Secretion of cytokines by human macrophages upon infection by pathogenic and non-pathogenic mycobacteria

Microb Pathog. 2000 May;28(5):313-8. doi: 10.1006/mpat.1999.0345.


The interaction of various pathogenic (Mycobacterium tuberculosis, M. avium, M. kansasii, M. xenopi), and non-pathogenic mycobacteria (M. smegmatis, M. phlei) with human macrophages at the level of macrophage cytokine expression (TNFalpha, IL1, IL6 and GM-CSF) was investigated. Both for TNFalpha and GM-CSF, the lowest levels were obtained with pathogenic mycobacterial species, whereas about 2-8 times higher levels were observed for non-pathogenic species. Contrary to the above, the differences for IL6 and IL1 were not marked, although IL6 appeared to be more elevated for non-pathogenic species. Heat-killed bacteria induced a lower level of the cytokines for all the three cytokines assayed (TNFalpha, IL6 and IL1), except for M. tuberculosis for whom a significantly higher proportion of TNFalpha was induced by killed bacilli. The RT-PCR experiments performed on M. avium (as a low inducer of the cytokines) and M. smegmatis (as a high inducer of the cytokines) showed that the differences observed among pathogenic vs non-pathogenic strains were also reflected at the transcriptional level for TNFalpha and to a lesser extent for IL6, but not for IL1. This investigation underlined important differences existing between the pathogenic and non-pathogenic species, particularly as regards TNFalpha and GM-CSF.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cells, Cultured
  • Cytokines / metabolism*
  • Enzyme-Linked Immunosorbent Assay
  • Granulocyte-Macrophage Colony-Stimulating Factor / metabolism
  • Heating
  • Humans
  • In Vitro Techniques
  • Interleukin-1 / metabolism
  • Interleukin-6 / metabolism
  • Macrophages / metabolism*
  • Macrophages / microbiology
  • Mycobacterium / metabolism*
  • Mycobacterium / pathogenicity
  • Mycobacterium Infections / metabolism*
  • Mycobacterium Infections / microbiology
  • Reverse Transcriptase Polymerase Chain Reaction
  • Tumor Necrosis Factor-alpha / metabolism
  • Virulence


  • Cytokines
  • Interleukin-1
  • Interleukin-6
  • Tumor Necrosis Factor-alpha
  • Granulocyte-Macrophage Colony-Stimulating Factor