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Infection and Immunity, February 2003, p. 697-707, Vol. 71, No. 2
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.2.697-707.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Different Innate Ability of I/St and A/Sn Mice To Combat Virulent Mycobacterium tuberculosis: Phenotypes Expressed in Lung and Extrapulmonary Macrophages

Konstantin B. Majorov, Irina V. Lyadova, Tatiana K. Kondratieva, Eugeny B. Eruslanov, Elvira I. Rubakova, Marianna O. Orlova, Vladimir V. Mischenko, and Alexander S. Apt*

Laboratory for Immunogenetics, Central Institute for Tuberculosis of the Russian Academy of Medical Sciences, Moscow 107564, Russia

Received 24 June 2002/ Returned for modification 26 August 2002/ Accepted 7 November 2002

Mice of the I/St and A/Sn inbred strains display a severe and moderate course, respectively, of disease caused by Mycobacterium tuberculosis. Earlier, we showed that the response to mycobacterial antigens in I/St mice compared to that in A/Sn mice is shifted toward Th2-like reactivity and a higher proliferative activity and turnover of T cells. However, the physiologic basis for different expressions of tuberculosis severity in these mice remains largely unknown. Here, we extend our previous observations with evidence that I/St interstitial lung macrophages are defective in the ability to inhibit mycobacterial growth and to survive following in vitro infection with M. tuberculosis H37Rv. A unique feature of this phenotype is its exclusive expression in freshly isolated lung macrophages. The defect is not displayed in ex vivo macrophages obtained from the peritoneal cavity nor in macrophages developed in vitro from progenitors extracted from various organs, including the lung itself. In addition, we show that, in sharp contrast to peritoneal macrophages, the mycobactericidal capacity of lung macrophages is not elevated in the presence of exogenous gamma interferon. Our data suggest that the in vivo differentiation in a particular anatomical microenvironment determines the pattern of macrophage-mycobacterium interaction. Thus, caution should be exercised when conclusions based upon the results obtained in a particular in vitro system are generalized to the functions of all phagocytes during M. tuberculosis infection.

* Corresponding author. Mailing address: Laboratory for Immunogenetics, Central Institute for Tuberculosis, Yauza Alley 2, Moscow 107564, Russia. Phone: (7095) 268 78 10. Fax: (7095) 963 80 00. E-mail: asapt{at}aha.ru.

Editor: W. A. Petri, Jr.

Infection and Immunity, February 2003, p. 697-707, Vol. 71, No. 2
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.2.697-707.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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