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Manipulation of host angioneogenesis: A critical link for understanding the pathogenesis of invasive mold infections?
1Department of Infectious Diseases, Infection Control and Employee Health, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. dkontoyi@mdanderson.org
Abstract:
Despite progress over the last decade, opportunistic mold infections continue to be associated with high rates of morbidity and mortality in immunocompromised patients. Given the propensity of molds to invade blood vessels, vasculopathy may be a barrier to effective delivery of antifungal drugs to infected tissue. In a recent study (Ben-Ami R et al. Blood, 2009), we found that A. fumigatus suppresses endothelial cell migration, differentiation and capillary tube formation both in vitro and in an animal model system. This effect is mediated by secreted secondary metabolites such as gliotoxin. Herein, I discuss the potential implications of how invasive molds modulate host angiogenesis in experimental and clinical mold infections. Strategies that employ reversal of vasculopathy, neutralization of metabolites that inhibit endothelial function, exploration of pro-angiogenic factors as diagnostic or prognostic markers affected patients will likely be the focus of future studies. This complex, yet emerging field might add another level of knowledge and therapeutic choices in the management of these devastated infections.
Insights
Opportunistic mold infections harm immunocompromised patients. Invasive molds like Aspergillus fumigatus disrupt blood vessel formation, hindering antifungal drug delivery and treatment effectiveness.
Area of Science:
- Medical Mycology
- Infectious Diseases
- Vascular Biology
Background:
- Opportunistic mold infections pose significant risks for immunocompromised individuals.
- Vasculopathy, driven by mold invasion of blood vessels, impedes effective antifungal drug delivery to infected tissues.
- Understanding mold-host interactions is crucial for improving patient outcomes.
Purpose of the Study:
- To investigate how invasive molds, specifically Aspergillus fumigatus, affect host angiogenesis.
- To explore the mechanisms by which molds modulate endothelial cell function.
- To discuss potential therapeutic strategies targeting vasculopathy in mold infections.
Main Methods:
- In vitro studies on endothelial cell migration, differentiation, and capillary tube formation.
- In vivo animal model system to assess the effects of Aspergillus fumigatus.
- Analysis of secondary metabolites, such as gliotoxin, secreted by molds.
Main Results:
- Aspergillus fumigatus was found to suppress endothelial cell migration and differentiation.
- Capillary tube formation was inhibited by Aspergillus fumigatus in vitro and in an animal model.
- Secreted fungal metabolites, including gliotoxin, mediate these anti-angiogenic effects.
Conclusions:
- Invasive molds actively modulate host angiogenesis, presenting a challenge in treating infections.
- Gliotoxin and other fungal metabolites play a role in suppressing endothelial cell function.
- Future research should focus on reversing vasculopathy and exploring pro-angiogenic factors for improved diagnostics and therapeutics.
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