scholarly journals Transcriptional Expression Profile of Toll Like Receptor 1 - 10 mRNA in Bovine Peripheral Mononuclear Cells in Response to Foot and Mouth Disease Antigens

2012 ◽  
Vol 02 (04) ◽  
pp. 417-425 ◽  
Author(s):  
Sathish Gaikwad ◽  
Sowmya Kumar ◽  
Thimmareddy Prashanth ◽  
Golla Rama Reddy ◽  
Veluvarthy Sanyasi Suryanarayana ◽  
...  
Keyword(s):  
Expression Profile ◽  
Mononuclear Cells ◽  
Foot And Mouth Disease ◽  
Mouth Disease ◽  
Toll Like Receptor ◽  
Transcriptional Expression ◽  
Foot And Mouth ◽  
Peripheral Mononuclear Cells

scholarly journals Myocarditis Associated with Foot-and-Mouth Disease Virus Type O in Lambs

2007 ◽  
Vol 44 (5) ◽  
pp. 589-599 ◽  
Author(s):  
M. Y. Gulbahar ◽  
W. C. Davis ◽  
T. Guvenc ◽  
M. Yarim ◽  
U. Parlak ◽  
...  
Keyword(s):  
Cardiac Myocytes ◽  
Disease Virus ◽  
Mononuclear Cells ◽  
Foot And Mouth Disease ◽  
Inflammatory Cells ◽  
Interstitial Cells ◽  
Mouth Disease ◽  
Mouth Disease Virus ◽  
Foot And Mouth ◽  
Fmdv Type

The present study describes the pathogenetic mechanisms of myocarditis in 9 lambs that died in a foot-and-mouth disease outbreak in Samsun, Turkey. In all the heart samples tested, ELISA and sequencing for phylogenetic analyses showed that the virus, namely O/TUR/Samsun/05, was associated with the PanAsia pandemic strain of foot-and-mouth disease virus (FMDV) type O. The lambs had myocardial lesions but no typical vesicular lesions. In situ reverse transcription showed that many cardiomyocytes and some interstitial cells were positive for FMDV type O. Inflammatory infiltration, hyaline degeneration, and necrosis of sheets of myocytes were observed. The cellular infiltrates were mononuclear cells, including many lymphocytes, macrophages, a few plasma cells, and neutrophils. Major histocompatibility complex Class II+ dendritic and mononuclear cells, γδ T cells, CD172A+ and CD14+ macrophages and monocytes, and IgM+ B cells were detected mainly in the infected hearts. Inducible nitric oxide synthetase (iNOS) was seen mostly in areas of inflammation infiltrated by large numbers of cells. Of the 2 α-subunits of integrin known to be used as receptors by FMDV in epithelial tissues, CD49e (integrin α5) was detected in the membranes of cardiac myocytes with intercalated discs, but CD51 (integrin αV) was not detected in cardiac myocytes from infected or normal lambs. Interstitial and inflammatory cells were positive for both integrin subunits. The terminal deoxynucleotidyl transferase mediated dUTP nick-end labeling (TUNEL)-positive signal was detected in the nuclei of both cardiac myocytes and interstitial cells from infected lambs. These findings suggest that the iNOS expressed by inflammatory cells in lesions may have a deleterious effect on cardiac myocytes in these lesions.

scholarly journals Type I Interferons Triggered through the Toll-Like Receptor 3–TRIF Pathway Control Coxsackievirus A16 Infection in Young Mice

2015 ◽  
Vol 89 (21) ◽  
pp. 10860-10867 ◽  
Author(s):  
Juhao Yang ◽  
Chunfu Yang ◽  
Nining Guo ◽  
Kai Zhu ◽  
Kaiming Luo ◽  
...  
Keyword(s):  
Protective Immunity ◽  
Foot And Mouth Disease ◽  
Therapeutic Strategies ◽  
Mouth Disease ◽  
Type I Interferons ◽  
Type I ◽  
Toll Like Receptor ◽  
Coxsackievirus A16 ◽  
Foot And Mouth ◽  
Young Mice

ABSTRACTCoxsackievirus A16 (CVA16) is one of the major etiological agents of hand, foot, and mouth disease (HFMD) in children. The host defense mechanisms against CVA16 infection remain almost entirely unknown. Unlike previous observations with enterovirus 71 (EV71) infection, here we show that gamma interferon (IFN-γ) or invariant NK T cell deficiency does not affect disease development or the survival of CVA16-infected mice. In contrast, type I interferon receptor deficiency resulted in the development of more severe disease in mice, and the mice had a lower survival rate than wild-type mice. Similarly, a deficiency of Toll-like receptor 3 (TLR3) and TRIF, but not other pattern recognition receptors, led to the decreased survival of CVA16-infected mice. TLR3-TRIF signaling was indispensable for the induction of type I interferons during CVA16 infection in mice and protected young mice from disease caused by the infection. In particular, TRIF-mediated immunity was critical for preventing CVA16 replication in the neuronal system before disease occurred. IFN-β treatment was also found to compensate for TRIF deficiency in mice and decreased the disease severity in and mortality of CVA16-infected mice. Altogether, type I interferons induced by TLR3-TRIF signaling mediate protective immunity against CVA16 infection. These findings may shed light on therapeutic strategies to combat HFMD caused by CVA16 infection.IMPORTANCEHand, foot, and mouth disease (HFMD) is a major threat to public health in the Asia-Pacific region. Both CVA16 and EV71 are major pathogens that are responsible for HFMD. The majority of research efforts have focused on the more virulent EV71, but little has been done with CVA16. Thus far, host immune responses to CVA16 infection have not yet been elucidated. The present study discovered an initial molecular mechanism underlying host protective immunity against CVA16 infection, providing the first explanation for why CVA16 and EV71 cause different clinical outcomes upon infection of humans. Therefore, different therapeutic strategies should be developed to treat HFMD cases caused by these two viruses.

scholarly journals Foot-and-mouth disease virus VP3 protein acts as a critical proinflammatory factor by promoting toll-like receptor 4-mediated signaling

2021 ◽  
Author(s):  
Jing Zhang ◽  
Dan Li ◽  
Wenping Yang ◽  
Yue Wang ◽  
Lulu Li ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Disease Virus ◽  
Foot And Mouth Disease ◽  
Mouth Disease ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Fmdv Infection ◽  
Mouth Disease Virus ◽  
Foot And Mouth ◽  
Proinflammatory Factor

Foot-and-mouth disease virus (FMDV) infection in cloven-hoofed animals causes severe inflammatory symptoms, including blisters on the oral mucosa, hoof, and breast; however, the molecular mechanism underlying the inflammatory response is unclear. In this study, we provide the first evidence that the FMDV protein VP3 activates lipopolysaccharide-triggered Toll-like receptor 4 (TLR4) signaling. FMDV VP3 increased the expression of TLR4 by downregulating the expression of the lysozyme-related protein Rab7b. Additionally, Rab7b can interact with VP3 to promote the replication of FMDV. Our findings suggested that VP3 regulates the Rab7b-TLR4 axis to mediate the inflammatory response to FMDV. Importance Foot-and-mouth disease virus (FMDV) infection causes a severe inflammatory response in cloven-hoofed animals, such as pigs, cattle, and sheep, with typical clinical manifestations of high fever, numerous blisters on the oral mucosa, hoof, and breast, as well as myocarditis (tigroid heart). However, the mechanism underlying the inflammatory response caused by FMDV is enigmatic. In this study, we identified the VP3 protein of FMDV as an important proinflammatory factor. Mechanistically, VP3 interacted with TLR4 to promote TLR4 expression by inhibiting the expression of the lysozyme-related protein Rab7b. Our findings suggest that FMDV VP3 is a major proinflammatory factor in FMDV-infected hosts.

Effect of Emodin on Coxsackievirus B3m-Mediated Encephalitis in Hand, Foot, and Mouth Disease by Inhibiting Toll-Like Receptor 3 Pathway In Vitro and In Vivo

2020 ◽  
Vol 222 (3) ◽  
pp. 443-455
Author(s):  
Yan Ding ◽  
Jie Xu ◽  
Liang-bin Cheng ◽  
Yong-qian Huang ◽  
You-qin Wang ◽  
...  
Keyword(s):  
Foot And Mouth Disease ◽  
Mouth Disease ◽  
Innate Immune ◽  
Enzyme Linked Immunosorbent Assay ◽  
Toll Like Receptor ◽  
Protein Levels ◽  
Foot And Mouth ◽  
Brain Tissues

Abstract Background Encephalitis in hand, foot, and mouth disease (HFMD) is a serious threat to children’s health and life. Toll-like receptor 3 (TLR3) is an innate immune-recognition receptor that can recognize virus and initiate innate immune responses. Emodin has the effects of anti-inflammatory and regulating immune function, but the mechanism is not very clear. Methods Cells and mice were pretreated with coxsackievirus B3m (CVB3) and treated with emodin. The messenger ribonucleic acid (mRNA) and protein levels of TLR3 and downstream molecules were detected by quantitative real-time polymearse chain reaction and western blotting analysis, respectively. TLR3 expression was also downregulated by anti-TLR3 antibody (TLR3Ab) or small interfering RNA (siRNA). Pathological changes were assessed with hematoxylin and eosin staining. Immunohistochemistry was used to examine the expression of TLR3 in brain tissues. The expression of interleukin (IL)-6, nuclear factor (NF)-κB, and interferon (IFN)-β in serum were tested with enzyme-linked immunosorbent assay. Results Emodin decreased the mRNA and protein levels of TLR3 and downstream molecules in vitro and in vivo. After downregulating TLR3 using anti-TLR3Ab or siRNA, emodin could still decrease the mRNA and protein levels of TLR3 and downstream molecules. Emodin also displayed notable effects on pathology, TLR3 protein in brain tissues, and expression of IL-6, NF-κB, IFN-β, in serum. Conclusions Emodin exerts a protective effect in CVB3-mediated encephalitis in HFMD by inhibiting the TLR3 pathway.

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