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15 January 2005

Volume 191, Number 2
The Journal of Infectious Diseases 2005;191:299–306
© 2004 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2005/19102-0020$15.00
DOI: 10.1086/426453
MAJOR ARTICLE

16α‐Bromoepiandrosterone Restores T Helper Cell Type 1 Activity and Accelerates Chemotherapy‐Induced Bacterial Clearance in a Model of Progressive Pulmonary Tuberculosis

Rogelio Hernández‐Pando,1

Diana Aguilar‐Leon,1

Hector Orozco,1

Alberto Serrano,1

Clarence Ahlem,2

Richard Trauger,2

Beatrix Schramm,2

Chris Reading,2

James Frincke,2 and

Graham A. W. Rook3

1Instituto Nacional de Ciencias Medicas y Nutricion “Salvador Zubiran,” Mexico City, Mexico; 2Hollis‐Eden Pharmaceuticals, San Diego, California; 3Centre for Infectious Diseases and International Health, Windeyer Institute for Medical Sciences, Royal Free and University College Medical School, London, United Kingdom

BALB/c mice with pulmonary tuberculosis develop a T helper cell type 1 response that peaks at 3 weeks, temporarily controlling bacterial growth. Then bacterial proliferation recommences, accompanied by increasing interleukin (IL)–4 levels and decreasing interferon (IFN)–γ, tumor necrosis factor (TNF)–α, and inducible nitric oxide synthase (iNOS) levels. These changes mimic those in the human disease. In a previous study, administration of dehydroepiandrosterone (DHEA) beginning on day 60 after infection reversed these changes and protected the mice. However, DHEA is suboptimal for human use, partly because it is readily metabolized into sex steroids. 16α‐Bromoepiandrosterone (EpiBr; 16α‐bromo‐5α‐androstan‐3β‐ol‐17‐one) is a synthetic adrenal steroid derivative that does not enter sex steroid pathways. In the present study, when tuberculous BALB/c mice were treated with EpiBr 3 times/week beginning on day 60, inhibition of bacterial proliferation and increased expression of TNF‐α, IFN‐γ, and iNOS were observed, although decreased expression of IL‐4 was also observed. Moreover, when given as an adjunct to conventional chemotherapy, EpiBr enhanced bacterial clearance. Trials for the use of EpiBr in the treatment of human tuberculosis are now justified.

Received 24 March 2004; accepted 27 July 2004; electronically published 9 December 2004.

Reprints or correspondence: Prof. Graham A. W. Rook, Centre for Infectious Diseases and International Health, Windeyer Institute for Medical Sciences, Royal Free and University College Medical School, 46 Cleveland St., London W1T 4JF, United Kingdom ().

Cited by

Dulce A Mata-Espinosa, Valentin Mendoza-Rodríguez, Diana Aguilar-León, Ricardo Rosales, Fernando López-Casillas, Rogelio Hernández-Pando. (2008) Therapeutic Effect of Recombinant Adenovirus Encoding Interferon-γ in a Murine Model of Progressive Pulmonary Tuberculosis. Molecular Therapy 16:6, 1065-1072
Online publication date: 1-Jul-2008.
CrossRef
Graham A. W. Rook, Douglas B. Lowrie, and Rogelio Hernàndez-Pando. (2007) Immunotherapeutics for Tuberculosis in Experimental Animals: Is There a Common Pathway Activated by Effective Protocols?. The Journal of Infectious Diseases 196:2, 191-198
Online publication date: 15-Jul-2007.
Abstract-Full Text-PDF Version (333 kB)
C. Reading, C. Dowding, B. Schramm, A. Garsd, N. Onizuka-Handa, D. Stickney, J. Frincke. (2006) Improvement in immune parameters and human immunodeficiency virus-1 viral response in individuals treated with 16?-bromoepiandrosterone (HE2000). Clinical Microbiology and Infection 12:11, 1082-1088
Online publication date: 1-Dec-2006.
CrossRef

  • Presented in part: Keystone Symposium, Keystone, CO, 28 March 2004 (abstract 321).

    Potential conflicts of interest: C.A., R.T., B.S., C.R., and J.F. are employees of Hollis‐Eden Pharmaceuticals.

    Financial support: Hollis‐Eden Pharmaceuticals.

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