Several studies have explored the origin and development mechanism of oral lichen planus (OLP) with limited attention to the role of bacteria in the progression of this common oral disease. Here we utilized MiSeq sequencing of 16S rRNA gene amplicons to identify complex oral microbiota associated with OLP from saliva samples of two subtypes (reticular and erosive) of OLP patients and healthy controls. Our analyses indicated that the overall structure of the salivary microbiome was not significantly affected by disease status. However, we did observe evident variations in abundance for several taxonomic groups in OLP. Porphyromonas and Solobacterium showed significantly higher relative abundances, whereas Haemophilus, Corynebacterium, Cellulosimicrobium and Campylobacter showed lower abundances in OLP patients, as compared with healthy controls. In addition, we explored specific microbial cooccurrence patterns in OLP, and revealed significantly fewer linkers of Streptococcus comprising species in erosive OLP. Furthermore, the disease severity and immune dysregulation were also genusassociated, including with Porphyromonas that correlated to disease scores and salivary levels of interleukin (IL)-17 and IL-23. Overall, this study provides a general description of oral microbiome in OLP, and it will be useful for further investigation of their potential roles in the initiation and immune modulation of OLP.Lichen planus is a common chronic mucocutaneous inflammatory disease affecting skin, oral, genital mucosa, scalp and nails. The prevalence of oral lichen planus (OLP) ranges from 0.1-4% in the general population, and females between 30 and 60 are more vulnerable to this disease 1 . Lesion manifestations can often persist for years alternating between periods of quiescence and exacerbation 2 . Intraorally, OLP presents as white striations, papules, plaques, mucosal atrophy, erosions or blisters, mainly affecting the buccal mucosa, tongue, gingiva and lips 3 . Among those clinical phenotypes, the reticular form is the most prevalent lesion characterized by the presence of Wickham striae and usually asymptomatic. Whereas the erosive type, although less frequent, always causes different degrees of discomfort and soreness, it may need ongoing concern due to its malignant potential 4 . Despite of numerous literatures appraising the OLP origin and development mechanism, its aetiology remains uncertain, and the pathogenesis of this disease still needs more investigations. Several internal and external factors have been implicated, such as immunodeficiencies and microbial infection 5 . Several lines of evidences have suggested that immune dysregulation and complex cytokine network played important roles in the exacerbation and perpetuation of OLP 6,7 . For instance, a high proportion of the novel CD4 + T helper cells subset-Th17 cells were detected in OLP lesions 8 . And interleukin (IL)-17 and IL-23, the newly discovered Th17-associated cytokines, were found to be important proinflammatory factors involved in OLP 9,10 . In...

Anthropogenic environments have been implicated in enrichment and exchange of antibiotic resistance genes and bacteria. Here we study the impact of confined and controlled swine farm environments on temporal changes in the gut microbiome and resistome of veterinary students with occupational exposure for 3 months. By analyzing 16S rRNA and whole metagenome shotgun sequencing data in tandem with culture-based methods, we show that farm exposure shapes the gut microbiome of students, resulting in enrichment of potentially pathogenic taxa and antimicrobial resistance genes. Comparison of students' gut microbiomes and resistomes to farm workers' and environmental samples revealed extensive sharing of resistance genes and bacteria following exposure and after three months of their visit. Notably, antibiotic resistance genes were found in similar genetic contexts in student samples and farm environmental samples. Dynamic Bayesian network modeling predicted that the observed changes partially reverse over a 4-6 month period. Our results indicate that acute changes in a human's living environment can persistently shape their gut microbiota and antibiotic resistome.

Persistent methicillin-resistant Staphylococcus aureus (MRSA) bacteremia (PB) represents an important subset of S. aureus endovascular infections. In this study, we investigated potential genetic mechanisms underlying the persistent outcomes. Compared with resolving bacteremia (RB) isolates (defined as isolates associated with negative results of blood cultures 2-4 days after initiation of therapy), PB strains (defined as isolates associated with positive results of blood cultures ≥7 days after initiation of therapy) had significantly earlier onset activation of key virulence regulons and structural genes (eg, sigB, sarA, sae, and cap5), higher expression of purine biosynthesis genes (eg, purF), and faster growth rates, with earlier entrance into stationary phase. Importantly, an isogenic strain set featuring a wild-type MRSA isolate, a purF mutant strain, and a purF-complemented strain and use of strategic purine biosynthesis inhibitors implicated a causal relationship between purine biosynthesis and the in vivo persistent outcomes. These observations suggest that purine biosynthesis plays a key role in the outcome of PB and may represent a new target for enhanced efficacy in treating life-threatening MRSA infections.