Pathogenic Yeast Cryptococcus neoformans Requires Reductive Iron Acquisition To Colonize Brain Tissue
The competition for iron is a key feature of many infectious diseases, including AIDS-associated meningoencephalitis caused by the fungus Cryptococcus neoformans. Saikia et al. (p. 839–850) find that a mutant of C. neoformans lacking the ferric reductase Fre2 has attenuated growth on heme and transferrin and reduced virulence in mice and colonization of brain tissue. These phenotypes are shared by mutants with defects in high-affinity iron uptake, and Fre2 may therefore be a new component of this pathway. In general, these functions are potential targets for antifungal drugs and candidates for vaccine development.
Protection from Clostridium difficile Infection in Immunocompromised Hosts by Mucosal and Systemic Antibodies
Clostridium difficile infection (CDI) arising from toxin A and/or B is treated with antibiotics. Most patients recover, but ∼20% undergo recurrent CDI. Although anti-toxin antibody (Ab) is protective, the contribution of systemic and mucosal Ab remains unclear. Utilizing the CDI mouse model, Johnston et al. (p. 522–531) show that in the absence of mucosal anti-toxin antibodies, systemic IgG anti-toxin antibodies mediate protection from CDI. However, in the absence of CD4+ T cells, protection is mediated solely by mucosal IgA anti-toxin antibodies. These findings underscore the importance of differing vaccine strategies depending on the immune competence of the host.
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