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Article ; Online: Altered gut microbiota of obesity subjects promotes colorectal carcinogenesis in mice.

Kang, Xing / Ng, Siu-Kin / Liu, Changan / Lin, Yufeng / Zhou, Yunfei / Kwong, Thomas N Y / Ni, Yunbi / Lam, Thomas Y T / Wu, William K K / Wei, Hong / Sung, Joseph J Y / Yu, Jun / Wong, Sunny H

EBioMedicine

2023 Volume 93, Page(s) 104670

Abstract: Background: Obesity is a risk factor for colorectal cancer (CRC). The role of gut microbiota in mediating the cancer-promoting effect of obesity is unknown.: Methods: Azoxymethane (AOM)-treated, Apc: Findings: Conventional AOM-treated and Apc: ... ...

Abstract	Background: Obesity is a risk factor for colorectal cancer (CRC). The role of gut microbiota in mediating the cancer-promoting effect of obesity is unknown. Methods: Azoxymethane (AOM)-treated, Apc Findings: Conventional AOM-treated and Apc Interpretation: Our results supported the role of obesity-associated microbiota in colorectal carcinogenesis and identified putative bacterial candidates that may mediate its mechanisms. Microbiota modulation in obese individuals may provide new approaches to prevent or treat obesity-related cancers including CRC. Funding: This work was funded by National Key Research and Development Program of China (2020YFA0509200/2020YFA0509203), National Natural Science Foundation of China (81922082), RGC Theme-based Research Scheme Hong Kong (T21-705/20-N), RGC Research Impact Fund Hong Kong (R4632-21F), RGC-CRF Hong Kong (C4039-19GF and C7065-18GF), RGC-GRF Hong Kong (14110819, 14111621), and NTU Start-Up Grant (021337-00001).
MeSH term(s)	Humans ; Mice ; Animals ; Gastrointestinal Microbiome ; Colonic Neoplasms ; Carcinogenesis ; Obesity/complications ; Azoxymethane/toxicity ; Colorectal Neoplasms/genetics ; Mice, Inbred C57BL ; Disease Models, Animal
Chemical Substances	Azoxymethane (MO0N1J0SEN)
Language	English
Publishing date	2023-06-19
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2851331-9
ISSN	2352-3964
ISSN (online)	2352-3964
DOI	10.1016/j.ebiom.2023.104670
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Article ; Online: Clinical applications of gut microbiota in cancer biology.

Wong, Sunny H / Kwong, Thomas N Y / Wu, Chun-Ying / Yu, Jun

Seminars in cancer biology

2018 Volume 55, Page(s) 28–36

Abstract: The involvement of microorganisms in cancer has been increasing recognized. Collectively, microorganisms have been estimated to account for ∼20% of all cancers worldwide. Recent advances in metagenomics and bioinformatics have provided new insights on ... ...

Abstract	The involvement of microorganisms in cancer has been increasing recognized. Collectively, microorganisms have been estimated to account for ∼20% of all cancers worldwide. Recent advances in metagenomics and bioinformatics have provided new insights on the microbial ecology in different tumors, pinpointing the roles of microorganisms in cancer formation, development and response to treatments. Furthermore, studies have emphasized the importance of host-microbial and inter-microbial interactions in the cancer microbiota. These studies have not only revolutionized our understanding of cancer biology, but also opened up new opportunities for cancer prevention, diagnosis, prognostication and treatment. This review article aims to summarize the microbiota in various cancers and their treatments, and explore clinical applications for such relevance.
MeSH term(s)	Computational Biology ; Gastrointestinal Microbiome/genetics ; Humans ; Metagenomics ; Neoplasms/diagnosis ; Neoplasms/genetics ; Neoplasms/microbiology ; Neoplasms/therapy
Language	English
Publishing date	2018-05-18
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1033980-2
ISSN	1096-3650 ; 1044-579X
ISSN (online)	1096-3650
ISSN	1044-579X
DOI	10.1016/j.semcancer.2018.05.003
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Article ; Online: Reply.

Kwong, Thomas N Y / Wu, William K K / Wong, Sunny H

Gastroenterology

2018 Volume 156, Issue 1, Page(s) 292

MeSH term(s)	Bacteremia ; Colorectal Neoplasms ; Humans ; Streptococcus gallolyticus
Language	English
Publishing date	2018-11-22
Publishing country	United States
Document type	Letter ; Comment
ZDB-ID	80112-4
ISSN	1528-0012 ; 0016-5085
ISSN (online)	1528-0012
ISSN	0016-5085
DOI	10.1053/j.gastro.2018.11.047
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Article ; Online: Disentangling the relationship of gut microbiota, functional gastrointestinal disorders and autism: a case-control study on prepubertal Chinese boys.

Wong, Oscar W H / Lam, Angela M W / Or, Brian P N / Mo, Flora Y M / Shea, Caroline K S / Lai, Kelly Y C / Ma, Suk Ling / Hung, Se Fong / Chan, Sandra / Kwong, Thomas N Y / Wong, Sunny / Leung, Patrick W L

Scientific reports

2022 Volume 12, Issue 1, Page(s) 10659

Abstract: Emerging evidence of an altered gut microbiome in autism spectrum disorder (ASD) suggests a pathomechanism through the gut-brain axis despite the inconsistent microbiome profile reported across studies. One of the knowledge gaps in the existing ASD ... ...

Abstract	Emerging evidence of an altered gut microbiome in autism spectrum disorder (ASD) suggests a pathomechanism through the gut-brain axis despite the inconsistent microbiome profile reported across studies. One of the knowledge gaps in the existing ASD microbiota studies is the lack of systematic exploration of the role of comorbid functional gastrointestinal disorder (FGID) in the association of ASD and altered gut microbiome. Consequently, 92 ASD and 112 age-matched typically developing (TD) boys were profiled on general psychopathology, FGID status by Rome IV classification, and gut microbiota using 16S ribosomal RNA amplicon sequencing at the V4 hypervariable region. Compared to TD, a significant decrease in the within-sample abundance of taxa was observed in ASD, regardless of FGID status. The microbiota of ASD FGID+ and ASD FGID- clustered apart from the TD groups. The microbiota of ASD FGID+ also showed qualitative differences from that of ASD FGID- and had the highest-level Firmicutes: Bacteroidetes ratio, which was paralleled by elevated levels of anxiety and overall psychopathology. The altered gastrointestinal microbiota composition in ASD appeared to be independent of comorbid FGID. Further studies should address how FGID may mediate neuropsychiatric symptoms in ASD through inflammation along the microbiota-gut-brain axis.
MeSH term(s)	Autism Spectrum Disorder ; Autistic Disorder ; Case-Control Studies ; China ; Gastrointestinal Diseases ; Gastrointestinal Microbiome/genetics ; Humans ; Male
Language	English
Publishing date	2022-06-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-14785-8
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Article ; Online: Trends in Incidence and Clinical Outcomes of Clostridioides difficile Infection, Hong Kong.

Guo, Cosmos L T / Kwong, Thomas N Y / Mak, Joyce W Y / Zhang, Lin / Lui, Grace C Y / Wong, Grace L H / Ip, Margaret / Yu, Jun / Sung, Joseph J Y / Wu, William K K / Wong, Sunny H

Emerging infectious diseases

2021 Volume 27, Issue 12

MeSH term(s)	Clostridioides difficile ; Clostridium Infections/diagnosis ; Clostridium Infections/epidemiology ; Hong Kong/epidemiology ; Humans ; Incidence
Language	English
Publishing date	2021-11-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1380686-5
ISSN	1080-6059 ; 1080-6040
ISSN (online)	1080-6059
ISSN	1080-6040
DOI	10.3201/eid2712.203769
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Article ; Online: Biological characteristics associated with virulence in

Kong, Ka Yi / Kwong, Thomas N Y / Chan, Hung / Wong, Kristine / Wong, Samuel S Y / Chaparala, Anu P / Chan, Raphael C Y / Zhang, Lin / Sung, Joseph J Y / Yu, Jun / Hawkey, Peter M / Ip, Margaret / Wu, William K K / Wong, Sunny H

Emerging microbes & infections

2020 Volume 9, Issue 1, Page(s) 631–638

Abstract: Clostridioides ... ...

Abstract	Clostridioides difficile
MeSH term(s)	Animals ; Clostridiales/pathogenicity ; Gram-Positive Bacterial Infections/microbiology ; Hong Kong ; Male ; Mice, Inbred C57BL ; Ribotyping ; Virulence
Language	English
Publishing date	2020-03-17
Publishing country	United States
Document type	Journal Article
ZDB-ID	2681359-2
ISSN	2222-1751 ; 2222-1751
ISSN (online)	2222-1751
ISSN	2222-1751
DOI	10.1080/22221751.2020.1739564
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Article ; Online: Real-time tracking of fluorescent magnetic spore-based microrobots for remote detection of

Zhang, Yabin / Zhang, Lin / Yang, Lidong / Vong, Chi Ian / Chan, Kai Fung / Wu, William K K / Kwong, Thomas N Y / Lo, Norman W S / Ip, Margaret / Wong, Sunny H / Sung, Joseph J Y / Chiu, Philip W Y / Zhang, Li

Science advances

2019 Volume 5, Issue 1, Page(s) eaau9650

Abstract: A rapid, direct, and low-cost method for detecting bacterial toxins associated with common gastrointestinal diseases remains a great challenge despite numerous studies and clinical assays. Motion-based detection through tracking the emerging micro- and ... ...

Abstract	A rapid, direct, and low-cost method for detecting bacterial toxins associated with common gastrointestinal diseases remains a great challenge despite numerous studies and clinical assays. Motion-based detection through tracking the emerging micro- and nanorobots has shown great potential in chemo- and biosensing due to accelerated "chemistry on the move". Here, we described the use of fluorescent magnetic spore-based microrobots (FMSMs) as a highly efficient mobile sensing platform for the detection of toxins secreted by
MeSH term(s)	Bacterial Proteins/analysis ; Bacterial Toxins/analysis ; Carbon/chemistry ; Clostridioides difficile/physiology ; Clostridium Infections/diagnosis ; Clostridium Infections/microbiology ; Feces/chemistry ; Feces/microbiology ; Ferrosoferric Oxide/chemistry ; Fluorescence ; Fluorescent Dyes/chemistry ; Humans ; Magnetite Nanoparticles/chemistry ; Nanomedicine/methods ; Remote Sensing Technology/methods ; Sensitivity and Specificity ; Spores, Bacterial
Chemical Substances	Bacterial Proteins ; Bacterial Toxins ; Fluorescent Dyes ; Magnetite Nanoparticles ; Carbon (7440-44-0) ; Ferrosoferric Oxide (XM0M87F357)
Language	English
Publishing date	2019-01-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.aau9650
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Article ; Online: Surveillance of antibiotic resistance among common Clostridium difficile ribotypes in Hong Kong.

Chow, Viola C Y / Kwong, Thomas N Y / So, Erica W M / Ho, Yolanda I I / Wong, Sunny H / Lai, Raymond W M / Chan, Raphael C Y

Scientific reports

2017 Volume 7, Issue 1, Page(s) 17218

Abstract: Incidence of Clostridium difficile infection (CDI) is rapidly increasing and it poses a major health burden globally. However, data regarding the epidemiology of CDI in Asia are limited. We aimed to characterize the antimicrobial susceptibility patterns ... ...

Abstract	Incidence of Clostridium difficile infection (CDI) is rapidly increasing and it poses a major health burden globally. However, data regarding the epidemiology of CDI in Asia are limited. We aimed to characterize the antimicrobial susceptibility patterns of common ribotypes of toxigenic C. difficile in Hong Kong. Fifty-three PCR ribotypes were identified among 284 toxigenic C. difficile clinical isolates. The five most prevalent ribotypes were 002 (13%), 017 (12%), 014 (10%), 012 (9.2%), and 020 (9.5%). All tested C. difficile strains remained susceptible to metronidazole, vancomycin, meropenem and piperacillin/tazobactam, but highly resistant to cephalosporins. Of the fluoroquinolones, highest resistance to ciprofloxacin was observed (99%), followed by levofloxacin (43%) and moxifloxacin (23%). The two newly emerged PCR ribotypes, 017 and 002, demonstrated high levels of co-resistance towards clindamycin, tetracycline, erythromycin and moxifloxacin. PCR ribotypes 017 and 002 with multi-drug resistance are rapidly emerging and continuous surveillance is important to monitor the epidemiology of C. difficile to prevent outbreaks of CDI.
MeSH term(s)	Anti-Bacterial Agents/pharmacology ; Clostridium difficile/classification ; Clostridium difficile/drug effects ; Clostridium difficile/genetics ; Drug Resistance, Bacterial ; Hong Kong ; Polymerase Chain Reaction ; Ribotyping
Chemical Substances	Anti-Bacterial Agents
Language	English
Publishing date	2017-12-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-017-17523-7
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Article ; Online: Clostridium difficile toxin B induces autophagic cell death in colonocytes.

Chan, Hung / Zhao, Shan / Zhang, Lin / Ho, Jeffery / Leung, Czarina C H / Wong, Wai T / Tian, Yuanyuan / Liu, Xiaodong / Kwong, Thomas N Y / Chan, Raphael C Y / Yu, Sidney S B / Wang, Maggie H T / Tse, Gary / Wong, Sunny H / Chan, Matthew T V / Wu, William K K

Journal of cellular and molecular medicine

2018 Volume 22, Issue 4, Page(s) 2469–2477

Abstract: Toxin B (TcdB) is a major pathogenic factor of Clostridum difficile. However, the mechanism by which TcdB exerts its cytotoxic action in host cells is still not completely known. Herein, we report for the first time that TcdB induced autophagic cell ... ...

Abstract	Toxin B (TcdB) is a major pathogenic factor of Clostridum difficile. However, the mechanism by which TcdB exerts its cytotoxic action in host cells is still not completely known. Herein, we report for the first time that TcdB induced autophagic cell death in cultured human colonocytes. The induction of autophagy was demonstrated by the increased levels of LC3-II, formation of LC3
MeSH term(s)	Apoptosis/drug effects ; Autophagosomes/drug effects ; Autophagosomes/metabolism ; Autophagosomes/microbiology ; Autophagy/genetics ; Autophagy-Related Protein 5 ; Autophagy-Related Protein 7 ; Bacterial Proteins/genetics ; Bacterial Proteins/metabolism ; Bacterial Toxins/genetics ; Bacterial Toxins/metabolism ; Beclin-1/genetics ; Clostridioides difficile/genetics ; Clostridioides difficile/pathogenicity ; Clostridium Infections/genetics ; Clostridium Infections/microbiology ; Clostridium Infections/therapy ; Colon/cytology ; Colon/microbiology ; Humans ; Phosphatidylinositol 3-Kinases/genetics ; Phosphorylation ; Sequestosome-1 Protein/genetics ; TOR Serine-Threonine Kinases/genetics
Chemical Substances	Autophagy-Related Protein 5 ; Bacterial Proteins ; Bacterial Toxins ; Beclin-1 ; SQSTM1 protein, human ; Sequestosome-1 Protein ; toxB protein, Clostridium difficile ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Autophagy-Related Protein 7 (EC 6.2.1.45)
Language	English
Publishing date	2018-01-31
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2074559-X
ISSN	1582-4934 ; 1582-4934 ; 1582-1838
ISSN (online)	1582-4934
ISSN	1582-4934 ; 1582-1838
DOI	10.1111/jcmm.13555
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Article ; Online: Gavage of Fecal Samples From Patients With Colorectal Cancer Promotes Intestinal Carcinogenesis in Germ-Free and Conventional Mice.

Wong, Sunny H / Zhao, Liuyang / Zhang, Xiang / Nakatsu, Geicho / Han, Juqiang / Xu, Weiqi / Xiao, Xue / Kwong, Thomas N Y / Tsoi, Ho / Wu, William K K / Benhua, Zeng / Chan, Francis K L / Sung, Joseph J Y / Wei, Hong / Yu, Jun

Gastroenterology

2017

Abstract: Background & aims: Altered gut microbiota is implicated in development of colorectal cancer (CRC). Some intestinal bacteria have been reported to potentiate intestinal carcinogenesis by producing genotoxins, altering the immune response and intestinal ... ...

Abstract	Background & aims: Altered gut microbiota is implicated in development of colorectal cancer (CRC). Some intestinal bacteria have been reported to potentiate intestinal carcinogenesis by producing genotoxins, altering the immune response and intestinal microenvironment, and activating oncogenic signaling pathways. We investigated whether stool from patients with CRC could directly induce colorectal carcinogenesis in mice. Methods: We obtained stored stool samples from participants in a metagenome study performed in Hong Kong. Conventional (male C57BL/6) mice were given azoxymethane to induce colon neoplasia after receiving a course of antibiotics in drinking water. Mice were gavaged twice weekly with stool from 5 patients with CRC or 5 healthy individuals (controls) for 5 weeks. Germ-free C57BL/6 mice were gavaged once with stool from 5 patients with CRC or 5 controls. We collected intestinal tissues from mice and performed histology, immunohistochemistry, expression microarray, quantitative polymerase chain reaction, immunoblot, and flow cytometry analyses. We performed 16S ribosomal RNA gene sequencing analysis of feces from mice. Results: Significantly higher proportions of conventional mice fed with stool from individuals with CRC than control stool developed high-grade dysplasia (P < .05) and macroscopic polyps (P < .01). We observed a higher proportion of proliferating (Ki-67-positive) cells in colons of germ-free mice fed with stool from patients with CRC vs those fed with stool from controls (P < .05). Feces from germ-free and conventional mice fed with stool from patients with CRC vs controls contained different microbial compositions, with lower richness in mice fed with stool from patients with CRC. Intestines collected from conventional and germ-free mice fed with stool from patients with CRC had increased expression of cytokines that modulate inflammation, including C-X-C motif chemokine receptor 1, C-X-C motif chemokine receptor 2, interleukin 17A (IL17A), IL22, and IL23A. Intestines from conventional and germ-free mice fed with stool from patients with CRC contained higher proportions of T-helper 1 (Th1) cells (2.25% vs 0.44%) and Th17 cells (2.08% vs 0.31%) (P < .05 for each) than mice fed with stool from controls. Real-time polymerase chain reaction arrays revealed up-regulation of genes involved in cell proliferation, stemness, apoptosis, angiogenesis, invasiveness, and metastasis in mice fed with stool from patients with CRC. Conclusions: We fed stool samples from patients with CRC and heathy individuals to germ-free mice and conventional mice with azoxymethane. We found stool from patients with CRC to increase the numbers of polyps, levels of intestinal dysplasia and proliferation, markers of inflammation, and proportions of Th1 and Th17 cells in colon, compared with stool from individuals without CRC. This study provides evidence that the fecal microbiota from patients with CRC can promote tumorigenesis in germ-free mice and mice given a carcinogen.
Language	English
Publishing date	2017-08-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	80112-4
ISSN	1528-0012 ; 0016-5085
ISSN (online)	1528-0012
ISSN	0016-5085
DOI	10.1053/j.gastro.2017.08.022
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