Skip to main content

Advertisement

Log in

TB comes to a sticky beginning

  • News & Views
  • Published:

From Nature Medicine

View current issue Submit your manuscript

Although the tuberculosis bacterium is most renowned for its ability to cause pulmonary infection, the bacilli colonize many sites in the body in addition to the lungs. The recent identification of a key player in the dissemination of infection sheds light on the route by which tuberculosis spreads from the lungs and opens the way to assessing the significance of dissemination to the course of disease.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Figure 1: Possible mechanisms by which inhaled M. tuberculosis might establish an infection in the lung and spread to extrapulmonary sites.

Stephen Horwitz

References

  1. Pethe, K. et al. The heparin-binding haemagglutinin of Mycobacterium tuberculosis is required for extrapulmonary dissemination. Nature 412, 190–194 (2001)

    Article  CAS  Google Scholar 

  2. Russell, D.G. Mycobacterium tuberculosis: Here today and here tomorrow. Nat. Rev. Mol. Cell Biol. (in the press).

  3. Bermudez, L.E. & Goodman, J. Mycobacterium tuberculosis invades and replicates within type II alveolar cells. Infect. Immun. 64, 1400–1406 (1996).

    CAS  PubMed  PubMed Central  Google Scholar 

  4. Menozzi, F.D. et al. Identification of a heparin-binding hemagglutinin present in mycobacteria. J. Exp. Med. 184, 993–1001 (1996).

    Article  CAS  Google Scholar 

  5. Menozzi, F.D., Bischoff, R., Fort, E., Brennan, M.J. & Locht, C. Molecular characterization of the mycobacterial heparin-binding hemagglutinin, a mycobacterial adhesin. Proc. Natl. Acad. Sci. USA 95, 12625–12630 (1998).

    Article  CAS  Google Scholar 

  6. Pethe, K. et al. Characterization of the heparin-binding site of the mycobacterial heparin-binding hemagglutinin adhesin. J. Biol. Chem. 275, 14273–14280 (2000).

    Article  CAS  Google Scholar 

  7. McDonough, K.A. & Kress, Y. Cytotoxicity for lung epithelial cells is a virulence-associated phenotype of Mycobacterium tuberculosis. Infect. Immun. 63, 4802–4811 (1995).

    CAS  PubMed  PubMed Central  Google Scholar 

  8. Lin, Y., Zhang, M. & Barnes, P.F. Chemokine production by a human alveolar epithelial cell line in response to Mycobacterium tuberculosis. Infect. Immun. 66, 1121–1126 (1998).

    CAS  PubMed  PubMed Central  Google Scholar 

  9. Dobos, K.M., Spotts, E.A., Quinn, F.D. & King, C.H. Necrosis of lung epithelial cells during infection with Mycobacterium tuberculosis is preceded by cell permeation. Infect. Immun. 68, 6300–6310 (2000).

    Article  CAS  Google Scholar 

  10. Birkness, K.A. et al. An in vitro tissue culture bilayer model to examine early events in Mycobacterium tuberculosis infection. Infect. Immun. 67, 653–658 (1999).

    CAS  PubMed  PubMed Central  Google Scholar 

  11. Hernandez-Pando, R. et al. Persistence of DNA from Mycobacterium tuberculosis in superficially normal lung tissue during latent infection. Lancet 356, 2133–2138 (2000).

    Article  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Rights and permissions

Reprints and permissions

About this article

Cite this article

Russell, D. TB comes to a sticky beginning. Nat Med 7, 894–895 (2001). https://doi.org/10.1038/90926

Download citation

  • Issue Date:

  • DOI: https://doi.org/10.1038/90926

  • Springer Nature America, Inc.

Navigation