Biomedical subjects

Hui-Min Feng

Publications and source records attributed to Hui-Min Feng.

10 recordsLinked to original sources

PubMed2006

Analysis of adsorption characteristics of 2,4-dichlorophenol from aqueous solutions by activated carbon fiber.

In this study experiments were conducted to investigate the adsorption of 2,4-dichlorophenol (2,4-DCP) by activated carbon fiber (ACF) activated by static air. With the results of batch experiments at various temperatures, the adsorption isotherms, kinetics and thermodynamics of this adsorption process were evaluated. Four adsorption isotherm models, Langmuir, Freundlich, Redlich-Peterson and Toth equations, were used to fit the experimental data and the results reveal that the adsorption isotherm models fitted the data in the order of: Langmuir>Redlich-Peterson>Toth>Freundlich isotherms. A pseudo second-order adsorption model was better to describe the adsorption data than the pseudo first-order model and the Bangham model at the temperatures tested. The activation energy was calculated to be 40.90 kJ/mol, while the thermodynamic parameters DeltaH and DeltaS were estimated to be -5.82 kJ/mol and 0.07 kJ/(molK), respectively.

Adsorption↗

PubMed2005

Analysis of ehrlichial p28 gene expression in a murine model of persistent infection.

Historically, ehrlichioses were tick-borne diseases of veterinary medical importance and are now important emerging infectious diseases in humans. p28s are encoded by multigene families with ORFs tandemly arranged with intergenic spaces of variable lengths. We reported initial sequencing of the Ehrlichia muris p28 locus. A model of persistent infection was described and provided tools for study of persistent ehrlichial infection. We completed the sequence of the E. muris p28 locus and examined mRNA expression.

Animals↗

PubMed2004

Overproduction of TNF-alpha by CD8+ type 1 cells and down-regulation of IFN-gamma production by CD4+ Th1 cells contribute to toxic shock-like syndrome in an animal model of fatal monocytotropic ehrlichiosis.

Human monocytotropic ehrlichiosis (HME) is an emerging, life-threatening, infectious disease caused by Ehrlichia chaffeensis, an obligate intracellular bacterium that lacks cell wall LPS. We have previously developed an animal model of severe HME using a strain of Ehrlichia isolated from Ixodes ovatus ticks (IOE). To understand the basis of susceptibility to severe monocytotropic ehrlichiosis, we compared low and high doses of the highly virulent IOE strain and the less virulent Ehrlichia muris strain that are closely related to E. chaffeensis in C57BL/6 mice. Lethal infections caused by high or low doses of IOE were accompanied by extensive liver damage, extremely elevated levels of TNF-alpha in the serum, high frequency of Ehrlichia-specific, TNF-alpha-producing CD8(+) T cells in the spleen, decreased Ehrlicha-specific CD4(+) T cell proliferation, low IL-12 levels in the spleen, and a 40-fold decrease in the number of IFN-gamma-producing CD4(+) Th1 cells. All groups contained negligible numbers of IL-4-producing cells in the spleen. Transfer of Ehrlichia-specific polyclonal Abs and IFN-gamma-producing Ehrlichia-specific CD4(+) and CD8(+) type 1 cells protected naive mice against lethal IOE challenge. Interestingly, infection with high dose E. muris provided protection against rechallenge with a lethal dose of IOE. Cross-protection was associated with substantial expansion of IFN-gamma-producing CD4(+) and CD8(+) cells, but not TNF-alpha-producing CD8(+) T cells, a high titer of IgG2a, and a low serum level of TNF-alpha. In conclusion, uncontrolled TNF-alpha production by CD8(+) T cells together with a weak CD4(+) Th1 cell response are associated with immunopathology and failure to clear IOE in the fatal model of HME.

Adoptive Transfer↗

PubMed2004

Histologic, serologic, and molecular analysis of persistent ehrlichiosis in a murine model.

Human monocytotropic ehrlichiosis caused by Ehrlichia chaffeensis was reported in 1987. An animal model to study acute fatal ehrlichiosis in mice that has been developed closely resembles the fatal form of human monocytotropic ehrlichiosis. However, animal models for persistent infection in the genus Ehrlichia in immunocompetent mice have not been characterized. We report the histopathological progression of Ehrlichia muris infection in immunocompetent mice (AKR and C57BL/6 strains) correlated with their antibody response determined by indirect immunofluorescence and Western immunoblotting, and the distribution and quantity of the ehrlichial load by immunohistochemistry, polymerase chain reaction (PCR), and real-time PCR in lungs, liver, and spleen. Mild to moderate correlation was observed between histopathological grading in these organs and relative ehrlichial loads. The highest ehrlichial loads were present between days 4 and 14 after infection. E. muris was detected in tissues examined up to 150 days after infection by real-time PCR. Analysis of the serological response revealed several immunodominant antigens, including 200-, 180-, 100-, 73/75-, 45-, and 28-kd proteins. In conclusion, we have provided for the first time a complete histopathological, serological, immunohistochemical, and quantitative analysis of an animal model for the study of persistent ehrlichial infection.

Animals↗

PubMed2004

Mechanisms of immunity to Ehrlichia muris: a model of monocytotropic ehrlichiosis.

Ehrlichia species can cause life-threatening infections or chronic persistent infections. Mechanisms of protective immunity were examined in an Ehrlichia muris mouse model of monocytotropic ehrlichiosis. C57BL/6 mice possessed strong genetic resistance to E. muris of an undetermined mechanism. CD8 T lymphocytes were particularly important, as revealed by 81% fatalities for E. muris-infected, major histocompatibility complex class I gene knockout mice compared with no deaths for wild-type C3H mice. Moreover, 80% of C3H mice depleted of CD8 and CD4 cells died of E. muris infection compared with only 44% of CD4 cell-depleted mice. CD8 T lymphocytes were demonstrated for the first time in an Ehrlichia infection to exhibit cytotoxic T-lymphocyte activity against Ehrlichia-infected target cells. Both gamma interferon and tumor necrosis factor were shown to play synergistic roles in protective immunity in vivo for the first time, as demonstrated by 75% fatalities when both cytokines were neutralized compared with minimal mortality when they were depleted separately. Passive transfer of antibodies, but not Fab fragments, to E. muris protected C3H/SCID mice against lethal infection. The mechanism of increased susceptibility (22% lethality) of C57BL/6 major histocompatibility complex class II gene knockout mice and CD4 cell-depleted C3H mice (i.e., through a gamma interferon or antibody mechanism), as well as the more important role of CD8 T lymphocytes (in the form of cytotoxic T-lymphocyte activity and/or gamma interferon production), remains to be elucidated. Protective immunity against monocytotropic E. muris is mediated by a combination of CD8 and CD4 T lymphocytes, gamma interferon, tumor necrosis factor alpha, and antibodies.

Animals↗

PubMed2004

Fc-dependent polyclonal antibodies and antibodies to outer membrane proteins A and B, but not to lipopolysaccharide, protect SCID mice against fatal Rickettsia conorii infection.

An emphasis on cellular immunity against Rickettsia has led to neglect of analysis of the role of antibody. The availability of an excellent mouse model of spotted fever rickettsiosis enabled investigation of a potential role of antibody in immunity to Rickettsia conorii. C3H severe combined immunodeficiency (SCID) mice were passively transfused with monoclonal antibodies against rickettsial outer membrane protein A (OmpA), OmpB, or lipopolysaccharide (LPS), polyclonal anti-R. conorii serum, Fab fragments of polyclonal antiserum, or no antibodies and then challenged 48 h later with 10 50% lethal doses (LD(50)) of R. conorii. All mice that received monoclonal antibodies against OmpA and two of four mice that received monoclonal antibodies against OmpB or polyclonal antisera were completely protected, but the recipients of anti-LPS antibodies or the Fab fragments were not protected. Polyclonal antibody treatment of C3H SCID mice that had been infected with 10 LD(50) of R. conorii 4 or 5 days earlier prolonged the life of the infected mice from 10.4 to 22.5 days and resulted in decreased levels of infectious rickettsiae in the spleen and liver 24 and 48 h later. Treatment with protective antibodies resulted in the development of large aggregates of R. conorii antigens in splenic macrophages and intraphagolysosomal rickettsial death and digestion. The kinetics of development of antibodies to R. conorii determined by immunoblotting revealed antibodies to LPS on day 6 and antibodies to OmpA and OmpB on day 12, when recovery from the infection had already occurred. Antibodies to particular epitopes of OmpA and OmpB may protect against reinfection, but they may not play a key role in immunity against primary infection. Antibodies might be useful for treating infections with antibiotic-resistant organisms, and some B-cell epitopes should be included in a subunit vaccine.

Animals↗

PubMed2004

Effect of antibody on the rickettsia-host cell interaction.

A recent study demonstrated that polyclonal antibodies to Rickettsia conorii and monoclonal antibodies to outer membrane proteins A (OmpA) and B (OmpB) provided effective, Fc-dependent, passive immunity, even in severe combined immunodeficient mice with an established infection. In order to determine the mechanism of protection, mouse endothelial and macrophage-like cell lines were infected with R. conorii that had been exposed to polyclonal antibodies, monoclonal antibodies to OmpA or OmpB, Fab fragments of the polyclonal antibodies, or normal serum or that were left untreated. At 0 h, Fc-dependent antibody enhancement of R. conorii adherence to endothelial and macrophage-like cell lines was inhibited by the presence of normal serum, suggesting Fc receptor-mediated adherence of opsonized rickettsiae. At 3 h, the opsonized rickettsiae had been internalized. After 72 h, inhibited survival of rickettsiae exposed to polyclonal antibodies or monoclonal antibodies to OmpA or OmpB was evident compared with growth of untreated and normal serum-treated and polyclonal Fab antibody-treated R. conorii. Polyclonal antibodies and an anti-OmpB monoclonal antibody inhibited the escape of R. conorii from the phagosome, resulting in intraphagolysosomal rickettsial death. At 48 h of infection, rickettsicidal activity of macrophages by opsonized rickettsiae was inhibited by NG-monomethyl-L-arginine, superoxide dismutase, mannitol, or supplemental L-tryptophan, and endothelial rickettsicidal activity against opsonized rickettsiae was inhibited by NG-monomethyl-L-arginine, superoxide dismutase, catalase, or supplemental L-tryptophan. Thus, Fc-dependent antibodies protected against R. conorii infection of endothelium and macrophages by opsonization that inhibited phagosomal escape and resulted in phagolysosomal killing mediated by nitric oxide, reactive oxygen intermediates, and L-tryptophan starvation.

Animals↗

PubMed2004

Ehrlichia chaffeensis: a prevalent, life-threatening, emerging pathogen.

Ehrlichia chaffeensis are small, obligately intracellular, endosomal bacteria with tropism for macrophages. Persistent infection in reservoir white-tailed deer is transmitted by lone star ticks. Flu-like illness can progress to severe multisystem disease with toxic shock-like syndrome, meningitis, or ARDS. The case-fatality rate is 2.7%. Leukopenia and thrombocytopenia are diagnostically useful. Granulomas are associated with control of the infection. Ehrlichial proteins and glycoproteins have been sequenced and expressed for diagnostic serology and vaccine development. Mouse models (mild disease and persistent infection with E. muris and fatal monocytotropic ehrlichiosis with a Japanese tick isolate) revealed that CD4 and CD8 T type 1 lymphocyte responses, IFN-gamma, TNF-alpha, and antibodies play roles in protective immunity, while a weak CD4 T-helper response, overproduction of TNF-alpha, and very high IL-10 are associated with toxic shock-like mortality. Protection against fatal ehrlichiosis was achieved by prior infection with low virulence E. muris. Acute clinical diagnosis is difficult except by PCR. Response to doxycycline is dramatic.

Animals↗

PubMed2003

Identification of CD8 T-lymphocyte epitopes in OmpB of Rickettsia conorii.

The 1.2-kb DNA fragment of the Rickettsia conorii outer membrane protein B gene (OmpB(451-846)) was subcloned using site-specific PCR primers and expressed as six smaller fragments: OmpB(458-652), OmpB(595-744), OmpB(595-654), OmpB(645-692), OmpB(689-744), and OmpB(739-848). NCTC cells transfected with a mammalian expression vector expressing the fragments OmpB(689-744) and OmpB(739-848) stimulated immune anti-R. conorii CD8 T lymphocytes, suggesting the presence of CD8 T-lymphocyte-stimulating epitopes on these fragments. In order to further characterize the CD8 T-lymphocyte-stimulatory elements, CD8 T-lymphocyte epitopes on OmpB(689-744) and OmpB(739-848) were mapped by overlapping synthetic peptides. The ability of these synthetic peptides to stimulate immune CD8 T lymphocytes was determined by gamma interferon (IFN-gamma) production and cell proliferation after incubation with simian virus 40-transformed murine vascular endothelial cells in the presence of a 20 micro M solution of each synthetic peptide. Five synthetic peptides, SKGVNVDTV (OmpB(708-716)), ANVGSFVFN (OmpB(735-743)), IVSGTVGGQ (OmpB(749-757)), ANSTLQIGG (OmpB(789-797)), and IVEFVNTGP (OmpB(812-820)), induced secretion of IFN-gamma at significantly higher levels than the controls. Three of these five peptides, SKGVNVDTV (OmpB(708-716)), ANSTLQIGG (OmpB(789-797)), and IVEFVNTGP (OmpB(812-820)), also stimulated the proliferation of immune CD8 T lymphocytes. Significantly higher levels of specific cytotoxic T-lymphocyte killing were observed with the same three synthetic peptides, SKGVNVDTV (OmpB(708-716)), ANSTLQIGG (OmpB(789-797)), and IVEFVNTGP (OmpB(812-820)).

Animals↗

PubMed2002

Current status of immune mechanisms of killing of intracellular microorganisms.

The interaction between intracellular pathogens and the mammalian host follows different pathways that reflect evolved survival mechanisms of both the pathogen and the host to assure each one's own survival. From the host's perspective, different immune mechanisms predominate at different stages of infection. Both phagocytic and non-phagocytic target cells participate in microbial uptake and, in some cases, intracellular destruction. In addition, the development of specific immunity ensures sustained activation of intracellular microbicidal mechanisms in the target cells, and induction of apoptotic or lytic target cell death by cytotoxic T lymphocytes. From the pathogen's perspective, different evasion strategies are employed to counteract host defenses. Understanding microbial survival strategies and the immune mechanisms that result in killing of intracellular pathogens will deepen our insight into the pathogenesis of infection that could be applied towards the development of effective vaccination and immunotherapy.

Animals↗