Microbiota-Immune Interactions in Ulcerative Colitis and Colitis Associated Cancer and Emerging Microbiota-Based Therapies

Popov, Jelena; Caputi, Valentina; Nandeesha, Nandini; Rodríguez, David Avelar; Pai, Nikhil

doi:10.3390/ijms222111365

Cited by 37 publications

(33 citation statements)

References 179 publications

(247 reference statements)

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“…Popov et al [ 43 ]proposed the three main theories about bacterial involvement in the development of IBD-associated CRC: The alpha-bug hypothesis, driver-passenger hypothesis, and common ground hypothesis. In the alpha-bug hypothesis, a single bacterium (normally ETBF) is thought to cause all modifications and damage that lead to carcinogenesis.…”

Section: Ibd-associated Crc and Gut Microbiotamentioning

confidence: 99%

“…The driver-passenger hypothesis is similar, but after the attack by the first bacteria, other opportunistic bacteria start to grow and contribute to cancer development. Finally, in the common ground hypothesis, endogenous and exogenous factors form a “leaky gut,” allowing the passage of bacteria into the submucosal tissue, leading to chronic inflammation and the consequent emergence of cancer[ 43 ].…”

Section: Ibd-associated Crc and Gut Microbiotamentioning

confidence: 99%

“…Increased quantities of Proteobacteria are associated with decreased levels of SCFAs and increased colonic inflammation[ 43 ]. In addition, intestinal Dysbiosis and barrier defects, associated with alterations in mucin secretion may happen even in the absence of active inflammation[ 43 ], perpetuating a favorable environment for the emergence of CRC.…”

Section: Ibd-associated Crc and Gut Microbiotamentioning

confidence: 99%

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Gut microbiota, inflammatory bowel disease and colorectal cancer

Quaglio¹,

Grillo²,

Oliveira³

et al. 2022

WJG

146

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The gut microbiota is a complex community of microorganisms that inhabit the digestive tracts of humans, living in symbiosis with the host. Dysbiosis, characterized by an imbalance between the beneficial and opportunistic gut microbiota, is associated with several gastrointestinal disorders, such as irritable bowel syndrome (IBS); inflammatory bowel disease (IBD), represented by ulcerative colitis and Crohn’s disease; and colorectal cancer (CRC). Dysbiosis can disrupt the mucosal barrier, resulting in perpetuation of inflammation and carcinogenesis. The increase in some specific groups of harmful bacteria, such as Escherichia coli ( E. coli ) and enterotoxigenic Bacteroides fragilis (ETBF), has been associated with chronic tissue inflammation and the release of pro-inflammatory and carcinogenic mediators, increasing the chance of developing CRC, following the inflammation-dysplasia-cancer sequence in IBD patients. Therefore, the aim of the present review was to analyze the correlation between changes in the gut microbiota and the development and maintenance of IBD, CRC, and IBD-associated CRC. Patients with IBD and CRC have shown reduced bacterial diversity and abundance compared to healthy individuals, with enrichment of Firmicute s and Bacteroidetes . Specific bacteria are also associated with the onset and progression of CRC, such as Fusobacterium nucleatum , E. coli , Enterococcus faecalis , Streptococcus gallolyticus , and ETBF. Future research can evaluate the advantages of modulating the gut microbiota as preventive measures in CRC high-risk patients, directly affecting the prognosis of the disease and the quality of life of patients.

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Section: Ibd-associated Crc and Gut Microbiotamentioning

confidence: 99%

Section: Ibd-associated Crc and Gut Microbiotamentioning

confidence: 99%

Section: Ibd-associated Crc and Gut Microbiotamentioning

confidence: 99%

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Gut microbiota, inflammatory bowel disease and colorectal cancer

Quaglio¹,

Grillo²,

Oliveira³

et al. 2022

WJG

146

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“…SCFAs generated by intestinal microorganisms are primary nutritional substrates for colonocytes [ 90 ]. By upregulating secretory IgA and cytokines, prebiotics can enhance host immunity [ 91 ]. Butyric acid protects against pathogenetic mechanisms mediated by reactive oxygen species and aids in understanding the apparent protection against CRC.…”

Section: Effect Of Bacterial Metabolitesmentioning

confidence: 99%

Effect of gut microbiota in the colorectal cancer and potential target therapy

Zhu

Yang

et al. 2022

Discov Onc

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The symbiotic interaction between gut microbiota and the digestive tract is an important factor in maintaining the intestinal environment balance. Colorectal cancer (CRC) is a complex disease involving the interaction between tumour cells and a large number of microorganisms. The microbiota is involved in the occurrence, development and prognosis of colorectal cancer. Several microbiota species have been studied, such as Fusobacterium nucleatum (F.nucleatum), Enterotoxigenic Bacteroidesfragilis (ETBF), Streptococcus bovis (S. bovis), Lactobacillus, and Bifidobacterium. Studies about the interaction between microbiota and CRC were retrieved from Embase, PubMed, Ovid and Web of Science up to 21 Oct 2021. This review expounded on the effect of microbiota on CRC, especially the dysregulation of bacteria and carcinogenicity. The methods of gut microbiota modifications representing novel prognostic markers and innovative therapeutic strategies were also described.

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“…Fungus, as an indispensable component of intestinal microbiota, take a crucial part in maintaining the gut homeostasis, and its dysbiosis might contribute to the pathogenesis of IBD ( 4 , 5 ). There are trillions of microorganisms resided in human gut, including bacteria, fungi, archaea and viruses ( 4 ), and metagenomic sequencing reveals that their collective genome are 100 times more than our own genome ( 6 , 7 ).…”

Section: Introductionmentioning

confidence: 99%

The Role of C-Type Lectin Receptor Signaling in the Intestinal Microbiota-Inflammation-Cancer Axis

Zhang

et al. 2022

Front. Immunol.

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As a subset of pattern recognition receptors (PRRs), C-type lectin-like receptors (CLRs) are mainly expressed by myeloid cells as both transmembrane and soluble forms. CLRs recognize not only pathogen associated molecular patterns (PAMPs), but also damage-associated molecular patterns (DAMPs) to promote innate immune responses and affect adaptive immune responses. Upon engagement by PAMPs or DAMPs, CLR signaling initiates various biological activities in vivo, such as cytokine secretion and immune cell recruitment. Recently, several CLRs have been implicated as contributory to the pathogenesis of intestinal inflammation, which represents a prominent risk factor for colorectal cancer (CRC). CLRs function as an interface among microbiota, intestinal epithelial barrier and immune system, so we firstly discussed the relationship between dysbiosis caused by microbiota alteration and inflammatory bowel disease (IBD), then focused on the role of CLRs signaling in pathogenesis of IBD (including Mincle, Dectin-3, Dectin-1, DCIR, DC-SIGN, LOX-1 and their downstream CARD9). Given that CLRs mediate intricate inflammatory signals and inflammation plays a significant role in tumorigenesis, we finally highlight the specific effects of CLRs on CRC, especially colitis-associated cancer (CAC), hoping to open new horizons on pathogenesis and therapeutics of IBD and CAC.

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Microbiota-Immune Interactions in Ulcerative Colitis and Colitis Associated Cancer and Emerging Microbiota-Based Therapies

Cited by 37 publications

References 179 publications

Gut microbiota, inflammatory bowel disease and colorectal cancer

Gut microbiota, inflammatory bowel disease and colorectal cancer

Effect of gut microbiota in the colorectal cancer and potential target therapy

The Role of C-Type Lectin Receptor Signaling in the Intestinal Microbiota-Inflammation-Cancer Axis

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