Corrigendum: Gut bacteria regulate the pathogenesis of Huntington's disease in Drosophila model

Abstract

[This corrects the article DOI: 10.3389/fnins.2022.902205.].

Keywords: Huntington's disease; crocin (PubChem CID: 5281233); gut-brain; microbiota; neurodegeneration.

Figure 4

Crocin ameliorates E. coli-induced motor defects and mortality in female FL-HD flies. (A) Freshly eclosed FL-HD flies were treated with rifaximin, luteolin, and crocin for 15 days and their climbing ability was evaluated. Data are reported as mean ± SEM and were analyzed by one-way ANOVA with Tukey's post hoc test. ***p < 0.001, n = 6 groups of 10 flies. (B) Climbing assay was performed to monitor the motor function of flies colonized with crocin, E. coli or E. coli plus crocin. Untreated FL-HD flies were used as control. Data are represented as mean ± SEM and were analyzed by one-way ANOVA with Tukey's post hoc test. ***p < 0.001; **p < 0.01, n = 6 groups of 10 flies. Part (C,D) show the percentage of FL-HD flies, which survived over time (days) under different treatments. Temperature was elevated to 25°C to accommodate E. coli growth. The data are represented as mean ± SEM, two-way ANOVA with Tukey's multiple-comparisons test. ***p < 0.001; **p < 0.01; *p < 0.05, n = 6 groups of 10 flies. (E) Representative confocal images of the GI tract of untreated (control) FL-HD flies or those treated with E. coli (curli) or E. coli plus crocin for 15 days showing bacterial colonization and suppression by crocin treatment. Immunostaining was performed using a monoclonal antibody reactive to E. coli. DAPI was used to stain the nuclei.