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Dive into the research topics where Mishell Evans is active.

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Featured researches published by Mishell Evans.


Journal of Medical Microbiology | 1995

Identification of pioneer viridans streptococci in the oral cavity of human neonates.

Cheryl L. Pearce; George H. Bowden; Mishell Evans; Sean P. Fitzsimmons; Jolene Johnson; Michael J. Sheridan; Raoul Wientzen; Michael F. Cole

Three hundred and sixty-seven strains of pioneer streptococci isolated from the mouths of 40 healthy, full-term infants during the first month of life were examined by two taxonomic schemes that incorporated biochemical and physiological characteristics, IgA1 protease production and glycosidase activities. Streptococcus mitis biovar 1 and S. oralis comprised 55.0% of the pioneer streptococci isolated from neonates. S. salivarius constituted 25.3% of the isolates, while S. anginosus, S. mitis biovar 2, S. sanguis and S. gordonii accounted collectively for 11.4%. Difficulties in identifying streptococci were encountered and 8.4% of the 367 isolates could not be assigned to a recognised species.


Journal of Clinical Immunology | 1990

Natural killer cell-mediated lysis of Mycobacterium avium complex-infected monocytes

Paul Katz; Henry Yeager; Gail Whalen; Mishell Evans; Rodney P. Swartz; Jennifer Roecklein

Since the precise mechanism of host responses to infection withMycobacterium-avium complex (MAC) is unclear and since cytotoxic lymphocytes may be involved in the destruction of cells infected with intracellular pathogens, we investigated the ability of normal peripheral blood lymphocytes to kill MAC-infected monocytes in a short-term isotope release assay. Nylon wool-passed lymphocytes lysed MAC-infected but not uninfected monocytes during a 4-hr assay. Infected monocytes were less sensitive to cell-mediated killing than the standard natural killer (NK) cell-sensitive cell line K562, although the kinetics of lysis were similar. The release of lymphocyte-derived mediators such as tumor necrosis factor, interleukin-2 (IL-2), and interferon-alpha and -gamma could not be implicated as a cause of monocyte death. Through the use of cell-specific monoclonal antibodies plus complement, the phenotype of the effector cell was that of an NK cell (CD3 negative, partially CD8 negative, and CD16 positive). The use of highly purified, negatively selected NK cells confirmed these results. NK cell-mediated lysis of infected monocytes decreased MAC viability, indicating that this cytotoxic activity would not favor dissemination of the organism. The killing of MAC-infected monocytes was reduced by K562 cells, suggesting that these targets shared common recognition/binding structures. These results suggest that NK-cell function may be important in the prevention of or response to MAC infection and may help explain the predilection of AIDS patients to develop widespread disease.


American Journal of Infection Control | 1998

Clonal diversity of vancomycin-resistant enterococci from an outbreak in a tertiary care university hospital

Cheryl L. Pearce; Mishell Evans; Stephen M. Peters; Michael F. Cole

BACKGROUND Enterococci have become important nosocomial pathogens and now account for approximately 12% of nosocomial infections. Enterococci can be transferred from patient to patient and from health care personnel to patient. We investigated the clonal diversity of vancomycinresistant enterococci (VRE) causing an outbreak of infections and attempted to determine the patterns of spread of these bacteria in a university hospital. METHODS Ribotyping was used to examine the clonal diversity of 50 VRE isolates, including 23 from wounds, 14 from urine, 8 from blood, 3 from the rectum, 1 from drainage, and 1 from the cornea. RESULTS Nine patients were infected with Enterococcus faecalis, 10 with Enterococcus faecium, 3 with both E faecalis and E faecium, and 1 with Enterococcus avium. The results suggest that the sources of the VRE infections included endogenous strains and strains acquired by transmission from attending staff or from the environment. Three patients were infected by both nosocomial and endogenous strains. CONCLUSIONS These data suggest that the collection and analysis of several isolates from repeated specimens is necessary to obtain a fuller understanding of the epidemiology and population structure of antibiotic-resistant enterococci.


Cellular Immunology | 1989

Suppression of B cell responses by natural killer cells is mediated through direct effects on T cells

Paul Katz; S. Ray Mitchell; Thomas R. Cupps; Mishell Evans; Gail Whalen

We examined the ability of human natural killer (NK) cells to modulate T cell-dependent mitogen-induced B cell responses. Highly purified NK cells inhibited the polyclonal antibody responses of autologous pokeweed mitogen (PWM)-stimulated unfractionated mononuclear cells in a reverse hemolytic plaque-forming cell (PFC) assay. Investigation of the possible mechanism(s) of the suppressor activity of NK cells revealed that lysis of mitogen-stimulated cells was unlikely. Chromium-51 release cytotoxicity assays of PWM-stimulated mononuclear cells did not demonstrate lysis by NK cells. Additionally, the monoclonal antibody 13.3, which abrogates NK cell cytolysis, did not reverse NK cell-dependent suppression of PFC formation. The putative lytic molecule elaborated by NK cells, NK cytotoxic factor, did not suppress B cell responses, further supporting a nonlytic inhibitory mechanism. That NK cell-derived lymphokines such as IFN-alpha, IFN-gamma, or IL-2 were uninvolved in the down-regulation of B cells was corroborated by the failure of antibodies to these mediators to reverse the suppression. NK cells did not suppress PFC formation when T cells were replaced by supernatants from PWM-stimulated T cells; additionally, NK cells had no effect on the generation of these necessary T cell factors. However, the coculture of T cells with NK cells resulted in the induction of suppressor activity within the T cell population suggesting that this was the mechanism of NK cell-mediated suppression of B cell responses.


Clinical and Vaccine Immunology | 2004

Study of humoral immunity to commensal oral bacteria in human infants demonstrates the presence of secretory immunoglobulin A antibodies reactive with Actinomyces naeslundii genospecies 1 and 2 ribotypes.

Michael F. Cole; Mishell Evans; Jennifer L. Kirchherr; Michael J. Sheridan; George H. Bowden

ABSTRACT The mouths of three human infants were examined from birth to age 2 years to detect colonization of Actinomyces naeslundii genospecies 1 and 2. These bacteria did not colonize until after tooth eruption. The diversity of posteruption isolates was determined by ribotyping. Using immunoblotting and enzyme-linked immunosorbent assay, we determined the reactivity of secretory immunoglobulin A (SIgA) antibodies in saliva samples collected from each infant before and after colonization against cell wall proteins from their own A. naeslundii strains and carbohydrates from standard A. naeslundii genospecies 1 and 2 strains. A. naeslundii genospecies 1 and 2 carbohydrate-reactive SIgA antibodies were not detected in any saliva sample. However, SIgA antibodies reactive with cell wall proteins were present in saliva before these bacteria colonized the mouth. These antibodies could be almost completely removed by absorption with A. odontolyticus, a species known to colonize the human mouth shortly after birth. However, after colonization by A. naeslundii genospecies 1 and 2, specific antibodies were induced that could not be removed by absorption with A. odontolyticus. Cluster analysis of the patterns of reactivity of postcolonization salivary antibodies from each infant with antigens from their own strains showed that not only could these antibodies discriminate among strains but antibodies in saliva samples collected at different times showed different reactivity patterns. Overall, these data suggest that, although much of the salivary SIgA antibodies reactive with A. naeslundii genospecies 1 and 2 are directed against genus-specific or more broadly cross-reactive antigens, species, genospecies, and possibly strain-specific antibodies are induced in response to colonization.


The Journal of Pediatrics | 1994

Immunoglobulin A subclasses in infants' saliva and in saliva and milk from their mothers

Sean P. Fitzsimmons; Mishell Evans; Cheryl L. Pearce; Michael J. Sheridan; Raoul Wientzen; Michael F. Cole


Clinical and Vaccine Immunology | 1996

Clonal diversity of Streptococcus mitis biovar 1 isolates from the oral cavity of human neonates.

Sean P. Fitzsimmons; Mishell Evans; Cheryl L. Pearce; Michael J. Sheridan; Raoul Wientzen; George H. Bowden; Michael F. Cole


Infection and Immunity | 1999

Humoral Immunity to Commensal Oral Bacteria in Human Infants: Salivary Secretory Immunoglobulin A Antibodies Reactive with Streptococcus mitis biovar 1, Streptococcus oralis, Streptococcus mutans, and Enterococcus faecalis during the First Two Years of Life

Michael F. Cole; Stacey Bryan; Mishell Evans; Cheryl L. Pearce; Michael J. Sheridan; Patricia A. Sura; Raoul Wientzen; George H. Bowden


Infection and Immunity | 1994

Pioneer oral streptococci produce immunoglobulin A1 protease.

Michael F. Cole; Mishell Evans; S Fitzsimmons; J Johnson; Cheryl L. Pearce; Michael J. Sheridan; Raoul Wientzen; George H. Bowden


Infection and Immunity | 1998

Humoral Immunity to Commensal Oral Bacteria in Human Infants: Salivary Antibodies Reactive with Actinomyces naeslundii Genospecies 1 and 2 during Colonization

Michael F. Cole; Stacey Bryan; Mishell Evans; Cheryl L. Pearce; Michael J. Sheridan; Patricia A. Sura; Raoul Wientzen; George H. Bowden

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Michael F. Cole

Georgetown University Medical Center

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Cheryl L. Pearce

Georgetown University Medical Center

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Raoul Wientzen

Georgetown University Medical Center

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Paul Katz

Georgetown University

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Sean P. Fitzsimmons

Georgetown University Medical Center

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S. Ray Mitchell

Georgetown University Medical Center

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Thomas R. Cupps

Georgetown University Medical Center

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