scholarly journals Immune Responses against Salmonella enterica Serovar Enteritidis Infection in Virally Immunosuppressed Chickens

2003 ◽  
Vol 10 (4) ◽  
pp. 670-679 ◽  
Author(s):  
Ruby R. Sheela ◽  
Uma Babu ◽  
Jie Mu ◽  
Subbiah Elankumaran ◽  
Daniel A. Bautista ◽  
...  
Keyword(s):  
Immune Responses ◽  
Salmonella Enterica ◽  
Immunoglobulin A ◽  
Chicken Anemia Virus ◽  
Salmonella Enterica Serovar Enteritidis ◽  
Limited Effect ◽  
Field Situation ◽  
Infected Cells ◽  
Anemia Virus

ABSTRACT To understand the role of immune mechanisms in protecting chickens from Salmonella infections, we examined the immune responses of Salmonella enterica serovar Enteritidis-infected chickens and the effect of chicken anemia virus (CAV), a T-cell-targeted virus, on S. enterica serovar Enteritidis-induced immune responses. One-day-old chicks were orally inoculated with S. enterica serovar Enteritidis with or without intramuscular injection of CAV. The bacterial infection, pathology, and immune responses of chickens were evaluated at 14, 28, and 56 days postinoculation. The infection increased the levels of S. enterica serovar Enteritidis-specific mucosal immunoglobulin A (IgA), the number of gut-associated T cells, and the titer of serum IgG specific for S. enterica serovar Enteritidis surface antigens. CAV infection depressed these immune responses, especially the mucosal immune responses, but did not increase the number of S. enterica serovar Enteritidis-infected cells in the intestine. The severity of pathological lesions appeared to be reciprocal to the level of immune responses, but the S. enterica serovar Enteritidis infection persisted. These results suggest that oral infection of S. enterica serovar Enteritidis in chickens induces both mucosal and systemic immune responses, which have a limited effect on the S. enterica serovar Enteritidis infection under conditions designed to mimic the field situation.

scholarly journals Vpr Enhances Tumor Necrosis Factor Production by HIV-1-Infected T Cells

2015 ◽  
Vol 89 (23) ◽  
pp. 12118-12130 ◽  
Author(s):  
Ferdinand Roesch ◽  
Léa Richard ◽  
Réjane Rua ◽  
Françoise Porrot ◽  
Nicoletta Casartelli ◽  
...  
Keyword(s):  
Immune Responses ◽  
Proinflammatory Cytokine ◽  
Tumor Necrosis ◽  
Cellular Proteins ◽  
Accessory Protein ◽  
Infected Cells ◽  
Hiv 1 ◽  
Necrosis Factor ◽  
Stimulation Of

ABSTRACTThe HIV-1 accessory protein Vpr displays different activities potentially impacting viral replication, including the arrest of the cell cycle in the G2phase and the stimulation of apoptosis and DNA damage response pathways. Vpr also modulates cytokine production by infected cells, but this property remains partly characterized. Here, we investigated the effect of Vpr on the production of the proinflammatory cytokine tumor necrosis factor (TNF). We report that Vpr significantly increases TNF secretion by infected lymphocytes.De novoproduction of Vpr is required for this effect. Vpr mutants known to be defective for G2cell cycle arrest induce lower levels of TNF secretion, suggesting a link between these two functions. Silencing experiments and the use of chemical inhibitors further implicated the cellular proteins DDB1 and TAK1 in this activity of Vpr. TNF secreted by HIV-1-infected cells triggers NF-κB activity in bystander cells and allows viral reactivation in a model of latently infected cells. Thus, the stimulation of the proinflammatory pathway by Vpr may impact HIV-1 replicationin vivo.IMPORTANCEThe role of the HIV-1 accessory protein Vpr remains only partially characterized. This protein is important for viral pathogenesis in infected individuals but is dispensable for viral replication in most cell culture systems. Some of the functions described for Vpr remain controversial. In particular, it remains unclear whether Vpr promotes or instead prevents proinflammatory and antiviral immune responses. In this report, we show that Vpr promotes the release of TNF, a proinflammatory cytokine associated with rapid disease progression. Using Vpr mutants or inhibiting selected cellular genes, we show that the cellular proteins DDB1 and TAK1 are involved in the release of TNF by HIV-infected cells. This report provides novel insights into how Vpr manipulates TNF production and helps clarify the role of Vpr in innate immune responses and inflammation.

scholarly journals Lactic Acid Bacteria Isolated From Korean Kimchi Activate the Vitamin D Receptor–autophagy Signaling Pathways

2020 ◽  
Vol 26 (8) ◽  
pp. 1199-1211 ◽  
Author(s):  
Rong Lu ◽  
Mei Shang ◽  
Yong-Guo Zhang ◽  
Yang Jiao ◽  
Yinglin Xia ◽  
...  
Keyword(s):  
Vitamin D ◽  
Lactic Acid ◽  
Lactic Acid Bacteria ◽  
Vitamin D Receptor ◽  
Salmonella Enterica ◽  
Conditional Knockout ◽  
Control Group ◽  
Salmonella Enterica Serovar Enteritidis ◽  
Anti Inflammation

Abstract Background Probiotic lactic acid bacteria (LAB) have been used in the anti-inflammation and anti-infection process of various diseases, including inflammatory bowel disease (IBD). Vitamin D receptor (VDR) plays an essential role in pathogenesis of IBD and infectious diseases. Previous studies have demonstrated that the human VDR gene is a key host factor to shape gut microbiome. Furthermore, intestinal epithelial VDR conditional knockout (VDRΔIEC) leads to dysbiosis. Low expressions of VDR is associated with impaired autophagy, accompanied by a reduction of ATG16L1 and LC3B. The purpose of this study is to investigate probiotic effects and mechanism in modulating the VDR-autophagy pathways. Methods Five LAB strains were isolated from Korean kimchi. Conditional medium (CM) from these strains was used to treat a human cell line HCT116 or intestinal organoids to measure the expression of VDR and autophagy. Mouse embryonic fibroblast (MEF) cells with or without VDR were used to investigate the dependence on the VDR signaling. To test the role of LAB in anti-inflammation, VDR+/+ organoids were treated with 121-CM before infection with Salmonella enterica serovar Enteritidis. In vivo, the role of LAB in regulating VDR-autophagy signaling was examined using LAB 121-CM orally administrated to VDRLoxp and VDRΔIEC mice. Results The LAB-CM-treated groups showed higher mRNA expression of VDR and its target genes cathelicidin compared with the control group. LAB treatment also enhanced expressions of Beclin-1 and ATG16L1 and changed the ratio of LC3B I and II, indicating the activation of autophagic responses. Furthermore, 121-CM treatment before Salmonella enterica serovar Enteritidis infection dramatically increased VDR and ATG16L1 and inhibited the inflammation. Administration of 121-CM to VDRLoxp and VDRΔIEC mice for 12 and 24 hours resulted in an increase of VDR and LC3B II:I ratio. Furthermore, we identified that probiotic proteins P40 and P75 in the LAB-CM contributed to the anti-inflammatory function by increasing VDR. Conclusions Probiotic LAB exert anti-inflammation activity and induces autophagy. These effects depend on the VDR expression. Our data highlight the beneficial effects of these 5 LAB strains isolated from food in anti-infection and anti-inflammation.

scholarly journals Flagellin from Recombinant Attenuated Salmonella enterica Serovar Typhimurium Reveals a Fundamental Role in Chicken Innate Immunity

2012 ◽  
Vol 19 (3) ◽  
pp. 304-312 ◽  
Author(s):  
Zhiming Pan ◽  
Qiuxia Cong ◽  
Shizhong Geng ◽  
Qiang Fang ◽  
Xilong Kang ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Immune Responses ◽  
Salmonella Enterica ◽  
Rational Design ◽  
Bacterial Load ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Content Type ◽  
Serovar Typhimurium

ABSTRACTRecombinant attenuatedSalmonellavaccines have been extensively studied, with a focus on eliciting specific immune responses against foreign antigens. However, very little is known about the innate immune responses, particularly the role of flagellin, in the induction of innate immunity triggered by recombinant attenuatedSalmonellain chickens. In the present report, we describe twoSalmonella entericaserovar Typhimurium vaccine strains, wild-type (WT) or flagellin-deficient (flhD)Salmonella, both expressing the fusion protein (F) gene of Newcastle disease virus. We examined the bacterial load and spatiotemporal kinetics of expression of inflammatory cytokine, chemokine, and Toll-like receptor 5 (TLR5) genes in the cecum, spleen, liver, and heterophils following oral immunization of chickens with the twoSalmonellastrains. TheflhDmutant exhibited an enhanced ability to establish systemic infection compared to the WT. In contrast, the WT strain induced higher levels of interleukin-1β (IL-1β), CXCLi2, and TLR5 mRNAs in cecum, the spleen, and the heterophils than theflhDmutant at different times postinfection. Collectively, the present data reveal a fundamental role of flagellin in the innate immune responses induced by recombinant attenuatedSalmonellavaccines in chickens that should be considered for the rational design of novel vaccines for poultry.

scholarly journals Site-directed mutagenesis of the VP2 gene of Chicken anemia virus affects virus replication, cytopathology and host-cell MHC class I expression

2006 ◽  
Vol 87 (4) ◽  
pp. 823-831 ◽  
Author(s):  
Michelle A. Peters ◽  
Brendan S. Crabb ◽  
Elizabeth A. Washington ◽  
Glenn F. Browning
Keyword(s):  
Mhc Class I ◽  
Virus Replication ◽  
Site Directed Mutagenesis ◽  
Class I ◽  
Chicken Anemia Virus ◽  
Directed Mutagenesis ◽  
Wild Type ◽  
Basic Residue ◽  
Infected Cells ◽  
Anemia Virus

Chicken anemia virus (CAV) is an immunosuppressive pathogen of chickens. To further examine the role of viral protein 2 (VP2), which possesses dual-specificity protein phosphatase (DSP) activity, in viral cytopathogenicity and its influence on viral growth and virulence, an infectious genomic clone of CAV was subjected to site-directed mutagenesis. Substitution mutations C87R, R101G, K102D and H103Y were introduced into the DSP catalytic motif and R129G, Q131P, R/K/K150/151/152G/A/A, D/E161/162G/G, L163P, D169G and E186G into a region predicted to have a high degree of secondary structure. All mutant constructs were infectious, but their growth curves differed. The growth curve for mutant virus R/K/K150/151/152G/A/A was similar to that for wild-type virus, a second cluster of mutant viruses had an extended latent period and a third cluster of mutant viruses had extended latent and eclipse periods. All mutants had a reduced cytopathogenic effect in infected cells and VP3 was restricted to the cytoplasm. Mutation of the second basic residue (K102D) in the atypical DSP signature motif resulted in a marked reduction in virus replication efficiency, whereas mutation of the first basic residue (R101G) attenuated cytopathogenicity, but did not reduce replication efficiency. Expression of major histocompatibility complex (MHC) class I was markedly downregulated in cells infected with wild-type CAV, but not in those infected with mutants. This study further demonstrates the significance of VP2 in CAV replication and shows that specific mutations introduced into the gene encoding this protein can reduce virus replication, cytopathogenicity and downregulation of MHC I in infected cells.

scholarly journals Susceptibility of Thymocytes for Infection by Chicken Anemia Virus is Related to Pre- and Posthatching Development

1992 ◽  
Vol 2 (2) ◽  
pp. 123-129 ◽  
Author(s):  
Suzan H. M. Jeurissen ◽  
Marga E. Janse ◽  
Dirk J. van Roozelaar ◽  
Guus Koch ◽  
Gerben F. de Boer
Keyword(s):  
Embryonic Development ◽  
Cell Lineage ◽  
Precursor Cells ◽  
Bursa Of Fabricius ◽  
Chicken Anemia Virus ◽  
Chicken Embryos ◽  
Infected Cells ◽  
Anemia Virus ◽  
Second Wave ◽  
Dependent Mechanism

To investigate the age-dependent mechanism of susceptibility for chicken anemia virus (CAV) infection, we inoculated embryos and chickens of ages between day 9 of embryonic development and day 28 after hatching with CAV. Chicken embryos inoculated at days 9 and 11 of development showed no CAV-infected cells in the thymus, nor in other lymphoid organs. Many CAV-infected cells were detected in the thymic cortex of all chicken embryos inoculated at days 13 and 16 of development and of all chickens inoculated 1, 3, and 7 days after hatching. All embryos and chickens that contained CAV-infected cells in the thymus also contained CAV-infected cells in the bone marrow, but not in the bursa of Fabricius or the spleen. In chickens inoculated at days 14 and 21, only few CAV-infected cells were detected in the thymus, whereas these cells were not detected in thymi of 28-day-old inoculated chickens. Depletion of the thymic cortex was only detected in chickens inoculated from day 16 of embryonic development till day 21 after hatching. Only hematocrit values of the chickens inoculated 1 and 3 days after hatching were below normal. The rationale for the simultaneous susceptibility of cells of the T-cell lineage and cells of the erythrocyte lineage is discussed. As far as the thymus is concerned, the absence of clinical and microscopical signs of CAV infection in older chickens and the inability of CAV to infect embryos at days 9 and 11 of embryonic development may be caused by a lack of susceptible thymocytes. In view of the three waves of thymic precursor cells that populate the thymus during ontogeny, as described by Le Douarin and colleagues, we hypothesize that CAV only infects thymocytes derived from the second wave of precursor cells.

scholarly journals Role of viral load in the pathogenesis of chicken anemia virus

2005 ◽  
Vol 86 (5) ◽  
pp. 1327-1333 ◽  
Author(s):  
Jianming Tan ◽  
Gregory A. Tannock
Keyword(s):  
Viral Load ◽  
Clinical Signs ◽  
Oral Route ◽  
High Titre ◽  
Chicken Anemia Virus ◽  
Chicken Embryos ◽  
Viral Loads ◽  
Msb1 Cell ◽  
Anemia Virus

The pathogenesis of strain 3711 of the chicken anemia virus (CAV), propagated in chickens, and two preparations of strain 3711 that had been adapted to grow to high titre in cells of the MDCC-MSB1 line were studied in chicken embryos and/or chickens. Highest viral loads in infected chickens, as measured by a microplate DNA-hybridization assay, were detected in the thymus, clotted blood and pancreas, and the lowest in the duodenum. The CAV DNA copy number in the organs of chicken embryos was significantly lower than in chickens. Route of infection was an important determinant of the course of disease in chickens, with clinical signs appearing earlier in birds infected by the intramuscular than those infected by the oral route; there was a direct relationship between viral load in particular organs and the extent of clinical signs. No reduction in the pathogenicity for chickens was noted for strain 3711 after 65 or 129 passages in the MDCC-MSB1 cell line.

Role of the Flagellar Basal-Body Protein, FlgC, in the Binding of Salmonella enterica Serovar Enteritidis to Host Cells

2014 ◽  
Vol 68 (5) ◽  
pp. 621-628 ◽  
Author(s):  
Daniel C. Shippy ◽  
Nicholas M. Eakley ◽  
Dareen M. Mikheil ◽  
Amin A. Fadl
Keyword(s):  
Basal Body ◽  
Salmonella Enterica ◽  
Host Cells ◽  
Salmonella Enterica Serovar Enteritidis ◽  
Body Protein

Role of the sseK1 gene in the pathogenicity of Salmonella enterica serovar enteritidis in vitro and in vivo

2018 ◽  
Vol 117 ◽  
pp. 270-275 ◽  
Author(s):  
Yadong Yang ◽  
Chuan Yu ◽  
Ke Ding ◽  
Chunjie Zhang ◽  
Chengshui Liao ◽  
...  
Keyword(s):  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Enteritidis

scholarly journals The Role of Extracellular Vesicles in Viral Infection and Transmission

Vaccines ◽  
2019 ◽  
Vol 7 (3) ◽  
pp. 102 ◽  
Author(s):  
Lorena Urbanelli ◽  
Sandra Buratta ◽  
Brunella Tancini ◽  
Krizia Sagini ◽  
Federica Delo ◽  
...  
Keyword(s):  
Immune Responses ◽  
Viral Infection ◽  
Extracellular Vesicles ◽  
Secretory Pathway ◽  
Cell Entry ◽  
Host Factors ◽  
Intercellular Signaling ◽  
Viral Pathogens ◽  
Infected Cells

Extracellular vesicles (EVs) have been found to be released by any type of cell and can be retrieved in every circulating body fluid, namely blood (plasma, serum), saliva, milk, and urine. EVs were initially considered a cellular garbage disposal tool, but later it became evident that they are involved in intercellular signaling. There is evidence that viruses can use EV endocytic routes to enter uninfected cells and hijack the EV secretory pathway to exit infected cells, thus illustrating that EVs and viruses share common cell entry and biogenesis mechanisms. Moreover, EVs play a role in immune response against viral pathogens. EVs incorporate and spread both viral and host factors, thereby prompting or inhibiting immune responses towards them via a multiplicity of mechanisms. The involvement of EVs in immune responses, and their potential use as agents modulating viral infection, will be examined. Although further studies are needed, the engineering of EVs could package viral elements or host factors selected for their immunostimulatory properties, to be used as vaccines or tolerogenic tools in autoimmune diseases.

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