Viral infection triggers interferon-induced expulsion of live Cryptococcus neoformans by macrophages.

Cryptococcus neoformans is an opportunistic human pathogen, which causes serious disease in immunocompromised hosts. Infection with this pathogen is particularly relevant in HIV+ patients, where it leads to around 200,000 deaths per annum. A key feature of cryptococcal pathogenesis is the ability of the fungus to survive and replicate within the phagosome of macrophages, as well as its ability to be expelled from host cells via a novel non-lytic mechanism known as vomocytosis.

Correction: Engineering microbial physiology with synthetic polymers: cationic polymers induce biofilm formation in and downregulate the expression of virulence genes.

[This corrects the article DOI: 10.1039/C7SC00615B.].

Characterizing the Mechanisms of Nonopsonic Uptake of Cryptococci by Macrophages.

The pathogenic fungus enters the human host via inhalation into the lung and is able to reside in a niche environment that is serum- (opsonin) limiting. Little is known about the mechanism by which nonopsonic phagocytosis occurs via phagocytes in such situations. Using a combination of soluble inhibitors of phagocytic receptors and macrophages derived from knockout mice and human volunteers, we show that uptake of nonopsonized and via the mannose receptor is dependent on macrophage activation by cytokines.

Quantifying donor-to-donor variation in macrophage responses to the human fungal pathogen Cryptococcus neoformans.

Cryptococcosis remains the leading cause of fungal meningitis worldwide, caused primarily by the pathogen Cryptococcus neoformans. Symptomatic cryptococcal infections typically affect immunocompromised patients. However, environmental exposure to cryptococcal spores is ubiquitous and most healthy individuals are thought to harbor infections from early childhood onwards that are either resolved, or become latent.

Cryptococcus-Epithelial Interactions.

The fungal pathogen, , causes devastating levels of morbidity and mortality. Infections with this fungus tend to be predominantly in immunocompromised individuals, such as those with HIV. Infections initiate with inhalation of cryptococcal cells and entry of the pathogen into the lungs.

Engineering microbial physiology with synthetic polymers: cationic polymers induce biofilm formation in and downregulate the expression of virulence genes.

Here we report the first application of non-bactericidal synthetic polymers to modulate the physiology of a bacterial pathogen. Poly(-[3-(dimethylamino)propyl] methacrylamide) () and poly(-(3-aminopropyl)methacrylamide) (), cationic polymers that bind to the surface of , the infectious agent causing cholera disease, can sequester the pathogen into clusters. Upon clustering, transitions to a sessile lifestyle, characterised by increased biofilm production and the repression of key virulence factors such as the cholera toxin (CTX).

New weapons in the Cryptococcus infection toolkit.

The global burden of fungal infections is unacceptably high. The human fungal pathogen Cryptococcus neoformans causes cryptococcosis and accounts for a significant proportion of this burden. Cryptococci undergo a number of elaborate interactions with their hosts, including survival and proliferation within phagocytes as well as dissemination to the central nervous system and other tissues.