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Lack of IL-10 alters inflammatory and immune responses during pulmonary Mycobacterium tuberculosis infection

David M Higgins1, Joaquin Sanchez-Campillo, Adrian G Rosas-Taraco

  • 1Department of Microbiology, Mycobacteria Research Laboratories, Colorado State University, Fort Collins, CO 80523, USA.

Tuberculosis (Edinburgh, Scotland)
|February 14, 2009
PubMed

Insights

Mice lacking interleukin-10 (IL-10) initially controlled Mycobacterium tuberculosis but later experienced bacterial regrowth and severe lung inflammation. This suggests IL-10 is crucial for managing chronic tuberculosis by regulating immune responses.

Area of Science:

  • Immunology
  • Microbiology
  • Pulmonology

Background:

  • Mycobacterium tuberculosis (M.tb) infection causes significant lung pathology.
  • Interleukin-10 (IL-10) is a key immunosuppressive cytokine with a complex role in host defense against M.tb.

Purpose of the Study:

  • To investigate the long-term role of IL-10 in the immune response to M.tb infection in mice.
  • To determine the impact of IL-10 deficiency on bacterial burden, host pathology, and immune cell populations during chronic M.tb infection.

Main Methods:

  • Generation and use of IL-10 gene-disrupted (IL-10 KO) mice and wild-type (WT) littermates.
  • Infection with M.tb and assessment of bacterial burden, survival, and clinical signs at multiple time points (60 and 185 days).
  • Analysis of lung lymphocyte populations and expression of Th1 (IL-12, IFNgamma) and immunosuppressive (TGFbeta, TNFalpha) cytokines.

Main Results:

  • IL-10 KO mice showed no difference in bacterial burden compared to WT mice during the early stages (4-5 months) of M.tb infection.
  • At 185 days post-infection, IL-10 KO mice exhibited bacterial regrowth, wasting, and morbidity.
  • Absence of IL-10 led to increased Th1 immunity and uncontrolled inflammation, with excessive pulmonary inflammation and elevated TNFalpha at later stages.

Conclusions:

  • IL-10 plays a critical role in dampening Th1 responses and preventing excessive pulmonary inflammation during chronic M.tb infection.
  • Complete removal of IL-10 leads to disease progression and pathology in the M.tb-infected lung.
  • IL-10 is essential for maintaining immune homeostasis and controlling chronic inflammation in tuberculosis.

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