Abstract
Mycotic infections and their effect on the human condition have been widely overlooked and poorly surveilled by many health organizations even though mortality rates have increased in recent years. The increased usage of immunosuppressive and myeloablative therapies for the treatment of malignant as well as non-malignant diseases has contributed significantly to the increased incidence of fungal infections. Invasive fungal infections have been found to be responsible for at least 1.5 million deaths worldwide. About 90% of these deaths can be attributed to Cryptococcus, Candida, Aspergillus, and Pneumocystis. A better understanding of how the host immune system contains fungal infection is likely to facilitate the development of much needed novel antifungal therapies. Innate cells are responsible for the rapid recognition and containment of fungal infections and have been found to play essential roles in defense against multiple fungal pathogens. In this review we summarize our current understanding of host-fungi interactions with a focus on mechanisms of innate cell-mediated recognition and control of pulmonary aspergillosis.
Highlights
Immunocompromised individuals comprise a growing population in today’s world
TLR9−/− neutropenic mice exhibited a decreased inflammatory response compared to wild-type 2 days post infection, but was significantly increased 4 days post infection indicating an immunoregulatory role for TLR9 in A. fumigatus infection (Ramaprakash et al, 2009)
A. fumigatus infection resulted in CCL3, CCL4, CXCL10, and CCL20 productions that induce the migration of effector memory Th1 cells (Gafa et al, 2007; Morton et al, 2011). Together these results indicate a dual role for dendritic cell (DC) in the innate as well as adaptive immune response against A. fumigatus (Margalit and Kavanagh, 2015)
Summary
Immunocompromised individuals comprise a growing population in today’s world. In part, this is due to the increased use of immunosuppressive drugs as therapies for diverse disease states. Aspergillus fumigatus is the etiological agent of over 90% of the invasive aspergillosis (IA) cases and it is considered the most common inhaled fungal pathogen (Dixon et al, 1996; Hohl and Feldmesser, 2007; Lehrnbecher et al, 2010). In this review we will focus our discussion on the recognition of the pathogen, the role of the innate immune system in response to respiratory fungal infection, and how diverse innate cell populations orchestrate antifungal defense against A. fumigatus
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