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Macrophages and Galectin 3 Control Bacterial Burden in Acute and Subacute Murine Leptospirosis That Determines

María F Ferrer1, Emilia Scharrig1, Nancy Charo2

  • 1Laboratory of Animal Viruses, Institute of Biotechnology and Molecular Biology, UNLP-CONICET, La Plata, Argentina.

Frontiers in Cellular and Infection Microbiology
|November 15, 2018
PubMed

Insights

Macrophages and galectin 3 (Gal-3) control Leptospira burden but have minor roles in kidney fibrosis. Bacterial burden, not these factors, correlates with fibrosis development in leptospirosis.

Area of Science:

  • Immunology
  • Pathology
  • Microbiology

Background:

  • Macrophages and galectin 3 (Gal-3) are implicated in acute Leptospira dissemination and kidney fibrosis.
  • Understanding their precise roles in experimental leptospirosis is crucial.

Purpose of the Study:

  • To investigate the roles of macrophages and Gal-3 in survival, clinical course, bacterial burden, nephritis, and kidney fibrosis in Leptospira interrogans serovar Copenhageni (LIC)-induced murine leptospirosis.
  • To determine the relationship between kidney fibrosis and bacterial burden, and the involvement of TGF-β1 and IL-13.

Main Methods:

  • Macrophage depletion using liposome-encapsulated clodronate in C57BL/6J mice.
  • Infection of Gal-3 knockout (Lgals3-/-) mice and wild-type controls with LIC.
  • Assessment of bacterial burden, nephritis, and kidney fibrosis.
  • Analysis of TGF-β1 and IL-13 transcription levels in kidneys.
  • In vitro study of human fibroblast differentiation.

Main Results:

  • Macrophage depletion led to higher bacterial burden, reduced subacute nephritis, and enhanced chronic kidney fibrosis.
  • Gal-3 deficiency resulted in increased bacterial burden, subacute nephritis, and chronic kidney fibrosis compared to wild-type mice.
  • Chronic fibrosis did not correlate with TGF-β1 or IL-13 levels but was associated with bacterial burden.
  • Human fibroblasts showed enhanced differentiation to myofibroblasts upon LIC treatment.

Conclusions:

  • Macrophages and Gal-3 are critical for controlling LIC bacterial burden but play a minor role in subsequent kidney fibrosis.
  • Kidney fibrosis in leptospirosis is primarily correlated with bacterial burden, not macrophage or Gal-3 activity.
  • Macrophages do not appear to disseminate leptospires during acute infection or contribute to chronic kidney fibrosis.
Keywords:
Leptospirafibrosisgalectin 3macrophagespathogenesis

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