ABSTRACT
BACKGROUND: Based on recent research reports, dysbiosis and improper concentrations of microbial metabolites in the gut may result into the carcinogenesis of colorectal cancer. Recent advancement also highlights the involvement of bacteria and their secreted metabolites in the cancer causation. Gut microbial metabolites are functional output of the host-microbiota interactions and produced by anaerobic fermentation of food components in the diet. They contribute to influence variety of biological mechanisms including inflammation, cell signaling, cell-cycle disruption which are majorly disrupted in carcinogenic activities. PURPOSE: In this review, we intend to discuss recent updates and possible molecular mechanisms to provide the role of bacterial metabolites, gut bacteria and diet in the colorectal carcinogenesis. Recent evidences have proposed the role of bacteria, such as Fusobacterium nucleaturm, Streptococcus bovis, Helicobacter pylori, Bacteroides fragilis and Clostridium septicum, in the carcinogenesis of CRC. Metagenomic study confirmed that these bacteria are in increased abundance in CRC patient as compared to healthy individuals and can cause inflammation and DNA damage which can lead to development of cancer. These bacteria produce metabolites, such as secondary bile salts from primary bile salts, hydrogen sulfide, trimethylamine-N-oxide (TMAO), which are likely to promote inflammation and subsequently cancer development. CONCLUSION: Recent studies suggest that gut microbiota-derived metabolites have a role in CRC progression and causation and hence, could be implicated in CRC diagnosis, prognosis and therapy.
Subject(s)
Colorectal Neoplasms/microbiology , Gastrointestinal Microbiome/physiology , Animals , Colorectal Neoplasms/pathology , Disease Progression , Gram-Negative Bacteria/metabolism , Gram-Positive Bacteria/metabolism , Humans , MetagenomicsABSTRACT
Although skin is the primary affected organ in Leprosy, the role of the skin microbiome in its pathogenesis is not well understood. Recent reports have shown that skin of leprosy patients (LP) harbours perturbed microbiota which grants inflammation and disease progression. Herein, we present the results of nested Polymerase Chain Reaction-Denaturing Gradient Gel Electrophoresis (PCR-DGGE) which was initially performed for investigating the diversity of bacterial communities from lesional skin (LS) and non-lesional skin (NLS) sites of LP (n = 11). Further, we performed comprehensive analysis of 16S rRNA profiles corresponding to skin samples from participants (n = 90) located in two geographical locations i.e. Hyderabad and Miraj in India. The genus Staphylococcus was observed to be one of the representative bacteria characterizing healthy controls (HC; n = 30), which in contrast was underrepresented in skin microbiota of LP. Taxa affiliated to phyla Firmicutes and Proteobacteria were found to be signatures of HC and LS, respectively. Observed diversity level changes, shifts in core microbiota, and community network structure support the evident dysbiosis in normal skin microbiota due to leprosy. Insights obtained indicate the need for exploring skin microbiota modulation as a potential therapeutic option for leprosy.
Subject(s)
Bacteria , Leprosy , Microbiota/genetics , Bacteria/classification , Bacteria/genetics , Female , Humans , India , Leprosy/genetics , Leprosy/microbiology , Male , Polymerase Chain Reaction , RNA, Bacterial/genetics , RNA, Ribosomal, 16S/geneticsABSTRACT
Leprosy is an infectious disease that has predilection in skin and peripheral nerves. Skin has its own microbiome, however it is not extensively studied in Indian leprosy patients. Here, by using next-generation 16S rDNA sequencing, we have attempted to assess the skin associated microbial diversity pertaining to affected and unaffected skin of Indian leprosy patients. A total of 90 skin swab samples were collected from 60 individuals (30 healthy controls, 30 patients) residing in Hyderabad and Miraj, two distinct geographical locations in India to assess the homo/heterogeneity of skin microbial signatures. While a large increase in genus Methylobacterium and Pseudomonas was seen in patients from Miraj and Hyderabad respectively, a considerable decrease in genus Staphylococcus in the leprosy patients (as compared to controls) from both geographical locations was also observed. We expect that, these datasets can not-only provide further interesting insights, but will also help to observe dynamics of microbiome in the diseased state and generate hypotheses to test for skin microbiome transplantation studies in leprosy.
