Failure of nitric oxide production by macrophages and decrease in CD4+ T cells in oral paracoccidioidomycosis:

Aline Carvalho Batista1, Cleverson Teixeira Soares, Vanessa Soares Lara

  • 1Department of Stomatology (Oral Pathology), Dental School, Federal University of Goiás, Goiânia, Goiás, Brazil.

Insights

Oral Paracoccidioidomycosis (OP) lesions show low expression of inducible nitric oxide synthase (iNOS) and fewer CD4+ T cells. These immune factors may allow the fungus Paracoccidioides brasiliensis to multiply, leading to persistent oral lesions.

Area of Science:

  • Immunology
  • Mycology
  • Oral Pathology

Background:

  • Paracoccidioidomycosis is a chronic granulomatous disease with specific immune responses.
  • Nitric oxide (NO), produced by inducible nitric oxide synthase (iNOS), is a known fungicidal molecule against Paracoccidioides brasiliensis.
  • Oral Paracoccidioidomycosis (OP) requires further characterization of its inflammatory and immune milieu.

Purpose of the Study:

  • To investigate the immunohistochemical expression of iNOS and immune cell markers in oral lesions of Paracoccidioidomycosis.
  • To correlate the presence of these markers with fungal load in oral tissues.

Main Methods:

  • Immunohistochemical analysis of iNOS, CD45RO, CD3, CD8, CD20, CD68, and mast cells in oral tissue samples.
  • Categorization of samples based on viable fungal counts per mm².
  • Comparison of marker expression between OP lesions and healthy oral tissue controls.

Main Results:

  • Weak immunolabeling for iNOS was observed in multinucleated giant cells (MNGC) and mononuclear (MN) cells in OP lesions.
  • The proportion of iNOS+ MN/MNGC cells in OP was comparable to controls.
  • Numbers of CD4+ T cells were similar in controls and OP groups with higher fungal loads.

Conclusions:

  • Low iNOS expression in OP lesions may impair the host's ability to control fungal growth.
  • A decrease in CD4+ T cells in OP could contribute to the persistence of oral lesions.
  • These findings suggest potential immune evasion mechanisms by Paracoccidioides brasiliensis in the oral cavity.

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