the virus infection. Infected tissues in the embryo exhibited an increased density of mature leukocytes compared to the same tissues in uninfected embryos. The responses we observed were almost completely restricted to the infected embryos. Uninfected littermates routinely exhibited small increases in innate immune components that rarely reached statistical significance compared to negative controls. Similarly, the placentae of infected embryos did not show any significant increase in transcription of innate immune cytokines. Since the placenta has both embryonic and maternal components, we suggest there is minimal involvement of the dam in the response to infection.IMPORTANCEInteraction between the small single-stranded vertebrate DNA viruses, the protoparvoviruses, and the host innate immune system has been unclear. The issue is important practically given the potential use of these viruses as oncotherapeutic agents. The data reported here stand in contrast to studies of innate immune response during protoparvovirus infection of adult hosts, which invariably reported no or minimal and sporadic induction of an interferon response during infection. We conclude that under conditions of robust and productive MVM infection, a normal murine host is able to mount a significant and broad innate immune response.

scholarly journals West Nile Virus Nonstructural Protein 1 Inhibits TLR3 Signal Transduction

2008 ◽  
Vol 82 (17) ◽  
pp. 8262-8271 ◽  
Author(s):  
Jason R. Wilson ◽  
Paola Florez de Sessions ◽  
Megan A. Leon ◽  
Frank Scholle
Keyword(s):  
Signal Transduction ◽  
Immune Response ◽  
West Nile Virus ◽  
Innate Immune Response ◽  
Mammalian Cells ◽  
Innate Immune ◽  
Productive Infection ◽  
West Nile ◽  
Antiviral State ◽  
Nonstructural Protein 1

ABSTRACT The innate immune response is the first line of defense against foreign pathogens. The recognition of virus-associated molecular patterns, including double- and single-stranded RNA, by pattern recognition receptors initiates a cascade of signaling reactions. These result in the transcriptional upregulation and secretion of proinflammatory cytokines that induce an antiviral state. Many viruses have evolved mechanisms to antagonize these responses in order to help them establish a productive infection. We have previously shown that West Nile virus (WNV) is able to inhibit Toll-like receptor 3 (TLR3)-mediated activation of interferon (IFN) regulatory factor 3 (IRF3) (F. Scholle and P. W. Mason, Virology 342:77-87, 2005). In the present study, the WNV nonstructural (NS) proteins were analyzed individually for their ability to antagonize signal transduction mediated by TLR3. We report that expression of WNV NS1 inhibits TLR3-induced transcriptional activation of the IFN-β promoter and of an NF-κB-responsive promoter. This inhibition was due to a failure of the TLR3 ligand poly(I:C) to induce nuclear translocation of IRF3 and NF-κB. Furthermore, NS1 expression also inhibited TLR3-dependent production of interleukin-6 and the establishment of an antiviral state. The function of NS1 in flavivirus infection is not well understood. NS1 is required for viral RNA replication and is also secreted from mammalian cells but not from insect cells. Here, we identify a previously unrecognized role for NS1 in the modulation of signaling pathways of the innate immune response to WNV infection.

scholarly journals Characterization of D-17 Canine Osteosarcoma Cell Line and Evaluation of Its Ability to Response to Infective Stressor Used as Alternative Anticancer Therapy

Animals ◽  
2020 ◽  
Vol 10 (11) ◽  
pp. 1981
Author(s):  
Paola Modesto ◽  
Jordi Leonardo Castrillo Fernandez ◽  
Isabella Martini ◽  
Roberto Zoccola ◽  
Maria Concetta Pugliano ◽  
...  
Keyword(s):  
Gene Expression ◽  
Immune Response ◽  
Cell Line ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Preliminary Evaluation ◽  
Osteosarcoma Cell ◽  
In Vitro Test ◽  
New Therapeutic Approaches

Osteosarcoma (OSA) is a rare cancer both in human and dog although the incidence rate in dogs is 27 times higher than in human. Many studies employed D-17 as cell line for in vitro test to evaluate conventional anticancer therapies; however, little is known about D-17 cell line. The aim of our study was to evaluate the basal level of gene expression of pivotal molecules in the innate immune response and cell cycle regulation and to establish the ability of this cell line to react to Salmonella typhimurium (ST) infective stressor. IL15, IL10, iNOS, TLR5, CD14, PTEN and IL18 were expressed in an inconsistent manner among experiments. The other genes under study were expressed in all samples. ST showed ability to penetrate D-17 causing pro-inflammatory response. Our results outline the expression in D-17 of important genes involved in innate immune response. These results provide important data on D-17 basal gene expression profile useful for in vitro preliminary evaluation of new therapeutic approaches.

scholarly journals Modulation of Ubiquitin Signaling in Innate Immune Response by Herpesviruses

2022 ◽  
Vol 23 (1) ◽  
pp. 492
Author(s):  
Sandrine-M. Soh ◽  
Yeong-Jun Kim ◽  
Hong-Hee Kim ◽  
Hye-Ra Lee
Keyword(s):  
Immune Response ◽  
Protein Degradation ◽  
Innate Immune Response ◽  
Defense Mechanisms ◽  
Ubiquitin Proteasome System ◽  
Innate Immune ◽  
Productive Infection ◽  
Antiviral Immune Response ◽  
E3 Ligases ◽  
Almost All

The ubiquitin proteasome system (UPS) is a protein degradation machinery that is crucial for cellular homeostasis in eukaryotes. Therefore, it is not surprising that the UPS coordinates almost all host cellular processes, including host–pathogen interactions. This protein degradation machinery acts predominantly by tagging substrate proteins designated for degradation with a ubiquitin molecule. These ubiquitin tags have been involved at various steps of the innate immune response. Hence, herpesviruses have evolved ways to antagonize the host defense mechanisms by targeting UPS components such as ubiquitin E3 ligases and deubiquitinases (DUBs) that establish a productive infection. This review delineates how herpesviruses usurp the critical roles of ubiquitin E3 ligases and DUBs in innate immune response to escape host-antiviral immune response, with particular focus on retinoic acid-inducible gene I (RIG-I)-like receptors (RLR), cyclic-GMP-AMP (cGAMP) synthase (cGAS), stimulator of interferon (IFN) genes (STING) pathways, and inflammasome signaling.

Oral Immune Activation by Disgust and Disease-Related Pictures

2015 ◽  
Vol 29 (3) ◽  
pp. 119-129 ◽  
Author(s):  
Richard J. Stevenson ◽  
Deborah Hodgson ◽  
Megan J. Oaten ◽  
Luba Sominsky ◽  
Mehmet Mahmut ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Innate Immune Response ◽  
Negative Control ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Immune Markers ◽  
Before And After ◽  
Secondary Analyses ◽  
Image Set

Abstract. Both disgust and disease-related images appear able to induce an innate immune response but it is unclear whether these effects are independent or rely upon a common shared factor (e.g., disgust or disease-related cognitions). In this study we directly compared these two inductions using specifically generated sets of images. One set was disease-related but evoked little disgust, while the other set was disgust evoking but with less disease-relatedness. These two image sets were then compared to a third set, a negative control condition. Using a wholly within-subject design, participants viewed one image set per week, and provided saliva samples, before and after each viewing occasion, which were later analyzed for innate immune markers. We found that both the disease related and disgust images, relative to the negative control images, were not able to generate an innate immune response. However, secondary analyses revealed innate immune responses in participants with greater propensity to feel disgust following exposure to disease-related and disgusting images. These findings suggest that disgust images relatively free of disease-related themes, and disease-related images relatively free of disgust may be suboptimal cues for generating an innate immune response. Not only may this explain why disgust propensity mediates these effects, it may also imply a common pathway.

Sign in / Sign up

Export Citation Format

Share Document