Roles of the Class II and Class V Myosins in Aspergillus fumigatus Hyphal Growth and Pathogenesis
Invasive aspergillosis, caused by the fungal pathogen Aspergillus fumigatus, is a leading cause of death in immunocompromised patients. Effective treatment is difficult, and new antifungals are needed due to increasing resistance to treatment options that are currently available. Renshaw et al. (p. 1556–1564) demonstrate that the class II and class V myosins in A. fumigatus are required for critical cellular processes, including septation, conidiation, conidium viability, germination, and hyphal polarity and branching. Furthermore, the class V myosin is required for virulence in a murine model of invasive aspergillosis, making it an attractive target for future drug development.
Infiltrated Macrophages Die of Necroptosis following Myocardial Invasion by Streptococcus pneumoniae
Gilley et al. (p. 1457–1469) find that myocardial invasion by Streptococcus pneumoniae occurs soon after the development of bacteremia and is continuous thereafter. Cardiac pathology in mice is bacterial strain specific, varying from nonpurulent bacterium-filled microlesions with readily visible pneumococci to areas of hydropic degeneration and infiltrated immune cells at sites where pneumococci could be detected only using immunofluorescence microscopy. Pneumolysin was found to be a major modulator of the cytokine and chemokine response and responsible for killing infiltrated macrophages by necroptosis. Mice challenged with pneumolysin-deficient mutants either failed to develop cardiac pathology or developed lesions characterized by robust immune cell infiltration.
- Copyright © 2016, American Society for Microbiology. All Rights Reserved.
