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Connective matrix organization in chronic granulomas of experimental paracoccidioidomycosis

I B Kerr1, P C de Oliveira, H L Lenzi

  • 1Department of Pathology, Instituto Oswaldo Cruz, Rio de Janeiro, Brazil.

Mycopathologia
|July 1, 1988
PubMed

Insights

Chronic granulomas in rats infected with Paracoccidioides brasiliensis show distinct zones and an extracellular matrix rich in collagen. Fibrosis progresses outwards, potentially driven by fungal or cellular interactions.

Area of Science:

  • Mycology
  • Immunology
  • Pathology

Background:

  • Paracoccidioides brasiliensis causes paracoccidioidomycosis, a granulomatous disease.
  • Chronic granulomas are key pathological features in persistent infections.
  • Understanding granuloma structure and extracellular matrix is crucial for infection control.

Purpose of the Study:

  • To describe the histological and ultrastructural features of chronic granulomas in a rat model of Paracoccidioides brasiliensis infection.
  • To analyze the composition of the extracellular matrix within these granulomas.
  • To investigate the cellular composition and directional progression of the fibrotic process.

Main Methods:

  • Histological examination of rat granulomas.
  • Ultrastructural analysis of granuloma components.
  • Identification of extracellular matrix constituents and cellular populations.

Main Results:

  • Granulomas exhibited a two-zone structure: a central zone with fungi and a peripheral zone.
  • The extracellular matrix comprised collagen types I and III, proteoglycans, glycoproteins, and amorphous substances.
  • Macrophages, epithelioid cells, and giant cells dominated the central zone, while fibroblasts were prevalent in the peripheral zone.
  • A centrifugal fibrotic process was observed, possibly induced by fungal elements or cell interactions.

Conclusions:

  • Chronic granulomas in Paracoccidioides brasiliensis infection have a defined zonal architecture and a complex extracellular matrix.
  • Fibrosis is a significant feature, progressing outwards from the central fungal core.
  • The findings suggest fungal components or host cell interactions drive the fibrotic response.

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