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Infect Immun, March 1998, p. 1190-1199, Vol. 66, No. 3
Divisions of
Pulmonary and Critical Care
Medicine1 and
Infectious
Diseases,
Received 2 December 1996/Returned for modification 30 January
1997/Accepted 9 December 1997
We assessed the applicability of an in vitro model of low-level
infection of human monocytes to the characterization of the virulence
of strains of the Mycobacterium tuberculosis family. Peripheral blood monocytes were infected at a 1:1 ratio with the virulent M. tuberculosis strain H37Rv, the avirulent
M. tuberculosis strain H37Ra, and the attenuated M. bovis strain BCG. Both the percentages of cells infected by the
three strains and the initial numbers of intracellular organisms were
equivalent, as were levels of monocyte viability up to 7 days following
infection. Intracellular growth reflected virulence, as H37Rv
replicated in logarithmic fashion throughout the assay, BCG growth
reached a plateau at 4 days, and H37Ra did not grow at all. The same
patterns of growth were observed following infection of human alveolar
macrophages with H37Rv and H37Ra. Monocyte production of tumor necrosis
factor alpha was significantly higher following infection with virulent H37Rv than with either BCG or H37Ra. In contrast, there was no clear
correlation of interleukin 10 production with virulence. Nonadherent
cells of purified-protein-derivative-positive donors mediated
equivalent degrees of reduction of the intracellular growth of H37Rv,
BCG, and H37Ra. Low-level infection of human monocytes with H37Rv, BCG,
and H37Ra thus provides an in vitro model for assessment of the
virulence of these M. tuberculosis family strains.
Furthermore, it is suggested that the virulence of these strains is
expressed primarily by their differing abilities to adapt to the
intracellular environment of the mononuclear phagocyte.
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Expression of Virulence of Mycobacterium tuberculosis
within Human Monocytes: Virulence Correlates with Intracellular
Growth and Induction of Tumor Necrosis Factor Alpha but Not with
Evasion of Lymphocyte-Dependent Monocyte Effector Functions
*
Corresponding author. Mailing address: Divisions of
Pulmonary and Critical Care Medicine and Infectious Diseases, Case
Western Reserve University School of Medicine, Biomedical Research
Building, Rm. 421, 10900 Euclid Ave., Cleveland, OH 44106-4941. Phone:
(216) 368-1151. Fax: (216) 368-2034. E-mail:
rfs4{at}po.cwru.edu.
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