Roger M. Loria

Virginia Commonwealth University

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David A. Padgett

Tennessee State University

Sidney Kibrick

Boston University

William Regelson

Virginia Commonwealth University

Martin R. Graf

Neurology, Inc

Gordon E. Madge

Virginia Commonwealth University

Louise B. Montgomery

Virginia Commonwealth University Medical Center

Mohammed Kalimi

Virginia Commonwealth University Medical Center

Selwyn A. Broitman

Boston University

Robert F. Diegelmann

Virginia Commonwealth University

Kevin R. Ward

University of Iowa Hospitals and Clinics

Cooperative Institutions

Virginia Commonwealth University

Virginia Commonwealth University Medical Center

University of Richmond

Istituti di Ricovero e Cura a Carattere Scientifico

University of Virginia

Children's Hospital of Richmond at VCU

National Cancer Institute

Uniformed Services University of the Health Sciences

Harvard University

Universidade de São Paulo

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Dehydroepiandrosterone (DHEA)‐the “Mother Steroid”

Annals of the New York Academy of Sciences (1994)

I. Immunologic Action William Regelson Roger M. Loria Mohammed Kalimi

10.1111/j.1749-6632.1994.tb56859.x

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Citations (91)

Suppression of aortic elastic tissue autofluorescence for the detection of viral antigen

Histochemistry (1979)

Roger M. Loria William L. Kos Ann E. Campbell Gordon E. Madge

Autofluorescence

Coxsackievirus

10.1007/bf00496527

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Citations (6)

Influence of diabetes mellitus heredity on susceptibility to coxsackievirus B4

Archives of Virology (1984)

Roger M. Loria Louise B. Montgomery Linda A. Corey Vernon M. Chinchilli

Coxsackievirus

Medical microbiology

Heredity

10.1007/bf01309997

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Citations (27)

Dietary hepatic cholesterol elevation: effects on coxsackievirus B infection and inflammation

Infection and Immunity (1982)

Ann E. Campbell Roger M. Loria Gordon E. Madge A M Kaplan

Mice made hypercholesterolemic (HC) by diet are highly susceptible to coxsackievirus (CV) B5, whereas normal adult animals remain resistant. In attempting to define those dietary-induced physiological changes which contribute to altered resistance, a strong association between accumulation of intrahepatic cholesterol and increased CV B5-induced mortality was demonstrated, with maximum susceptibility to CV coinciding with a 2.5-fold increase in the ratio of hepatic cholesterol to protein. This metabolic imbalance was associated with a lower clearance rate of CV from the blood and liver of C57BL/6 mice, although virus-specific neutralizing antibody production was unaltered. In addition to CV, HC mice were more susceptible to an intravenous inoculation of Listeria monocytogenes in comparison to controls. The macrophage stimulant Corynebacterium parvum failed to increase resistance of HC mice to a high dose of CV B4 and L. monocytogenes and failed to induce the hepatomegaly, splenomegaly, and cellular infiltrate seen in the liver and spleen of normal animals. Furthermore, the peritoneal monocytic infiltrate induced by thioglycolate in normal animals was absent in HC mice. Results from these experiments suggest that decreased resistance to CV in the HC host is attributed to a defect in the nonspecific immune responses of macrophages and monocytes which are of primary importance in resistance to this virus and other infectious agents.

Coxsackievirus

10.1128/iai.37.1.307-317.1982

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Citations (21)

Coxsackie B4-Induced Pancreopathy

Springer eBooks (1987)

Sallie S. Cook Roger M. Loria

Etiology

Pathogenesis

10.1007/978-1-4613-2085-2_10

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Regulation of the immune response by dehydroepiandrosterone and its metabolites.

PubMed (1996)

Roger M. Loria David A. Padgett Phuong Nguyen Hoai Huynh

Dehydroepiandrosterone (5-androsten-3 beta-ol-17-one, DHEA) has been shown to protect mice from a variety of lethal infections. This includes, but is not limited to, infection with viruses (herpes virus type 2, coxsackie virus B4 (CB4)), bacteria (Enterococcus faecalis, Pseudomonas aeruginosa), and a parasite (Cryptosporidium parvum). We have previously reported that androstenediol (5-androstene-3 beta, 17 beta-diol, AED), derived from DHEA, is at least 100 x more effective in up-regulating systemic resistance against CB4 infection than its precursor. Furthermore, androstenetriol (5-androstene-3 beta,7 beta, 17 beta-triol, AET) which is formed by 7 beta hydroxylation of AED, was more effective against CB4 infection than its precursor, AED. Neither steroid, however, has shown any significant direct antiviral effects. The in vitro influences of DHEA, AED and AET on a mitogen-induced mixed splenocyte proliferation assay were determined. The results showed that DHEA suppressed the proliferation of concanavalin A (ConA)- or lipopolysaccharide-activated cultures in a dose-dependent manner. AED had little influence on the activation response. However, AET potentiated the response to both mitogens significantly above the control level. The regulation of interleukin (IL)-2 and IL-3 secretion from ConA-activated lymphocytes was analogous to these observations. These functions were depressed by DHEA, unaffected by AED, and potently increased by AET. Moreover, the classic immunosuppressive effects of hydrocortisone on ConA-induced lymphocyte proliferation, as well as IL-2 and IL-3 production, were unaffected by co-culture with DHEA and only minimally counteracted by AED. In contrast. AET significantly counteracted the effect of hydrocortisone when co-cultured together. These data show that while DHEA, AED and AET each function in a similar manner in vivo, in vitro their effects are dramatically different from one another with only AET potentiating the cellular response by increasing lymphocyte activation and counteracting the immunosuppressive activity of hydrocortisone.

Androstenediol

Splenocyte

Pokeweed mitogen

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Citations (84)

Enhancing host resistance to infections

Journal of Antivirals & Antiretrovirals (2017)

Roger M. Loria

Host resistance

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Endocrine regulation of the immune response to influenza virus infection with a metabolite of DHEA-androstenediol

Journal of Neuroimmunology (1997)

David A. Padgett Roger M. Loria John F. Sheridan

Androstenediol

Corticosterone

Pathogenesis

10.1016/s0165-5728(97)00102-1

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Citations (73)

Androstenetriol and Androstenediol: Protection Against Lethal Radiation and Restoration of Immunity After Radiation Injury

Annals of the New York Academy of Sciences (2000)

Roger M. Loria Daniel H. Conrad Thomas Huff H. CARTER D. Ben‐Nathan

A bstract : Androstenetriol (AET) and Androstenediol (AED) upregulate host immunity, leading to increased resistance against infections. AET augments IL‐2, IL‐3, IFNγ levels, and counteracts hydrocortisone immune suppression. AET and AED at a dose of 0.75 mg/‐ and 8.0 mg/25‐g mouse, protected 60 and 70%, respectively, of C57/BL/6J mice irradiated with a lethal dose. These hormones also protected mice irradiated with 6 Gy and infected with a coxsackievirus B4 LD50. AET significantly increased spleen lymphocyte numbers at 7, 14, and 21 days after a 6‐Gy exposure. Fluorescent activated cell‐sorter analysis of irradiated mice, spleen, and bone marrow showed that AET significantly augmented the myeloid precursor markers, CD11b/Mac‐1, and B220 (pan B), as well as the absolute numbers of CD4+/CD8+ cells over the 21 days of testing. Overall, the data are consistent with AET/AED inducing a more rapid recovery of all hematopoietic precursors from the small number of surviving stem cells.

Acute Radiation Syndrome

10.1111/j.1749-6632.2000.tb05452.x

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Citations (43)

#87 Androstenetriol improves survival in a trauma-hemorrhage shock model

Brain Behavior and Immunity (2005)

Roger M. Loria Andreea C. Marcu Hans W. Carter R. Wayne Barbee Rao R. Ivatury

Extracorporeal

Lumen (anatomy)

Hemorrhagic shock

10.1016/j.bbi.2005.10.094

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