scholarly journals Cellular immune response in chickens infected with avian infectious bronchitis virus (IBV)

2017 ◽  
Vol 15 (1) ◽  
pp. 35-41 ◽  
Author(s):  
Tong Zhang ◽  
Deyin Li ◽  
Zhihua Jia ◽  
Jianyu Chang ◽  
Xiaolin Hou
Keyword(s):  
Infectious Bronchitis Virus ◽  
Interferon Α ◽  
Mrna Transcription ◽  
Infectious Bronchitis ◽  
Over Expression ◽  
Tnf Α ◽  
Mechanistic Basis ◽  
Gene Transcription Profile ◽  
Factor Α ◽  
Cellular Immune

To understand the mechanistic basis of innate immunity against the infectious bronchitis virus (IBV), the gene transcription profile of pattern recognition receptors (PRRs) in SPF chicken tissues infected with an IBV-M41 strain was examined. IBV infection induced mRNA transcription of TLRs, RLRs, and NODs. TLR7, MyD88, TRAF6, MDA5, LGP2, and NLRC5 were stimulated, as well as mRNA activation of the downstream genes of NF-κB and IRF3. And mRNA for the pro-inflammatory cytokines of interferon-α (IFN)-α, IFN-β, tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) showed over-expression. The IBV load in tissues gradually reduced. These results suggested that the three kinds of PRRs signaling pathways and innate immune cytokine were induced after IBV infection.

scholarly journals Design and Characterization of a DNA Vaccine Based on Spike with Consensus Nucleotide Sequence against Infectious Bronchitis Virus

Vaccines ◽  
2021 ◽  
Vol 9 (1) ◽  
pp. 50
Author(s):  
Lei Zuo ◽  
Wenjun Yan ◽  
Zhou Song ◽  
Hao Li ◽  
Xin Xie ◽  
...  
Keyword(s):  
Nucleotide Sequence ◽  
Dna Vaccine ◽  
Infectious Bronchitis Virus ◽  
Neutralizing Antibody ◽  
Economic Losses ◽  
Post Translational Modification ◽  
Virus Shedding ◽  
Infectious Bronchitis ◽  
Specific Pathogen ◽  
Cellular Immune

Avian coronavirus infectious bronchitis virus (IBV) causes severe economic losses in the poultry industry, but its control is hampered by the continuous emergence of new genotypes and the lack of cross-protection among different IBV genotypes. We designed a new immunogen based on a spike with the consensus nucleotide sequence (S_con) that may overcome the extraordinary genetic diversity of IBV. S_con was cloned into a pVAX1 vector to form a new IBV DNA vaccine, pV-S_con. pV-S_con could be correctly expressed in HD11 cells with corresponding post-translational modification, and induced a neutralizing antibody response to the Vero-cell-adapted IBV strain Beaudette (p65) in mice. To further evaluate its immunogenicity, specific-pathogen-free (SPF) chickens were immunized with the pV-S_con plasmid and compared with the control pVAX1 vector and the H120 vaccine. Detection of IBV-specific antibodies and cell cytokines (IL-4 and IFN-γ) indicated that vaccination with pV-S_con efficiently induced both humoral and cellular immune responses. After challenge with the heterologous strain M41, virus shedding and virus loading in tissues was significantly reduced both by pV-S_con and its homologous vaccine H120. Thus, pV-S_con is a promising vaccine candidate for IBV, and the consensus approach is an appealing method for vaccine design in viruses with high variability.

scholarly journals Antibody-Mediated Porcine Reproductive and Respiratory Syndrome Virus Infection Downregulates the Production of Interferon-α and Tumor Necrosis Factor-α in Porcine Alveolar Macrophages via Fc Gamma Receptor I and III

Viruses ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 187
Author(s):  
Liujun Zhang ◽  
Wen Li ◽  
Yangyang Sun ◽  
Linghao Kong ◽  
Pengli Xu ◽  
...  
Keyword(s):  
Virus Infection ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Respiratory Syndrome Virus ◽  
Interferon Α ◽  
Fc Gamma Receptor ◽  
Gamma Receptor ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Antibody-dependent enhancement (ADE) contributes to the pathogenesis of porcine reproductive and respiratory syndrome virus (PRRSV)-persistent infection. However, the mechanisms of PRRSV-ADE infection are still confusing. A clear understanding of the event upon virus infection by the ADE pathway has become crucial for developing efficient intervention of the PRRSV infection. In this study, an ADE assay showed that PRRSV-ADE infection in porcine alveolar macrophages (AMs) significantly decreased the production of interferon-α (IFN-α) and tumor necrosis factor-α (TNF-α), and significantly increased the production of interleukine-10 (IL-10). A gene knockdown assay based on small interfering RNA (siRNA) showed that both Fc gamma receptor I (FcγRI) and FcγRIII in porcine AMs were involved in PRRSV-ADE infection. An activation assay showed that specific activation of FcγRI or FcγRIII in porcine AMs during PRRSV infection not only significantly decreased the production of IFN-α and TNF-α, but also significantly increased the production of IL-10 and significantly facilitated PRRSV replication. In conclusion, our studies suggested that ADE downregulated the production of IFN-α and TNF-α in porcine AMs maybe via FcγRI and FcγRIII, thereby leading to enhanced PRRSV infection.

scholarly journals Effects of porcine MyD88 knockdown on the expression of TLR4 pathway-related genes and proinflammatory cytokines

2016 ◽  
Vol 36 (6) ◽  
Author(s):  
Chaohui Dai ◽  
Li Sun ◽  
Lihuai Yu ◽  
Guoqiang Zhu ◽  
Shenglong Wu ◽  
...  
Keyword(s):  
Cell Line ◽  
Proinflammatory Cytokines ◽  
Negative Control ◽  
Signalling Pathway ◽  
Mechanistic Study ◽  
Interferon Α ◽  
Toll Like Receptor ◽  
Pk15 Cell ◽  
Tnf Α ◽  
Factor Α

As a critical adapter protein in Toll-like receptor (TLR)/Interleukin (IL)-1R signalling pathway, myeloid differentiation protein 88 (MyD88) plays an important role in immune responses and host defence against pathogens. The present study was designed to provide a foundation and an important reagent for the mechanistic study of MyD88 and its role TLR/IL-1R signalling pathways in porcine immunity. Lentivirus-mediated RNAi was used to generate a porcine PK15 cell line with a silenced MyD88 gene and quantitative real-time PCR (qPCR) and Western blotting were used to detect changes in the expression of critical genes in the Toll-like receptor 4 (TLR4) signalling pathway. ELISA was used to measure the levels of seven proinflammatory cytokines–interleukin-1β (IL-1β), tumour necrosis factor-α (TNF-α), IL-6, IL-8, IL-12, macrophage inflammatory protein (MIP)-1α and MIP-1β–in cell culture supernatants after MyD88 silencing. We successfully obtained a PK15 cell line with 61% MyD88 mRNA transcript down-regulated. In PK15 cells with MyD88 silencing, the transcript levels of TLR4 and IL-1β were significantly reduced, whereas there were no significant changes in the expression levels of cluster of differentiation antigen 14 (CD14), interferon-α (IFN-α) or TNF-α. The ELISA results showed that the levels of most cytokines were not significantly changed apart from IL-8 without stimulation, which was significantly up-regulated. When cells were induced by lipopolysaccharide (LPS) (0.1 μg/ml) for 6 h, the global level of seven proinflammatory cytokines up-regulated and the level of IL-1β, TNF-α, IL-6, IL-8 and IL-12 of Blank and negative control (NC) group up-regulated more significantly than RNAi group (P<0.05), which revealed that the MyD88 silencing could reduce the TLR4 signal transduction which inhibited the release of proinflammatory cytokines and finally leaded to immunosuppression.

scholarly journals Particle size and activation threshold: a new dimension of danger signaling

Blood ◽  
2010 ◽  
Vol 115 (22) ◽  
pp. 4533-4541 ◽  
Author(s):  
Lorna Rettig ◽  
Sebastian P. Haen ◽  
Anne Greet Bittermann ◽  
Lotta von Boehmer ◽  
Alessandra Curioni ◽  
...  
Keyword(s):  
Immune Cells ◽  
Interferon Α ◽  
Innate Response ◽  
Activation Threshold ◽  
Tnf Α ◽  
Nanometric Particles ◽  
Human Immune ◽  
Factor Α ◽  
Molecular Patterns ◽  
Necrosis Factor

Abstract Previous studies have shown that single-stranded RNA (ssRNA) mixed with protamine forms particles and activates immune cells through Toll-like receptors (TLRs). We have found that the size of protamine-RNA particles generated depends on the electrolyte content when mixing the 2 components. Moreover, we have evidenced that (1) nanometric particles induce production of interferon-α, whereas (2) micrometric particles mainly induce production of tumor necrosis factor-α (TNF-α) in human immune cells. We found that the mechanisms underlying these observations are (1) nanoparticles but not microparticles are selectively phagocytosed by plasmacytoid dendritic cells (pDCs), which produce interferon-α and (2) monocytes that produce TNF-α have a higher activation threshold than that of pDCs. Thus, at the same time as sensing pathogen-associated molecular patterns such as ssRNA, the immune system distinguishes the size of the associated structure in such a way as to trigger the adapted antivirus (nanometric) or antibacterial/antifungal (micrometric) immune response. Our results introduce a new dimension in danger signaling—how size qualitatively affects innate response.

scholarly journals Glutathione Supplementation as an Adjunctive Therapy in COVID-19

Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 914
Author(s):  
Vika Guloyan ◽  
Buzand Oganesian ◽  
Nicole Baghdasaryan ◽  
Christopher Yeh ◽  
Manpreet Singh ◽  
...  
Keyword(s):  
Disease Process ◽  
Current Treatment ◽  
Treatment Modalities ◽  
Adjunctive Treatment ◽  
Interferon Α ◽  
Beneficial Effects ◽  
Tnf Α ◽  
Immunodeficiency Virus ◽  
Factor Α ◽  
Necrosis Factor

Morbidity and mortality of coronavirus disease 2019 (COVID-19) are due in large part to severe cytokine storm and hypercoagulable state brought on by dysregulated host-inflammatory immune response, ultimately leading to multi-organ failure. Exacerbated oxidative stress caused by increased levels of interleukin (IL)-6 and tumor necrosis factor α (TNF-α) along with decreased levels of interferon α and interferon β (IFN-α, IFN-β) are mainly believed to drive the disease process. Based on the evidence attesting to the ability of glutathione (GSH) to inhibit viral replication and decrease levels of IL-6 in human immunodeficiency virus (HIV) and tuberculosis (TB) patients, as well as beneficial effects of GSH on other pulmonary diseases processes, we believe the use of liposomal GSH could be beneficial in COVID-19 patients. This review discusses the epidemiology, transmission, and clinical presentation of COVID-19 with a focus on its pathogenesis and the possible use of liposomal GSH as an adjunctive treatment to the current treatment modalities in COVID-19 patients.

scholarly journals Effect of different anesthetic methods on cellular immune functioning and the prognosis of patients with ovarian cancer undergoing oophorectomy

2017 ◽  
Vol 37 (5) ◽  
Author(s):  
Xin-Rui Han ◽  
Xin Wen ◽  
Yan-Yi Li ◽  
Shao-Hua Fan ◽  
Zi-Feng Zhang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Ovarian Cancer ◽  
Ca 125 ◽  
Red Cell ◽  
Post Surgery ◽  
Tnf Α ◽  
C3b Receptor ◽  
Factor Α ◽  
Cellular Immune ◽  
Necrosis Factor

The present study aimed to explore the effects of different anesthetic methods on cellular immune function and prognosis of patients with ovarian cancer (OC) undergoing oophorectomy. A total of 167 patients who received general anesthesia (GA) treatment (GA group) and 154 patients who received combined general/epidural anesthesia (GEA) treatment (GEA group) were collected retrospectively. Each group selected 124 patients that met the inclusion and exclusion criteria for further study. ELISA and radioimmunoassay were employed to detect levels of IL-2, TNF-α, and CA-125. The rates of tumor-red cell rosette (RTRR), red cell immune complex rosette (RRICR), and red cell C3b receptor rosette (RRCR) were also measured. Systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR) were determined by hemodynamics. The levels of tumor necrosis factor-α (TNF-α) and interleukin (IL)-2 decreased at 1 h intraoperation (T2), but increased 24-h post surgery (T3). The levels of TNF-α and IL-2 were recovered faster in the GEA group than in the GA group. The GA group exhibited greater levels of CA-125 expression than in the GEA group. The levels of RTRR, RRICR, and RRCR; ratios of CD3+, CD4+, CD4+/CD8+, CD16+, and CD56+ at 30 min after anesthesia (T1), T2, T3 and 48 h after the operation (T4) and levels of SBP, DBP, and HR at T1, T2, and T3 displayed increased levels in the GEA group than in the GA group. At 72-h post surgery (T5), the 5-year survival rate significantly increased in the GEA group compared with the GA group. GEA to be more suitable than GA for surgery on OC patients.

Response of hairy cells to IFN-α involves induction of apoptosis through autocrine TNF-α and protection by adhesion

Blood ◽  
2002 ◽  
Vol 100 (2) ◽  
pp. 647-653 ◽  
Author(s):  
Peter K. Baker ◽  
Andrew R. Pettitt ◽  
Joseph R. Slupsky ◽  
Hai J. Chen ◽  
Mark A. Glenn ◽  
...  
Keyword(s):  
Nuclear Factor Κb ◽  
Interferon Α ◽  
The Novel ◽  
Tnf Α ◽  
Hairy Cells ◽  
Induced Apoptosis ◽  
Factor Α ◽  
Blocking Antibodies ◽  
Biologic Basis ◽  
Necrosis Factor

Abstract Although hairy cell leukemia is uniquely sensitive to interferon-α (IFN-α), the biologic basis for this phenomenon remains unclear. Here we examine the effects of IFN-α on cultured hairy cells (HCs), taking into account the possible modifying influence of cell adhesion. We make the novel observation that therapeutic concentrations of IFN-α kill nonadherent HCs by inducing apoptosis. In keeping with the persistence of HCs in tissues during therapy, such killing was inhibited by integrin-mediated adhesion to vitronectin or fibronectin. Exposure of HCs to IFN-α resulted in a marked increase in tumor necrosis factor-α (TNF-α) secretion. Furthermore, blocking antibodies to TNF-RI or TNF-RII protected HCs from IFN-α–induced apoptosis, demonstrating that such killing was mediated by TNF-α. In the absence of IFN-α, exogenous TNF-α did not induce HC apoptosis, showing that IFN-α sensitized HCs to the proapoptotic effect of autocrine TNF-α. This sensitization to TNF-α–induced killing was attributable to suppression of IAP (inhibitors of apoptosis) production known to be regulated by the cytoprotective nuclear factor–κB–dependent arm of TNF-α signaling. Moreover, engagement of the receptors for fibronectin or vitronectin prevented this IFN-α–induced down-regulation of IAPs. Understanding of the signals involved in the combined effects of IFN-α and TNF-α and abrogation of those induced by integrin engagement offers the possibility of sensitizing other malignant cells to IFN-α–induced killing and thereby extending the therapeutic use of this cytokine.

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