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Funatsu, O.

Publications and source records attributed to Funatsu, O..

2 recordsLinked to original sources
bioRxiv2023

Detailed microbiome analysis of sticker-stripped surface materials of acne lesions revealed acne-related Cutibacterium acnes subtypes: A pilot study

Cutibacterium acnes (C. acnes) is known to play a central role in pathogenesis of acne vulgaris. It has been understood that multiple phylotypes of C. acnes exist, with certain types being more prevalent in patient with acne vulgaris and others more common in healthy individuals. In this context, we conducted a preliminary study using self-collected samples via an adhesive sticker (MySkin(R) patch) to analyze the skin microbiome of Japanese women. The study aimed to determine the role of C. acnes and its specific phylotypes in the development of acne vulgaris. Participants in this study were Japanese females aged between their 20s and 40s. Dermatologists evaluate the data from web-based questionnaires and smartphone image submissions to classify subjects into either Acne group (n = 219) or Non-acne group (n = 77). Quality assessment of DNA extracted from the sticker was conducted, followed by amplification of the 16S rRNA region using PCR. Subsequent microbial community analysis was performed using next-generation sequencing techniques. Genetic classification of C. acnes was accomplished through single locus sequence typing. Results indicated a bacterial community composition on the facial skin surface predominantly consisting of C. acnes clusters, with over half of these clusters constituted by C. acnes. Notably, the Acne group exhibited a significantly higher proportion of C. acnes relative to total bacterial presence compared to the Non-acne group. Analysis of C. acnes phylotypes revealed a markedly lower presence of type III (subspecies elongatum) in the Acne group (vs. Non-acne group, p < 0.05). No significant differences were observed in the prevalence of Types IA1, IA2, II, and IB between the two groups. The predominantsequence types (ST) of C. acnes identified were IA2_2_F0 (23.9%), IA1_4_A0 (20.6%), and II_2_K0 (18.6%). Within the Acne group, an increase in IA2_1_F1 and a decrease in III_1_L0 were observed (vs. Non-acne group, p < 0.05). This study underscores the feasibility of using self-collected and mailed-in samples for qPCR and microbiome analysis, maintaining diagnostic quality comparable to in-person assessments. Furthermore, the variation in the expression of C. acnes phylotypes across skin surfaces between acne-afflicted and healthy individuals could suggest that shifts in phylotype expression patterns may be indicative of skin susceptibilities to acne development.

microbiology↗
bioRxiv2021

The Mechanism of Neurite Outgrowth Induction by Novel Synthetic Retinobenzoic Acids

Retinoids are a family of vitamin A-derived molecules and include the biologically active metabolite, retinoic acid (RA). RA acts as a specific modulator of neuronal differentiation and proliferation. However, teratogenicity and a large excess of RA have been found in animal studies. Thus, development of effective and stable retinoids is desirable. In this study, we showed that treatment with novel synthetic retinobenzoic acids promotes neurite outgrowth in a selected subpopulation of the human neuroblastoma cell line SK-N-SH. Furthermore, we found that, although acting via a different mechanism, retinobenzoic acids have the same neurite outgrowth-inducing effect as RA. Retinoids, including RA, bind to nuclear retinoic acid receptors (RARs). Therefore, we examined the expression of RARs in retinobenzoic acid-treated cells. Similar to already known retinoids, novel synthetic retinobenzoic acids promote the upregulation of RAR{beta} and have no effect on RAR or {gamma}. These results suggest that retinobenzoic acids act via RAR{beta} during neurite outgrowth. Moreover, stimulation with RA or retinobenzoic acids significantly increased the phosphorylation levels of both ERK1/2 and mTOR. ERK1/2 and mTOR inhibition blocked the retinobenzoic acid-induced increase in neurite outgrowth, suggesting that retinobenzoic acids promoted neurite outgrowth by activating the ERK1/2 and mTOR signaling pathways. Notably, the RA-induced increase in neurite outgrowth was blocked by the ERK1/2 inhibitor U0126, but not by the mTOR inhibitor rapamycin. In addition, ERK1/2 inhibition blocked the upregulation of RAR{beta} promoted by RA and retinobenzoic acids. In contrast, mTOR inhibition had no effect on upregulation of RAR{beta}. Our results show that novel synthetic retinobenzoic acids induce neurite outgrowth by a different mechanism than RA. These findings suggest that activation of both ERK1/2, which results in downstream regulation of RAR{beta}, and mTOR, are responsible for the novel synthetic retinobenzoic acid-induced neurite outgrowth in human neuroblastoma cells.

cell biology↗