Bacteroides fragilis toxin's role in colon cancer development
Journal name: The Malaysian Journal of Medical Sciences
Original article title: The Mechanism of Bacteroides fragilis Toxin Contributes to Colon Cancer Formation
The Malaysian Journal of Medical Sciences (MJMS) is a peer-reviewed, open-access journal published online at least six times a year. It covers all aspects of medical sciences and prioritizes high-quality research.
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Original source:
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Wai Teng Cheng, Haresh Kumar Kantilal, Fabian Davamani
The Malaysian Journal of Medical Sciences:
(A peer-reviewed, open-access journal)
Full text available for: The Mechanism of Bacteroides fragilis Toxin Contributes to Colon Cancer Formation
Year: 2020 | Doi: 10.21315/mjms2020.27.4.2
Copyright (license): CC BY 4.0
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Summary of article contents:
Introduction
The intestinal tract is home to numerous microbial species, including Bacteroides fragilis (B. fragilis), which can exist in two forms: non-toxigenic (NTBF) and enterotoxigenic (ETBF). While NTBF is typically non-harmful, ETBF produces a toxin known as Bacteroides fragilis toxin (BFT), which is associated with various inflammatory responses and chronic intestinal conditions. Chronic inflammation is a significant risk factor for colorectal cancer (CRC), as it alters the microenvironment of the intestinal tract, leading to cellular changes that can promote carcinogenesis. Understanding the interactions between ETBF, the immune system, and inflammation is crucial for elucidating the molecular mechanisms underlying CRC development.
The Role of STAT3 Activation in Colorectal Carcinogenesis
One of the pivotal mechanisms through which ETBF contributes to CRC is the activation of the signal transducer and activator of transcription 3 (STAT3) pathway. STAT3 is essential in regulating immune responses and promoting inflammation. In the presence of BFT, STAT3 activation occurs in colonic mucosal immune cells and epithelial cells, fostering an environment conducive to tumor growth. Specifically, activated STAT3 encourages the differentiation of T-helper 17 (Th17) cells, which lead to increased production of pro-inflammatory cytokines like IL-17 and IL-6. This cascade initiates chronic inflammation and alters various signaling pathways, including the cyclooxygenase-2 (COX-2) pathway, which further enhances pro-inflammatory responses and promotes cancer cell proliferation. The persistent activation of STAT3 ultimately mitigates anti-tumor immune responses, exacerbating carcinogenesis within the colon.
Conclusion
In conclusion, the enterotoxigenic strains of Bacteroides fragilis, particularly through the actions of BFT, significantly impact intestinal health by triggering chronic inflammation and promoting CRC. The STAT3 signaling pathway plays a central role in this process by mediating immune responses that favor inflammation and tumorigenesis. Given the established link between ETBF colonization and colorectal cancer development, this highlights the importance of understanding microbial influences on cancer biology, which could pave the way for new therapeutic strategies targeting inflammation and its related mechanisms in CRC prevention and treatment.
FAQ section (important questions/answers):
What role does Bacteroides fragilis play in colorectal cancer?
Bacteroides fragilis, specifically enterotoxigenic B. fragilis (ETBF), produces a toxin that contributes to inflammation and carcinogenesis in the colon, increasing the risk of colorectal cancer (CRC). The non-toxigenic variant does not have this cancer-promoting effect.
How does the Bacteroides fragilis toxin affect intestinal health?
The Bacteroides fragilis toxin (BFT) damages the intestinal epithelial cells, disrupts tight junctions, increases permeability, and triggers chronic inflammation, all of which are key factors in the progression toward colorectal cancer.
What is the connection between chronic inflammation and colorectal cancer?
Chronic inflammation leads to cellular changes, mutations, and an abnormal immune response, which can contribute to tumorigenesis. Specifically, cytokines produced during inflammation activate pathways that promote cancer cell survival and growth.
What genetic factors are associated with increased colorectal cancer risk?
Familial adenomatous polyposis (FAP) is linked to mutations in the adenomatous polyposis coli (APC) gene, which enhances bacterial adherence and increases the risk of colorectal cancer. The genetic predisposition, combined with microbial factors, heightens this risk.
Glossary definitions and references:
Scientific and Ayurvedic Glossary list for “Bacteroides fragilis toxin's role in colon cancer development”. This list explains important keywords that occur in this article and links it to the glossary for a better understanding of that concept in the context of Ayurveda and other topics.
1) Cancer:
Cancer refers to a group of diseases characterized by uncontrolled cell growth, leading to the formation of tumors. Colorectal cancer (CRC) is particularly noted for its association with chronic inflammation caused by microbial factors, such as enterotoxigenic Bacteroides fragilis, which plays a crucial role in the disease's development and progression.
2) Inflammation:
Inflammation is a vital immune response to injury or infection that can, when chronic, lead to several diseases including cancer. In the context of colorectal cancer, inflammation induced by bacteria such as Bacteroides fragilis can perpetuate tumorigenesis through various signaling pathways, including STAT3 activation.
3) Disease:
Disease refers to any condition that causes dysfunction within the body and can be caused by various factors including genetics, infections, and environmental conditions. Colorectal cancer is a prominent disease linked to alterations in gut microbiota and prolonged inflammatory responses, showing the intersection between microbial health and human disease.
4) Mutation:
Mutation denotes a change in the DNA sequence, which can lead to altered protein functions and contribute to diseases such as cancer. In familial adenomatous polyposis, mutations in the adenomatous polyposis coli (APC) gene are crucial for the initiation of tumorigenesis, illustrating the genetic basis of certain colorectal cancers.
5) Species:
Species refers to a group of organisms capable of interbreeding. Within this context, Bacteroides fragilis exists in both non-toxigenic and enterotoxigenic forms. The enterotoxigenic species is specifically linked to colorectal cancer development through its ability to produce toxins and induce inflammation within the gut.
6) Blood:
Blood is a bodily fluid that circulates in humans, serving critical roles in transport and immune response. In cancer-related studies, blood biomarkers such as COX-2 and inflammatory cytokines are often measured to assess cancer presence and link systemic inflammation and immune response to tumor progression.
7) Table:
Table, in scientific writing, often refers to data presentation in a structured format to display complex information clearly. In the context of literature reviews, tables summarize findings, results from studies on diseases like colorectal cancer, and datasets linking microbial activity, inflammation, and cancer pathways for easier analysis and reference.
8) Activity:
Activity in this context refers to the biological responses or functions of various agents, including microbes, toxins, and immune cells. The activity of enterotoxigenic Bacteroides fragilis contributes to gastrointestinal inflammation and tissue injury, highlighting its role in the pathogenesis of colorectal cancer.
9) Science (Scientific):
Science is the systematic pursuit of knowledge, encompassing various disciplines including biology and medicine. Research into the relationship between gut microbiota and colorectal cancer is an emerging field, emphasizing the importance of microbial interactions in understanding disease mechanisms and identifying potential therapeutic targets.
10) Surface:
Surface often relates to the outer layer of cells or tissues. In microbial contexts, the surface characteristics of pathogens like Bacteroides fragilis can influence adhesion to gut epithelium, playing a role in colonization, inflammation, and ultimately carcinogenesis in colorectal cancer.
11) Nature:
Nature refers to the inherent qualities and characteristics of organisms and their environment. Understanding the nature of microbial interactions within the gut provides insights into how disturbances in such ecosystems contribute to diseases like colorectal cancer, emphasizing the interplay between health and microbial environments.
12) Ter:
Short for therapy or therapeutic, it relates to treatment options for diseases. In the realm of cancer, understanding microbial contributions to inflammation and tumorigenesis is crucial for developing targeted therapies to mitigate colorectal cancer risk and improve treatment outcomes.
13) Sho (So):
Shao likely refers to a researcher contributing to the literature on the relationship between microbial activity and cancer. Their findings may advance understanding of how specific bacteria influence inflammation and drive the progression of diseases like colorectal cancer, illustrating the importance of research in health.
14) Developing:
Developing refers to the process of growth or advancement. In the context of colorectal cancer, developing a deeper understanding of microbial influences on inflammation and tumorigenesis is essential for crafting effective interventions aimed at reducing disease risk and improving patient outcomes.
15) Substance:
Substance pertains to the materials or compounds involved in biological processes. In the context of colorectal cancer, substances like toxins produced by Bacteroides fragilis play a significant role in promoting inflammation, altering signaling pathways, and facilitating carcinogenesis in the gut.
16) Medicine:
Medicine encompasses various fields dedicated to the diagnosis, treatment, and prevention of diseases. Insights gained from studying the interactions between gut microbiota and colorectal cancer may lead to innovative medical approaches, shaping future practices aimed at managing cancer and associated inflammatory conditions.
17) Death:
Death signifies the cessation of biological functions that sustain life and is a critical outcome related to diseases, including cancer. Understanding the factors leading to mortality in colorectal cancer patients, including microbial influences, is vital for improving treatment strategies and patient care.
18) Drug:
Drug refers to a substance used in the diagnosis, treatment, or prevention of disease. In the context of cancer, approaches involving anti-inflammatory drugs targeting pathways activated by microbes like Bacteroides fragilis are explored for their potential to mitigate cancer risks and enhance therapeutic efficacy.
19) Chan:
Chan may represent a researcher or authority in the field whose insights and findings contribute to the understanding of microbial roles in cancer. Their work enriches the understanding of how microbial influences intersect with immune responses to contribute to diseases like colorectal cancer.
20) Accumulation (Accumulating, Accumulate):
Accumulating emphasizes the process of gradual gathering of substances, cells, or influences over time. In the context of colorectal cancer, accumulating evidence about the role of inflammation and microbial factors lays the groundwork for potential preventive strategies and targeted therapies.
21) Pantiyar (Pantiyan):
Pandiyan could refer to a researcher known for contributions to immunology, particularly in the area concerning microbial influences on immune responses. Their work on T helper cells and inflammation links microbial dynamics to cancer progression, particularly in colorectal cancer contexts.
22) Karin (Kari):
Karin likely refers to a notable figure in cancer research, especially concerning the inflammatory pathways and their roles in tumorigenesis. Their contributions enhance the understanding of how chronic inflammation links microbial activity to cancer development, aiding in identifying potential treatment targets.
23) Varga:
Varga may denote a researcher whose work focuses on the interplay between inflammation and cancer. Their studies could provide valuable insights into how immune pathways contribute to tumorigenesis, particularly in the context of colorectal cancer driven by microbial factors.
24) Study (Studying):
Study indicates a systematic investigation into a specific area of research, such as the impacts of gut microbiota on colorectal cancer. Research studies contribute significant findings to our understanding of disease mechanisms, risk factors, and potential therapeutic strategies.
25) Rich (Rch):
Rich refers to a researcher likely involved in cancer studies, particularly those exploring inflammatory responses and their implications in tumor biology. Their work might focus on the intersection of microbiology and cancer, contributing to the understanding of disease dynamics.
26) Line:
Line often signifies a lineage or sequence, in scientific studies referring to experimental models or genetic lines. In colorectal cancer research, analyzing genetic lines can elucidate the roles of specific genes and microbes in disease susceptibility and progression.
27) Transformation (Transform, Transforming):
Transform signifies the act of changing or causing change. In cancer biology, transforming factors, including certain bacteria and their products, can alter cellular pathways, driving the progression from inflammation to malignancy, particularly in colorectal cancer.
28) Killing (Killed):
Killing pertains to the process of destroying pathogens or cancer cells, a crucial aspect of immune response and therapeutic strategies. Targeted therapies are designed to enhance the body's ability to kill cancer cells, addressing the influences of microbial factors linked to cancer.
29) Family:
Family may refer to related organisms or cells within the context of microbiology. Understanding the family of bacteria in the gut, especially those like Bacteroides fragilis, is essential for evaluating their roles in health and disease, particularly in inflammatory and oncological contexts.
30) Kappa:
Kappa typically refers to a subtype of proteins or pathways like the NF-kappaB signaling pathway, which is crucial in inflammation and cancer. The Kappa factor serves as a bridge connecting microbial-induced inflammation to the carcinogenic processes occurring in colorectal cancer.
31) Pain:
Pain is a complex experience often associated with inflammation or injury. In the context of colorectal cancer, pain can be a significant symptom influenced by inflammatory processes, where microbial activity may exacerbate discomfort and indicate underlying disease progression.
32) Post:
Post refers to various contexts but often denotes subsequent events or conditions following an occurrence. In cancer research, post-therapeutic outcomes and monitoring the patient's response after treatments are essential for assessing effectiveness and managing any residual disease activity.
Other Science Concepts:
Discover the significance of concepts within the article: ‘Bacteroides fragilis toxin's role in colon cancer development’. Further sources in the context of Science might help you critically compare this page with similair documents:
Ro, Inflammation, Intestinal tract, Chronic inflammation, Oxidative stress, Reactive oxygen species, Genetic predisposition, Immune response, Bacterial flora, Apoptosis, Candida albicans, PGE2, Inflammatory cells, Nitric oxide, Cell proliferation, Inflammatory bowel disease, Tumor microenvironment, Tumor formation, Colorectal Cancer, Skin cancer, Metastasis, Genetic testing, Gene mutation, Cancerous cells, T-helper cells, Cox-2, Epithelial Cells, Redox homeostasis, Mucosal inflammation, Mouse model, Wnt signaling pathway, Intestinal microflora, Th17 cells, Colon cancer, Bacteroides fragilis, Proinflammatory cytokine, Interleukin-17, Interleukin -8, Nitric oxide synthase, IL-6, Tumor Proliferation, COX-2 expression, Tumor load, L-arginine, Epithelial mesenchymal transition, Epithelial barrier, Signal transduction, Tumor development, Intestinal epithelial cells, Gene regulation, Interleukin, Colorectal carcinoma, Tumor suppressor protein, MicroRNA, Neoplastic Cells, Tumour cells, Intestinal Inflammation, Germline mutation, Somatic mutation, Chloride secretion, Heme oxygenase-1, Biofilm producers, Cyclooxygenase, APC gene, Genetic alteration, Proto-oncogene.