Jenny M. Bator

University of Illinois Chicago

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Co-Authors

Ronald M. Burch

Consumer VOICE

Moshe Weitzberg

Abbott Fund

Jane R. Connor

AstraZeneca (United States)

Duke E. Cameron

Massachusetts General Hospital

Kenton J. Zehr

University of Cincinnati Medical Center

A. Marc Gillinov

Cleveland Clinic

Janice Redmond

St. James's Hospital

Christopher L. Reading

AbbVie (United States)

William E. Curtis

University of Washington

Donald K. Martin

Université Grenoble Alpes

Cooperative Institutions

Johns Hopkins University

Johns Hopkins Medicine

Nova Medical (United States)

Johns Hopkins Hospital

National Institutes of Health

Freeport-McMoRan (United States)

Eunice Kennedy Shriver National Institute of Child Health and Human Development

University of Maryland, Baltimore

The University of Texas MD Anderson Cancer Center

Cleveland Clinic

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Neutrophil adhesion molecule expression during cardiopulmonary bypass with bubble and membrane oxygenators

The Annals of Thoracic Surgery (1993)

A. Marc Gillinov Jenny M. Bator Kenton J. Zehr Janice Redmond Ronald M. Burch

The neutrophil-mediated tissue injury associated with cardiopulmonary bypass (CPB) is thought to require the interaction of specific neutrophil and endothelial adhesion molecules. In this study, the effects of CPB on the expression of neutrophil CD11b and CD18 (the components of the Mac-1 adhesion molecule) were examined; the effects of membrane versus bubble oxygenators on the expression of neutrophil CD11b and CD18 were compared; and the plasma levels of the intercellular adhesion molecule-1 (cICAM-1), an inducible endothelial adhesion molecule, were measured. In addition, the time courses of complement activation and neutrophil granule release were measured to determine their temporal relationship to the expression of the neutrophil adhesion molecule. Fifteen adult patients underwent procedures requiring cardiopulmonary bypass; hollow-fiber membrane oxygenators were used in 8 (group M) and bubble oxygenators were used in 7 (group B). Blood samples were drawn before, during, and after CPB for determination of the expression of neutrophil CD11b and CD18 (immunofluorescent flow cytometry), and the plasma cICAM-1, elastase, lactoferrin (enzyme-linked immunoabsorbent assay), and plasma C3a (radioimmunoassay) levels. CPB caused an immediate and sustained increase in the neutrophil CD11b and CD18 expression in both groups; after 60 minutes of CPB, CD11b expression had increased by 116.9% +/- 19.1% in group B and by 79.3% +/- 8.5% in group M (p = 0.78). Over the same period, CD18 expression increased by 97.2% +/- 17.9% in group B and by 72.4% +/- 16.8% in group M (p = 0.67).(ABSTRACT TRUNCATED AT 250 WORDS)

Neutrophil elastase

10.1016/0003-4975(93)90342-f

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Citations (115)

Inhibition of neutrophil adhesion reduces myocardial infarct size

The Annals of Thoracic Surgery (1993)

William E. Curtis A. Marc Gillinov Ian C. Wilson Jenny M. Bator Ronald M. Burch

Neutrophil accumulation and activation within the myocardium during ischemia and reperfusion has been shown to play a prominent role in the development of myocardial stunning and infarction.To determine if a simple inhibitor of neutrophil adhesion could reduce myocardial infarct size, we administered NPC 15669 (a new antiinflammatory agent that inhibits neutrophil adhesion) to 12 pigs (6 controls, 6 NPC-treated) in a porcine model of ischemia and reperfusion injury.Each animal received a continuous infusion of either NPC (10 mg/kg intravenous bolus followed by 6 mgkg-' * h-' intravenous infusion) or an equal volume of normal saline solution during 1 hour of left anterior descending artery occlusion and 2 hours of reperfusion.There were no eutrophil accumulation and activation within myo-N cardium has been shown to play a prominent role in extension of myocardial infarction [ 1-61.Activated neutrophils release numerous cytotoxic metabolites, including oxygen free radicals and proteolytic enzymes that are highly damaging to tissue [7, 81.Recent work indicates that activated neutrophils have increased adhesiveness to endothelial cells after modulation of their cell surface adhesion molecules [9].Most notable among these adhesion molecules is a neutrophil membrane glycoprotein known as the Mac-1, or CDllb/CD18, adhesion molecule.Several studies have demonstrated that inhibition of neutrophil adherence by monoclonal antibodies directed against the Mac-1 protein attenuates myocardial infarction and stunning [3, 5, lo].Such antibodies, although important as research tools, are too costly and in limited supply to be useful as therapeutic agents.Recently, a new class of antiinflammatory agents that inhibit neutrophil recruitment was introduced into clinical trials for treatment of several inflammatory diseases.These "leumedins" are amino acids that have been shown in several animal models to reduce neutrophil recruitment and infiltration into areas of inflammation [ll, 121.One of the principal activities of leumedins appears to be inhibition of up-regulation of the Mac-1 adhesion molecule.In this present study, we report the use of the leumedin

Myocardial Stunning

10.1016/0003-4975(95)90015-2

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N-(fluorenyl-9-methoxycarbonyl) amino acids, a class of antiinflammatory agents with a different mechanism of action.

Proceedings of the National Academy of Sciences (1991)

Ronald M. Burch Moshe Weitzberg Natalie Blok Richard O. Muhlhauser Donald K. Martin

Several members of a series of N-(fluorenyl-9-methoxycarbonyl) amino acids were found to possess a broad spectrum of antiinflammatory activity. The compounds were active against oxazolone dermatitis in mice and adjuvant arthritis in rats, models in which activated T lymphocytes are implicated. The compounds also inhibited T-lymphocyte activation in vitro, assessed by using the mixed lymphocyte reaction. The compounds inhibited the reversed passive Arthus reaction in rats and arachidonic acid-induced dermatitis in mice, models in which leukocyte infiltration is responsible for the inflammatory reaction. More complete evaluation was made of one compound, N-(fluorenyl-9-methoxycarbonyl)leucine (NPC 15199). On histologic examination after arachidonic acid administration, NPC 15199 was found to block recruitment of neutrophils into the inflammatory site. The compound was not a general myelotoxin. Prolonged treatment of animals did not alter bone-marrow progenitor number or the numbers of circulating white blood cells. Further, several white cell functions were not inhibited in vitro, including neutrophil respiratory burst and macrophage phagocytosis. NPC 15199 was effective in blocking antigen arthritis in rabbits and was effective in a therapeutic protocol, reversing oxazolone edema. These studies suggest that N-(fluorenyl-9-methoxycarbonyl) amino acids may be valuable therapeutic agents for inflammatory diseases.

Oxazolone

Arthus reaction

Mechanism of Action

10.1073/pnas.88.2.355

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Citations (111)

Estrogen Dependence of a Gonadotropin-induced Steroidogenic Lesion in Rat Testicular Leydig Cells

Journal of Clinical Investigation (1980)

S. B. Cicorraga Susan H. Sorrell Jenny M. Bator Kevin Catt Maria Dufau

Leydig cells isolated from the testes of rats treated with intravenous exogenous gonadotropin (hCG) or subcutaneous gonadotropin-releasing hormone (GnRH) show markedly decreased luteinizing hormone (LH) receptors and a partial block in testicular 17,20 desmolase activity. In contrast, Leydig cells from animals with equivalent degrees of LH receptor loss induced by subcutaneous hCG treatment show no change in 17,20 desmolase activity. These findings indicated that the acuteness of gonadotrophic stimulation, rather than the extent of LH receptor loss, was responsible for the steroidogenic lesion. A role of estradiol in the enzymatic block produced in vivo by acute elevation of circulating gonadotropin (intravenous hCG or GnRH-stimulated endogenous LH) was suggested by rapid elevations of testicular 17beta-estradiol within 30 min after intravenous hCG, whereas more gradual increases in estradiol occurred 4-8 h after subcutaneous hCG. The inhibitory effect of endogenous estrogen on testicular steroidogenesis was confirmed by the ability of an estrogen antagonist (Tamoxifen) to prevent the reduction of testosterone responses caused by intravenous hCG and subcutaneous GnRH. In addition, Tamoxifen significantly increased the number of LH receptors in Leydig cells from both control and gonadotropin-desensitized animals. These findings indicate that the acute elevations of intratesticular estrogen produced by treatment with hCG or GnRH are responsible for the steroidogenic lesion seen in gonadotropin-desensitized Leydig cells. These results also suggest that locally produced estrogens contribute to the regulation of testicular LH receptors and 17,20 desmolase activity.

Gonadotropin

10.1172/jci109716

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Citations (111)

A microassay for the determination of iodide and its application to the measurement of the iodination of proteins and the catalytic activities of iodo compounds

Analytical Biochemistry (1989)

Richard O’Kennedy Jenny M. Bator Christopher L. Reading

Hapten

10.1016/0003-2697(89)90214-5

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Citations (21)

Inhibition of neutrophil adhesion during cardiopulmonary bypass

The Annals of Thoracic Surgery (1994)

A. Marc Gillinov Janice Redmond Kenton J. Zehr Ian C. Wilson William E. Curtis

Room air distribution

10.1016/0003-4975(94)90380-8

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Citations (106)

NPC 15669 inhibits the reversed passive Arthus reaction in rats by blocking neutrophil recruitment.

Journal of Pharmacology and Experimental Therapeutics (1992)

Ronald M. Burch James R. Connor Jenny M. Bator Moshe Weitzberg Keith D. Laemont

NPC 15669, N-carboxy-L-leucine,N-[(2,7-dimethylfluoren-9-yl)methyl]ester, has been shown to inhibit several inflammatory reactions that depend upon recruitment of neutrophils into the primary lesion. In the present study we examined the effects of NPC 15669 in the reversed passive Arthus reaction, an inflammatory reaction occurring in the skin of rats in response to intracutaneous injection of antigen followed by intravenous administration of antibody. In this model, immune complex formation activates complement, resulting in rapid recruitment of neutrophils to the site, which releases free radicals and proteases that damage capillaries, resulting in plasma leak. NPC 15669 inhibited the increased capillary permeability occurring in the reversed passive Arthus reaction in a dose-dependent manner, with an ED50 of 4 mg/kg. The agent similarly inhibited the recruitment of radiolabeled neutrophils as well as the accumulation of myeloperoxidase, a neutrophil marker. NPC 15669 in vitro inhibited the adherence of formyl-L-Met-L-Leu-L-Phe- or human recombinant C5a-activated neutrophils to endothelium, with IC50 values of 15 to 30 microM (ca. 4-9 micrograms/ml). Measurement of plasma NPC 15669 showed that at the ED50 dose, the average circulating concentration of drug was 5 micrograms/ml, consistent with the hypothesis that NPC 15669 exerts its anti-inflammatory effects by inhibiting neutrophil adherence to endothelium and recruitment into the inflammatory lesion.

Arthus reaction

ED50

Vascular permeability

10.1016/s0022-3565(25)10498-9

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Citations (19)

Measurement of antibody affinity for cell surface antigens using an enzyme-linked immunosorbent assay

Journal of Immunological Methods (1989)

Jenny M. Bator Christopher L. Reading

Serial dilution

Microtiter plate

10.1016/0022-1759(89)90090-2