In Murine Disseminated Candidiasis, Serum Amyloid P Component Inhibits Inflammation and C-Reactive Protein...

Area of Science:

• Immunology
• Mycology
• Pathology

Background:

• Candida albicans is a fungus that can cause lethal bloodstream infections.
• Innate immune effectors modulate the course of systemic candidiasis.
• The roles of human serum amyloid P component (hSAP) and human C-reactive protein (hCRP) in candidiasis are not fully understood.

Purpose of the Study:

• To investigate the pathological basis for the differential effects of hSAP and hCRP on systemic Candida albicans infection in mice.

Main Methods:

• Murine model of disseminated candidiasis induced by intravenous C. albicans injection.
• Administration of hSAP or hCRP to infected mice.
• Histological examination of kidneys, including collagen deposition and inflammatory cell infiltration.
• Immunohistochemical staining for CD45 and Ly-6G.

Main Results:

• hSAP administration reduced collagen deposition and preserved kidney structure, prolonging survival.
• hCRP administration increased collagen deposition, caused loss of kidney structure, and hastened death.
• hSAP bound to C. albicans yeasts and hyphae, while hCRP bound to damaged tissue.
• hSAP reduced inflammatory cell infiltration, whereas hCRP did not.

Conclusions:

• hSAP confers protection against systemic candidiasis by dampening inflammation and collagen production.
• hCRP exacerbates candidiasis by promoting tissue damage and destructive inflammation.
• Differential binding of hSAP and hCRP to fungi or host tissues underlies their opposing effects on infection outcome.