Do Visually Impaired People Develop Superior Smell Ability?

It is well known that visually impaired people perform better in orientation by sound than sighted individuals, but it is not clear whether this enhanced awareness also extends to other senses. Therefore, the aim of this study was to observe whether visually impaired subjects develop superior abilities in olfactory perception to compensate for their lack of vision. We investigated the odor perception of visually impaired individuals aged 7 to 89 ( n = 99; 52 women, 47 men) and compared them with subjects of a control group aged 8 to 82 years ( n = 100; 45 women, 55 men) without any visual impairment. The participants were evaluated by Sniffin' Sticks odor identification and discrimination test. Identification ability was assessed for 16 common odors presented in felt-tip pens. In the odor discrimination task, subjects had to determine which of three pens in 16 triplets had a different odor. The median number of correctly identified odorant pens in both groups was the same, 13 of the offered 16. In the discrimination test, there was also no significant difference observed. Gender did not influence results. Age-related changes were observed in both groups with olfactory perception decreasing after the age of 51. We could not confirm that visually impaired people were better in smell identification and discrimination ability than sighted individuals.

IL-18BP mediates the balance between protective and pathological immune responses to Toxoplasma gondii.

Interleukin-18 (IL-18) promotes natural killer (NK) and T cell production of interferon (IFN)-γ, a key factor in resistance to Toxoplasma gondii, but previous work has shown a limited role for endogenous IL-18 in control of this parasite. Although infection with T. gondii results in release of IL-18, the production of IFN-γ induces high levels of the IL-18 binding protein (IL-18BP). Antagonism of IL-18BP with a "decoy-to-the-decoy" (D2D) IL-18 construct that does not signal but rather binds IL-18BP results in enhanced innate lymphoid cell (ILC) and T cell responses and improved parasite control. In addition, the use of IL-18 resistant to IL-18BP ("decoy-resistant" IL-18 [DR-18]) is more effective than exogenous IL-18 at promoting innate resistance to infection. DR-18 enhances CD4+ T cell production of IFN-γ but results in CD4+ T cell-mediated pathology. Thus, endogenous IL-18BP restrains aberrant immune pathology, and this study highlights strategies that can be used to tune this regulatory pathway for optimal anti-pathogen responses.

A positive feedback loop controls Toxoplasma chronic differentiation.

Successful infection strategies must balance pathogen amplification and persistence. In the obligate intracellular parasite Toxoplasma gondii this is accomplished through differentiation into dedicated cyst-forming chronic stages that avoid clearance by the host immune system. The transcription factor BFD1 is both necessary and sufficient for stage conversion; however, its regulation is not understood. In this study we examine five factors that are transcriptionally activated by BFD1. One of these is a cytosolic RNA-binding protein of the CCCH-type zinc-finger family, which we name bradyzoite formation deficient 2 (BFD2). Parasites lacking BFD2 fail to induce BFD1 and are consequently unable to fully differentiate in culture or in mice. BFD2 interacts with the BFD1 transcript under stress, and deletion of BFD2 reduces BFD1 protein levels but not messenger RNA abundance. The reciprocal effects on BFD2 transcription and BFD1 translation outline a positive feedback loop that enforces the chronic-stage gene-expression programme. Thus, our findings help explain how parasites both initiate and commit to chronic differentiation. This work provides new mechanistic insight into the regulation of T. gondii persistence, and can be exploited in the design of strategies to prevent and treat these key reservoirs of human infection.