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ABSTRACT: Coxsackievirus B (CVB) and enterovirus 71 (EV71) are important causes of severe enteroviral diseases in neonates or young children in Taiwan. CVB can cause fulminant hepatitis, myocarditis, or meningoencephalitis. This study was designed to explore the role of coxsackievirus-adenovirus receptor (CAR) in pathogenesis of CVB3 infected hepatocyte via in vitro and mice study. CVB3 (CVB3/2630) was isolated from liver tissue of a neonate with fulminant hepatitis. Cell lines A549, HeLa, HEp2 and Huh-7 were maintained in Dulbecco's modified Eagle's medium. One-day-old or seven-day-old mice progeny were used in the experiments. Viraemia was noted in seven-day-old ICR mice 2 hours of an intraperitoneal injection. Thereafter the highest viral titers were detected in blood, liver and spleen. Histopathological studies of the liver demonstrated polymorphonuclear cells infiltration, massive hepatic cells necrosis and apoptosis. CAR was more expressed in liver than other tissues. Expression of CAR decreased with mice age. Anti-CAR monoclonal antibody prevented infection of Huh-7 cells from CVB3. Furthermore, anti-CAR monoclonal antibody pretreatment can reduce mortality and decrease level of liver enzymes in CVB3-infected mice. These findings indicate that CAR plays an important role in the initiation of CVB infections and is closely associated with hepatotropism and age-specific susceptibility. This article is protected by copyright. All rights reserved.
Pathogens and disease. 04/2013;
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ABSTRACT: Antibody-dependent enhancement (ADE) of virus infections can be induced by subneutralizing concentrations of specific antibodies. We recently demonstrated ADE in human monocytes infected with enterovirus 71 (EV71). The current study was designed to extend these observations by determining the effect of ADE on the pathogenesis of EV71 infection in newborn mice. We compared the clinical manifestations, mortality, virus titer, histopathology, and serum levels of cytokines and chemokines in newborn mice pretreated with subneutralizing antibodies to EV71 or normal mouse IgG with and without virus. Seven-day-old ICR mice were pretreated with a wide range of mouse anti-EV71 IgG 24 h prior to intraperitoneal injection of EV71. Mice were protected from infection by neutralizing doses of anti-EV71 IgG ranging from 6.43 × 10(-1) to 329.6 μg/ml. Subneutralizing doses ranging from 2.01 × 10(-2) to 3.21 × 10(-1) μg/ml were found to significantly increase 14-day mortality compared to virus alone. The ADE effect was not evident at lower doses. Histopathological examination of mice given a subneutralizing dose of 8.04 × 10(-2) μg/ml revealed extensive neuronal and muscular damage compared to untreated infected controls. Higher serum levels of interferon (IFN)-γ and monocyte chemoattractant protein (MCP)-1 were noted in mice pretreated with subneutralizing doses than untreated infected controls. These findings support the concept that subneutralizing antibodies directed enhance EV71 induce ADE in newborn mice.
Medical Microbiology and Immunology 02/2013; · 3.83 Impact Factor
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ABSTRACT: Type I interferons (IFNs) represent an essential innate defense mechanism for controlling enterovirus 71 (EV 71) infection. Mice inoculated with EV 71 produced a significantly lower amount of type I IFNs than those inoculated with poly (I:C), adenovirus type V, or coxsackievirus B3 (CB3). EV 71 infection, however, mounted a proinflammatory response with a significant increase in the levels of serum and brain interleukin (IL)-6, monocyte chemoattractant protein-1, tumor necrosis factor, and IFN-γ. EV 71 infection abolished both poly (I:C)- and CB3-induced type I IFN production of mice. Such effect was not extended to other enteroviruses including coxsackievirus A24, B2, B3, and echovirus 9, as mice infected with these viruses retained type I IFN responsiveness upon poly (I:C) challenge. In addition, EV 71-infected RAW264.7 cells produced significantly lower amount of type I IFNs than non-infected cells upon poly (I:C) stimulation. The inhibitory effect of EV 71 on type I IFN production was attributed to the viral protein 3C, which was confirmed using over-expression systems in both mice and RAW264.7 cells. The 3C over-expression, however, did not interfere with poly (I:C)-induced proinflammatory cytokine production. These findings indicate that EV 71 can hamper the host innate defense by blocking selectively type I IFN synthesis through the 3C viral protein. J. Med. Virol. 84:1779-1789, 2012. © 2012 Wiley Periodicals, Inc.
Journal of Medical Virology 11/2012; 84(11):1779-89. · 2.82 Impact Factor
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ABSTRACT: Enterovirus 71 (EV71) is a major causative agent of hand-foot-and-mouth disease (HFMD), and infection of EV71 to central nerve system (CNS) may result in a high mortality in children less than 2 years old. Although there are two highly glycosylated membrane proteins, SCARB2 and PSGL-1, which have been identified as the cellular and functional receptors of EV71, the role of glycosylation in EV71 infection is still unclear.
We demonstrated that the attachment of EV71 to RD and SK-N-SH cells was diminished after the removal of cell surface sialic acids by neuraminidase. Sialic acid specific lectins, Maackia amurensis (MAA) and Sambucus Nigra (SNA), could compete with EV71 and restrained the binding of EV71 significantly. Preincubation of RD cells with fetuin also reduced the binding of EV71. In addition, we found that SCARB2 was a sialylated glycoprotein and interaction between SCARB2 and EV71 was retarded after desialylation.
In this study, we demonstrated that cell surface sialic acids assist in the attachment of EV71 to host cells. Cell surface sialylation should be a key regulator that facilitates the binding and infection of EV71 to RD and SK-N-SH cells.
BMC Microbiology 08/2012; 12:162. · 3.04 Impact Factor
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ABSTRACT: Enterovirus 71 (EV71) is a major cause of hand-foot-and-mouth disease. EV71 infection occasionally associates with severe neurological sequelae such as brainstem encephalitis or poliovirus-like paralysis. We demonstrated that mouse-adapted strain increases infectivity, resulting in higher cytotoxicity of neuron cells and mortality to neonatal mice than a non-adapted strain. Results pointed to EV71 capsid region determining viral infectivity and mouse lethality. Mutant virus with lysine to methionine substitution at VP2(149) (VP2(149M)) or glutamine to glutamic acid substitution at VP1(145) (VP1(145E)) showed greater viral titers and apoptosis. Synergistic effect of VP2(149M) and VP1(145E) double mutations enhanced viral binding and RNA accumulation in infected Neuro-2a cells. The dual substitution mutants markedly reduced value of 50% lethal dose in neonatal mice infection, indicating they raised mouse lethality in vivo. In sum, VP2(149M) and VP1(145E) mutations cooperatively promote viral binding and RNA accumulation of EV71, contributing to viral infectivity in vitro and mouse lethality in vivo.
Virology 11/2011; 422(1):132-43. · 3.35 Impact Factor
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ABSTRACT: Neonatal mice developed neurological disease and pulmonary dysfunction after an infection with a mouse-adapted human Enterovirus 71 (EV71) strain MP4. However, the hallmark of severe human EV71 infection, pulmonary edema (PE), was not evident.
To test whether EV71-induced PE required a proinflammatory cytokine response, exogenous pro-inflammatory cytokines were administered to EV71-infected mice during the late stage of infection.
After intracranial infection of EV71/MP4, 7-day-old mice developed hind-limb paralysis, pulmonary dysfunction, and emphysema. A transient increase was observed in serum IL-6, IL-10, IL-13, and IFN-γ, but not noradrenaline. At day 3 post infection, treatment with IL-6, IL-13, and IFN-γ provoked mild PE and severe emphysema that were accompanied by pulmonary dysfunction in EV71-infected, but not herpes simplex virus-1 (HSV-1)-infected control mice. Adult mice did not develop PE after an intracerebral microinjection of EV71 into the nucleus tractus solitarii (NTS). While viral antigen accumulated in the ventral medulla and the NTS of intracerebrally injected mice, neuronal loss was observed in the ventral medulla only.
Exogenous IL-6, IL-13, and IFN-γ treatment could induce mild PE and exacerbate pulmonary abnormality of EV71-infected mice. However, other factors such as over-activation of the sympathetic nervous system may also be required for the development of classic PE symptoms.
Respiratory research 11/2011; 12:147. · 3.36 Impact Factor
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ABSTRACT: In this study we tested the effectiveness of a formaldehyde-inactivated EV71 vaccine and its compatibility for co-immunization with a pentavalent vaccine that contained inactivated poliovirus (PV) vaccine. The inactivated EV71 vaccine (C2 genogroup) elicited an antibody response which broadly neutralized homologous and heterologous genogroups, including B4, C4, and B5. Pups from vaccinated dams were resistant to the EV71 challenge and had a high survival rate and a low tissue viral burden when compared to those from non-vaccinated counterparts. Co-immunization with pentavalent and inactivated EV71 vaccines elicited antibodies against the major components of the pentavalent vaccine including the PV, Bordetella pertussis, Haemophilus influenzae type b, diphtheria toxoid, and tetanus toxoid at the same levels as in mice immunized with pentavalent vaccine alone. Likewise, EV71 neutralizing antibody titers were comparable between EV71-vaccinated mice and mice co-immunized with the two vaccines. These results indicate that formaldehyde-inactivated whole virus EV71 vaccine is feasible for designing multivalent vaccines.
Vaccine 02/2011; 29(15):2772-6. · 3.77 Impact Factor
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ABSTRACT: Enterovirus 71 (EV71) has emerged as a neuroinvasive virus responsible for several large outbreaks in the Asia-Pacific region while virulence determinant remains unexplored.
In this report, we investigated increased virulence of unadapted EV71 clinical isolate 237 as compared with isolate 4643 in mice. A fragment 12 nucleotides in length in stem loop (SL) II of 237 5'-untranslated region (UTR) visibly reduced survival time and rate in mice was identified by constructing a series of infectious clones harboring chimeric 5'-UTR. In cells transfected with bicistronic plasmids, and replicon RNAs, the 12-nt fragment of isolate 237 enhanced translational activities and accelerated replication of subgenomic EV71. Finally, single nucleotide change from cytosine to uridine at base 158 in this short fragment of 5'-UTR was proven to reduce viral translation and EV71 virulence in mice. Results collectively indicated a pivotal role of novel virulence determinant C158 on virus translation in vitro and EV71 virulence in vivo.
These results presented the first reported virulence determinant in EV71 5'-UTR and first position discovered from unadapted isolates.
PLoS ONE 01/2011; 6(11):e27082. · 4.09 Impact Factor
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ABSTRACT: We tested whether methylene blue, an inexpensive and safe photosensitizer, is feasible for photodynamic inactivation of enterovirus 71 (EV71) in the environment.
By escalating light doses and photosensitizer concentrations, photoinactivation of EV71 and other enteroviruses was examined in vitro. Viral transmission in the environment was simulated with a neonatal mouse model in vivo. Possible mechanisms were analysed with alterations of viral DNA and proteins after treatments.
Photodynamic inactivation of EV71 in suspensions occurred in a dose-dependent manner. The optimal condition for photoinactivating EV71 required a light dose of 200 J/cm(2) in the presence of methylene blue. This photodynamic condition was also able to inactivate other enteroviruses, including poliovirus 1 and coxsackieviruses A2, A3, A16 and B3. In an imitation environment, EV71 spread on a solid surface was inactivated by methylene blue-mediated photodynamic inactivation and prevented EV71 transmission to mice. Western blot and RT-PCR analysis indicated that both the viral proteins and the genome were disrupted after photodynamic inactivation.
Methylene blue-mediated photodynamic inactivation may provide a novel way to eliminate environmentally contaminated sources of EV71 to prevent infection.
Journal of Antimicrobial Chemotherapy 10/2010; 65(10):2176-82. · 5.07 Impact Factor
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ABSTRACT: The objective of this study is to evaluate the passive protective efficiency of immunoglobulin in yolk (IgY) specific against human enterovirus type 71 (EV71). The antibody was raised by intramuscular immunization to 10 White Leghorn hens, with inactivated human EV71 serving as the antigen. The titer and specificity of the antibody were analyzed from purified IgY in the egg yolks of immunized hens. Results indicate that the titer of IgY specific against EV71 increased from the third week after the first immunization. The content of total IgY was 190 ± 26 mg/yolk, with an average concentration of specific IgY of 6.34 ± 3.38 mg/yolk in the eggs from 3 to 18 wk after immunization. The results of the neutralization effect of specific IgY in EV71-challenged mice demonstrate that the EV71-specific IgY, either by intraperitoneal injection or oral administration, was able to significantly reduce the morbidity and mortality in EV71 infected mice pups.
Vaccine 10/2010; 28(51):8189-96. · 3.77 Impact Factor
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ABSTRACT: In 1998, an enterovirus 71 (EV71) epidemic in Taiwan resulted in 78 deaths; however, the molecular basis of EV71 pathogenicity remains poorly understood. Comparison of the deduced amino acid sequences in 3D polymerases of EV71clinical isolates showed the T251V or T251I substitution from 1986 and 1998 outbreaks. An EV71 replicon system showed that introducing an I251T mutation did not affect luciferase activities at 35 degrees C when compared with wild type; however, lower luciferase activities were observed when they were incubated at 39.5 degrees C. In addition, the I251T mutation in the EV71 infectious clone not only reduced viral replication at 39.5 degrees C in vitro but also decreased the virulence of the mouse adaptive strain MP4 in neonatal mice in an i.p. infection model. Therefore, these results suggested that the threonine at position 251 results in a temperature sensitivity phenotype of EV71 which may contribute to the attenuation of circulating strains.
Virology 11/2009; 396(1):1-9. · 3.35 Impact Factor
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Chung-Tiang Liang,
Amy Shih,
Yu-Hsiu Chang,
Chiung-Wen Liu,
Ya-Tien Lee,
Wei-Chun Hsieh,
Yuan-Ling Huang,
Wan-Tsang Huang,
Chih-Hui Kuang,
Kan-Hung Lee,
Yi-Xing Zhuo,
Sheng-Yu Ho,
Shiow-Ling Liao,
Yi-Ying Chiu,
Chieh-Ning Hsu,
San-Chi Liang, Chun-Keung Yu
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ABSTRACT: Limited data are available on the pathogen status of contemporary rodent colonies in Taiwan. Here we summarized the rodent pathogen diagnostic records of the Taiwan National Laboratory Animal Center during a 4-y period that representing approximately 10% of the rodent colonies in Taiwan. Demand for pathogen diagnostic service increased continuously from 2004 to 2007, with a 20% increase each year. In 2007, more than 20% of the mouse colonies were positive for mouse parvovirus, mouse hepatitis virus, Theiler murine encephalomyelitis virus, and Mycoplasma pulmonis, with fewer colonies diagnosed as having infections of pneumonia virus of mice, mouse adenovirus, lymphocytic choriomeningitis virus, and reovirus. Almost 40% of tested rat colonies were positive for Mycoplasma pulmonis and rat parvovirus, with fewer colonies containing Kilham rat virus, sialodacryoadenitis virus, pneumonia virus of mice, Sendai virus, and Syphacia spp. These data provide a sound overall picture of the health status of mouse and rat colonies in Taiwan.
Journal of the American Association for Laboratory Animal Science: JAALAS 08/2009; 48(4):381-6. · 0.71 Impact Factor
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ABSTRACT: Brainstem encephalitis (BE) is a serious neurological complication of enterovirus 71 (EV71) infection. The present study was designed to determine the characteristics of the chemokine response in the blood and cerebrospinal fluid (CSF) of patients with EV71-associated BE.
Thirty-one patients with BE were studied. They consisted of 12 with uncomplicated BE, 9 with autonomic nervous system (ANS) dysregulation, and 10 with pulmonary edema (PE); 13 healthy control subjects were also studied. Plasma and CSF concentrations of various chemokines were determined by a particle-based flow cytometry immunoassay.
Plasma levels of interferon (IFN)-gamma-induced protein (IP)-10, monocyte chemoattractant protein (MCP)-1, monokine induced by IFN-gamma (MIG), and interleukin (IL)-8 were significantly higher in patients with PE than in those with uncomplicated BE. CSF levels of MIG were significantly higher in patients with PE than in those with uncomplicated BE and ANS dysregulation. The ratios of mean CSF to plasma levels for MCP-1 and IL-8 were highest in patients with uncomplicated BE and tended to fall with increasing severity of the disease.
Overexpression of the chemokine cascade in the central nervous system compartment appears to play an important role in the elicitation of the immune response to EV71. The chemokine CSF to plasma ratios suggest that IL-8, IP-10, MCP-1, and possibly MIG-but not RANTES-are synthesized in the brain in response to encephalitis.
The Journal of Infectious Diseases 11/2008; 198(7):1002-6. · 6.41 Impact Factor
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ABSTRACT: Enterovirus 71 (EV71) causes fatal encephalitis in young children. However, there is no effective antiviral drug available for infected patients. Ribavirin is currently used for the treatment of several RNA virus infections clinically, so its anti-EV71 efficacy was evaluated. In vitro results showed that ribavirin effectively reduced the viral yields (with an IC50 of 65 microg/mL) and virus-induced cytopathic effect in human and mouse cell lines. In vivo results showed that ribavirin reduced the mortality, morbidity, and subsequent paralysis sequelae in infected mice by decreasing viral loads in tissues. Thus, ribavirin could be a potential anti-EV71 drug.
The Journal of Infectious Diseases 04/2008; 197(6):854-7. · 6.41 Impact Factor
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ABSTRACT: The molecular mechanism behind what causes an infection of Enterovirus 71 (EV71) in young children to result in severe neurological diseases is unclear. Herein, we show that Cdk5, a critical signalling effector of various neurotoxic insults in the brain, is activated by EV71 infection of neuronal cells. EV71-induced neuronal apoptosis could be effectively repressed by blocking either Cdk5 kinase activity or its protein expression. Moreover, EV71-induced Cdk5 activation was modulated by c-Abl. The suppression of c-Abl kinase activity by STI571 notably repressed both the Cdk5 activation and neuronal apoptosis in cells infected with EV71. Although EV71 also induces apoptosis in non-neuronal cells, it did not affect Abl and Cdk5 activities in several non-neuronal cell lines. Intriguingly, coxsackievirus A16 (CA16), a genetically closely related serotype to EV71 that usually does not induce severe neurological disorders, could only weakly stimulate Abl, but not Cdk5 kinase activity. Taken together, our data suggest a serotype- and cell type-specific mechanism, by which EV71 induces Abl kinase activity, which in turn triggers Cdk5-signalling for neuronal apoptosis.
Cellular Microbiology 12/2007; 9(11):2676-88. · 5.46 Impact Factor
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ABSTRACT: In this study, we sought to determine whether intratypic and intertypic cross-reactivity protected against enterovirus 71 (EV71) infection in a murine infection model. We demonstrate that active immunization of 1-day-old mice with avirulent EV71 strain or coxsackie A16 virus (CA16) by the oral route developed anti-EV71 antibodies with neutralizing activity (1:16 and 1:2, respectively). Splenocytes from both EV71- and CA16-immunized mice proliferated upon EV71 or CA16, but not coxsackie B3 virus (CB3), antigen stimulation. Immunized mice became more resistant to virulent EV71 strain challenge than nonimmunized mice. There was an increase in the percentage of activated splenic T cells and B cells in the immunized mice 2 days after EV71 challenge. The CA16 immune serum reacted with EV71 antigens in an enzyme-linked immunosorbent assay and neutralized EV71 but not CB3 or poliovirus at a titer of 1:4. Passive immunization with the CA16 immune serum reduced the clinical score, diminished the organ viral load, and increased the survival rate of mice upon EV71 challenge. CB3 neither shared in vitro cross-reactivity with EV71 nor provided in vivo protection after both active and passive immunization. These results illustrated that live vaccine is feasible for EV71 and that intertypic cross-reactivity of enteroviruses may provide a way to determine the prevalence of EV71.
Journal of Virology 11/2007; 81(19):10310-5. · 5.40 Impact Factor
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ABSTRACT: Inoculation of enterovirus 71 (EV71) by the oral (p.o.), intramuscular (i.m.), or intracranial route resulted in brain infection, flaccid paralysis, pulmonary dysfunction, and death of 7-day-old mice. The lag time of disease progression indicated that neuroinvasion from the inoculation sites was a prerequisite for the development of the clinical signs. Although EV71 p.o. inoculation led to a persistent viremia and a transient increase in blood-brain barrier permeability at the early stage of the infection, only low levels of virus, which led to neither severe infection nor clinical illness, could be detected in the brain, suggesting that hematogenous transport might not represent a major transmission route. In the spinal cord, following both p.o. and hind limb i.m. inoculation, the virus first appeared and increased rapidly in the lower segments, especially at the anterior horn areas, and then spread to the upper segments and brain in the presence of viremia. A reverse pattern, with the virus being first detected in the upper segment, was observed when the virus was i.m. inoculated in the forelimb. Colchicine, a fast axonal transport inhibitor, but not sciatic nerve transection reduced EV71 neuroinvasion in a dose-dependent manner, indicating a neuronal transmission of the virus.
Journal of Virology 10/2007; 81(17):8996-9003. · 5.40 Impact Factor
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ABSTRACT: Several epidemics of enterovirus 71 (EV71) infections occurred in Taiwan since 1998.
We performed the study to determine the changes in cytokine profiles associated with administration of intravenous immunoglobulin (IVIG) in patients with EV71-associated brainstem encephalitis complicated by autonomic nervous system (ANS) dysfunction and pulmonary edema.
Plasma cytokine concentrations (IL-1beta, IL-6, IL-8, IFN-gamma, TNF-alpha, IL-2, IL-4, IL-5, IL-10, and IL-13) were monitored on admission and within 12-24h after administration of IVIG in a cohort of children (n=22) with virologically confirmed EV71 infection, from March 2000 through April 2004.
Plasma levels of IFN-gamma, IL-6, IL-8, IL-10, and IL-13 levels significantly decreased in patients with pulmonary edema after administration of IVIG, P<0.05. Plasma levels of IL-6 and IL-8 were significantly decreased in patients with ANS dysregulation after administration of IVIG, P<0.05. Administration of IVIG was not associated with significant changes in plasma concentration of IL-1beta, IL-2, IL-4, IL-5 IL-10, IL-13 and TNF-alpha in patients with ANS dysregulation.
These findings suggest that IVIG might be considered to have a therapeutic role in EV71-associated brainstem encephalitis. A clinical trial is needed to support this hypothesis.
Journal of Clinical Virology 09/2006; 37(1):47-52. · 3.97 Impact Factor
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ABSTRACT: Serine proteases such as mast cell tryptase and certain allergens are important in the pathogenesis of allergic inflammation of asthma.
We sought to investigate the effects of serine protease inhibitors nafamostat mesilate (FUT), gabexate mesilate (FOY), and ulinastatin (UTI) on airway inflammation in a mouse model of allergic asthma.
BALB/c mice were sensitized to Dermatophagoides pteronyssinus (Der p) and intratracheally challenged with Der p (0.5 mg/mL). Therapeutic doses of FUT (0.0625 mg/kg), FOY (20 mg/kg), and UTI (10,000 U/kg) were intra-peritoneally injected into 3 corresponding sensitized mice during the sensitization phase (protocol 1) or 24 hours after allergen challenge (protocol 2).
Both FUT-treated and FOY-treated sensitized mice had reduced mast cells activation, airway hyperresponsiveness, attenuated eosinophils infiltrations, and decreased Der p-induced IL-4 and TNF-alpha, but increased IL-12 cytokine production in bronchoalveolar lavage fluid compared with nontreated mice. Furthermore, FUT treatment downregulated the expression of IL-1beta, TNF-alpha, IL-6, eotaxin, inducible NO synthase, CD86, and nuclear factor-kappaB activation, but enhanced the expression of IL-12 and IL-10 in Der p-stimulated alveolar macrophages. UTI-treated mice have no significant change of the aforementioned measurements compared with nontreated sensitized mice.
Nafamostat mesilate and FOY exerting the therapeutic effect in allergen-induced airway inflammation was a result not only of their inhibitory action in the early phase of mast cells activation but also of immunoregulatory function in the late phase of allergic inflammation. Such properties of FUT and FOY might be a potential therapeutic approach for asthma.
The clinical used of serine protease inhibitors FUT and FOY may also have implications for treating airway inflammation of asthma.
Journal of Allergy and Clinical Immunology 08/2006; 118(1):105-12. · 11.00 Impact Factor
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ABSTRACT: T-cell depletion is found in enterovirus 71 (EV71)-infected patients with pulmonary edema. However, the mechanism that causes T-cell depletion is unclear. To address this question, the effects of EV71 infection on the cell viability of human Jurkat T cells were studied. Viable viruses were recovered from both the culture supernatant and the cell lysate of Jurkat cells after EV71 infection. Results from reverse-transcription polymerase chain reaction (RT-PCR) and immunofluorescence assay confirmed further the presence of EV71 negative-strand RNA and antigen, respectively, in EV71-infected Jurkat cells. The viability of the Jurkat cells decreased after 48 hr of EV71 infection. Both terminal transferase end labeling (TUNEL) and DNA fragmentation assays demonstrated that the apoptosis of EV71-infected Jurkat cells had increased. In addition, the expression of Fas ligand (FasL) in EV71-infected Jurkat cells increased at both mRNA and surface expression levels. Taken together, these results confirmed that EV71 infected T cells and induced FasL expression, which may contribute to T-cell apoptosis during EV71 infection.
Journal of Medical Virology 07/2006; 78(6):780-6. · 2.82 Impact Factor
