RESUMO
Liver disease has been reported to associate with oral microbiota. This study aimed to identify the salivary microbial structure in liver disease patients and determine whether the disease progression influence the bacterial composition. 16S rDNA high-throughput sequencing and bioinformatic analysis were used to examine oral bacterial diversity in the different status of hepatitis patients including 6 patients with Hepatitis B (Y), 6 patients with Hepatitis B Cirrhosis (YY) and 6 patients with liver cancer (C), and 6 healthy controls (T). Phylogenetic analysis revealed that the genera of Streptococcus, Prevotella, Actinomyces, Veillonella and Neisseria are predominant genus in the saliva of Y, YY, C patients and T group. Lautropia, Abiotrophia and Veillonella were enriched in Y patients, while Treponema, Selenomonas and Oribacterium were also existed in YY patients. Haemophilus, Porphyromonas and Filifactor had high abundance in C patients. The genera of Moryella, Leptotrichia, Lactobacillus, Dialister, Serratia, Enterococcus and Actinobacillus were decreased in all patient samples compared with healthy control samples which may be used for treatment of liver disease. Diversity analyses showed decreased diversity of salivary bacterial communities was discovered in the progress of the liver disease. These findings identified the oral microbiota dysbiosis in liver disease, which may providing available information and possible diagnostic biomarkers for liver patients.
Assuntos
Neoplasias Hepáticas , Microbiota , Humanos , Filogenia , RNA Ribossômico 16S/genética , SalivaRESUMO
Chronic periodontitis (CP) is a common oral disease characterized by the slow progression of alveolar attachment loss and bone destruction. Genetic components have been reported to play an important role in the onset and development of CP. In the present study, we aimed to replicate the association signals of NIN and SIGLEC5 identified in previous genome-wide association studies (GWASs) of samples from Chinese Han individuals. Association signals between clinical severity indicators of CP and relevant single nucleotide polymorphisms (SNPs) were also examined. A total of 3,160 study subjects, including 1,076 CP patients and 2,084 healthy controls, were recruited. A total of 32 SNPs, including 22 from NIN and 10 from SIGLEC5, were selected for genotyping. SNPs rs12883458 (OR = 1.45, P = 1.22 × 10-5, NIN) and rs4284742 (OR = 0.75, P = 1.69 × 10-5, SIGLEC5) were significantly associated with CP disease status. rs4284742 was significantly associated with all 3 clinical severity indicators, including bleeding on probing (BOP), probing depth (PD) and clinical attachment loss (CAL). According to evidence from bioinformatics analyses, both significant SNPs, rs12883458 and rs4284742, are likely surrogates of underlying variants with true effects. In summary, our findings provide direct evidence for the association of NIN and SIGLEC5 with CP susceptibility.