Enterohemorrhagic Escherichia coli (EHEC) is a specific subset of Shiga toxin-producing Escherichia coli (STEC) strains
that are characterized by their ability to cause bloody diarrhea (hemorrhagic colitis) and potentially life-threatening,
extraintestinal complications such as hemolytic uremic syndrome (HUS), which is associated with acute renal failure.,
contributing to severe clinical outcomes. The Shiga toxins (Stxs), produced by EHEC, are primary virulence factors. These
potent cytotoxins are composed of one enzymatically active A subunit (StxA) and five receptor-binding B subunits (StxB).
Although the toxins are primarily associated with cytotoxic effects, they also elicit other pathogenic consequences due to
their induction of a number of biological processes, including apoptosis through ER-stress, pro-inflammatory responses,
autophagy, and post-translational modification (PTM). Moreover, several studies have reported the association between Stxs
and extracellular vesicles (EVs), including microvesicles and exosomes, demonstrating that Stx-containing EVs secreted
by intoxicated macrophages are taken up by recipient cells, such as toxin-sensitive renal proximal tubular epithelial cells.
This mechanism likely contributes to the spreading of Stxs within the host, and may exacerbate gastrointestinal illnesses
and kidney dysfunction. In this review, we summarize recent findings relating to the host responses, in different types of
cells in vitro and in animal models, mediated by Stxs-containing exosomes. Due to their unique properties, EVs have been
explored as therapeutic agents, drug delivery systems, and diagnostic tools. Thus, potential therapeutic applications of EVs
in EHEC Stxs-mediated pathogenesis are also briefly reviewed.
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A number of pathogenic species of basidiomycete fungi are
either life-threatening pathogens of humans or major economic
pests for crop production. Sensing the host is a key
aspect of pathogen proliferation during disease, and signal
transduction pathways are critically important for detecting
environmental conditions and facilitating adaptation. This
review focuses on the contributions of the cAMP/protein
kinase A (PKA) signaling pathway in Cryptococcus neoformans,
a species that causes meningitis in humans, and Ustilago
maydis, a model phytopathogen that causes a smut disease on
maize. Environmental sensing by the cAMP/PKA pathway
regulates the production of key virulence traits in C. neoformans
including the polysaccharide capsule and melanin.
For U. maydis, the pathway controls the dimorphic transition
from budding growth to the filamentous cell type required
for proliferation in plant tissue. We discuss recent advances
in identifying new components of the cAMP/PKA pathway
in these pathogens and highlight an emerging theme that
pathway signaling influences iron acquisition.
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