12 research outputs found
Phospholipids Trigger Cryptococcus neoformans Capsular Enlargement during Interactions with Amoebae and Macrophages
A remarkable aspect of the interaction of Cryptococcus
neoformans with mammalian hosts is a consistent increase in capsule
volume. Given that many aspects of the interaction of C.
neoformans with macrophages are also observed with amoebae, we
hypothesized that the capsule enlargement phenomenon also had a protozoan
parallel. Incubation of C. neoformans with Acanthamoeba
castellanii resulted in C. neoformans capsular
enlargement. The phenomenon required contact between fungal and protozoan cells
but did not require amoeba viability. Analysis of amoebae extracts showed that
the likely stimuli for capsule enlargement were protozoan polar lipids. Extracts
from macrophages and mammalian serum also triggered cryptococcal capsular
enlargement. C. neoformans capsule enlargement required
expression of fungal phospholipase B, but not phospholipase C. Purified
phospholipids, in particular, phosphatidylcholine, and derived molecules
triggered capsular enlargement with the subsequent formation of giant cells.
These results implicate phospholipids as a trigger for both C.
neoformans capsule enlargement in vivo and
exopolysaccharide production. The observation that the incubation of C.
neoformans with phospholipids led to the formation of giant cells
provides the means to generate these enigmatic cells in vitro.
Protozoan- or mammalian-derived polar lipids could represent a danger signal for
C. neoformans that triggers capsular enlargement as a
non-specific defense mechanism against potential predatory cells. Hence,
phospholipids are the first host-derived molecules identified to trigger
capsular enlargement. The parallels apparent in the capsular response of
C. neoformans to both amoebae and macrophages provide
additional support for the notion that certain aspects of cryptococcal virulence
emerged as a consequence of environmental interactions with other microorganisms
such as protists