オーバーツーリズムの発生と持続可能な観光発展の課題

　近年、増加し続けている国際観光客数はさらに拡大することが見込まれている。それによる経済効果は大きく、世界各国では観光産業を重要産業として育ててきた。一方で観光客の急増や集中によって思わぬ被害を受けている観光地も続出している。それは許容量を超える観光客が訪れ、観光地の社会に悪影響を与えていることを指していて、数年前からオーバーツーリズムという言葉が登場した。本研究は世界各地で発生しているオーバーツーリズム現象の状況を把握するとともに、どのような対応策が講じられているのか調べたものである

The microbiology of oral lichen planus: Is microbial infection the cause of oral lichen planus?

Oral lichen planus (OLP) is a variant of lichen planus (LP), a common chronic mucocu-taneous inflammatory disease. Cutaneous lesions of LP are self- limiting, but OLP le-sions are non- remissive, alternating periods of exacerbation and quiescence, and only symptomatic treatments exist for OLP. The precise etiology and pathogenesis of OLP are hardly understood, which is a major obstacle to the development of new therapeu-tics for this disease. OLP is considered a T- cell- mediated inflammatory disease. Although various antigens have been considered, what actually triggers the inflamma-tory response of T cells is unknown. Suggested predisposing factors include genetic factors, stress, trauma, and infection. The aim of this review was to determine whether microbial infection can cause OLP. We first reviewed the association between OLP and microbial factors, including viral, fungal, and bacterial infections. In addition, each microbial factor associated with OLP was assessed by modified guidelines of Fredricks and Relman to determine whether it establishes a causal relationship. In conclusion, no microbial factor yet fulfills the guidelines to establish the causality of OLP. By focusing on the unclarified issues, however, the potential roles of microbial factors in the patho-genesis of OLP will be soon elucidated.This research was supported by Basic Science Research Program through the National Research Foundation of Korea (No. 2016R1E1A1A01942402).OAIID:RECH_ACHV_DSTSH_NO:T201714477RECH_ACHV_FG:RR00200001ADJUST_YN:EMP_ID:A075701CITE_RATE:2.908FILENAME:Baek_et_al-2017-Molecular_Oral_Microbiology.pdfDEPT_NM:치의과학과EMAIL:[email protected]_YN:YFILEURL:https://srnd.snu.ac.kr/eXrepEIR/fws/file/a720edb9-946a-4d68-811e-ebebd2045d18/linkCONFIRM:

Characterization of intratissue bacterial communities and isolation of Escherichia coli from oral lichen planus lesions

© 2020, The Author(s).Oral lichen planus (OLP) is a chronic T cell-mediated inflammatory disease of unknown etiology. We previously proposed that the intracellular bacteria detected in OLP lesions are important triggering factors for T cell infiltration. This study aimed to identify OLP-associated bacterial species through the characterization of intratissue bacterial communities of OLP lesions. Seven pairs of bacterial communities collected from the mucosal surface and biopsied tissues of OLP lesions were analyzed by high-throughput sequencing of the 16S rRNA gene. The intratissue bacterial communities were characterized by decreased alpha diversity but increased beta diversity compared with those on the mucosal surface. While the relative abundance of most taxa was decreased within the tissues, that of Escherichia coli was significantly increased. Four E. coli strains were isolated from additional OLP biopsies and verified as K12 strains by whole-genome sequencing. The distribution of E. coli in sections of control (n = 12) and OLP (n = 22) tissues was examined by in situ hybridization. E. coli was detected in most OLP tissues, suggesting its potential role in the pathogenesis of OLP. The oral E. coli strains isolated from OLP tissues will be useful to investigate their role as triggering factors for T cell infiltration.

Treponema denticola enolase contributes to the production of antibodies against ENO1 but not to the progression of periodontitis

Autoantibodies against alpha-enolase (ENO1) are often detected in various infectious and autoimmune diseases. Anti-ENO1 antibody titers were reported to be associated with the severity of periodontitis in patients with rheumatoid arthritis. Because the enolase of the periodontal pathogen Treponema denticola (TdEno) has the highest homology with ENO1 among the enolases of human-associated bacteria, we hypothesized that anti-ENO1 autoantibodies produced during the immune response to TdEno may contribute to the progression of periodontitis and tested it in human and mouse systems. In human subjects with healthy periodontium or chronic periodontitis, a strong positive correlation between the levels of anti-TdEno and anti-ENO1 antibodies was observed. In addition, the purified anti-TdEno antibodies recognized ENO1 as well as TdEno in a dot blot, confirming the cross-reactivity between TdEno and ENO1. However, anti-ENO1 antibody titers were not associated with the severity of periodontitis. To further investigate the role of TdEno in the production of anti-ENO1 antibodies and the progression of periodontitis, mice received an oral gavage of P. gingivalis alone, subcutaneous immunization with TdEno alone, or both P. gingivalis oral gavage and TdEno immunization. Immunization with TdEno induced not only anti-TdEno but also anti-mouse Eno1 (mEno1) antibodies and increased the expression of TNFα in the gingival tissues. However, alveolar bone loss was not increased by TdEno immunization. In conclusion, autoreactive anti-ENO1/mEno1 antibodies that are produced as byproducts during the antibody response to TdEno play a minimal role in the progression of periodontitis in the absence of rheumatoid arthritis