Editorial: the influence of genetic factors in mediating the effects of tobacco smoke in <scp>IBD</scp>

Adams, Alexander T.; Kalla, Rahul; Satsangi, Jack

doi:10.1111/apt.14434

Cited by 4 publications

(4 citation statements)

References 8 publications

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“…With regard to intestinal bowel diseases, we can state that smoking plays a key dual role in their development, as smoking appears to play a protective role in ulcerative colitis (CU), while it is a risk factor for Crohn’s disease (CD), though the mechanisms underlying this relationship appear to be intricate [ 77 , 78 ]. The lack of solid results relies on the fact that IBDs are extremely complex diseases with a multifactorial pathogenesis, so that it is extremely difficult to put confounding factors on the back burner.…”

Section: Discussionmentioning

confidence: 99%

The Impact of Smoking on Microbiota: A Narrative Review

et al. 2023

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Cigarette smoke is a classic risk factor for many diseases. The microbiota has been recently indicated as a new, major player in human health. Its deregulation—dysbiosis—is considered a new risk factor for several illnesses. Some studies highlight a cross-interaction between these two risk factors—smoke and dysbiosis—that may explain the pathogenesis of some diseases. We searched the keywords “smoking OR smoke AND microbiota” in the title of articles on PubMed®, UptoDate®, and Cochrane®. We included articles published in English over the last 25 years. We collected approximately 70 articles, grouped into four topics: oral cavity, airways, gut, and other organs. Smoke may impair microbiota homeostasis through the same harmful mechanisms exerted on the host cells. Surprisingly, dysbiosis and its consequences affect not only those organs that are in direct contact with the smoke, such as the oral cavity or the airways, but also involve distant organs, such as the gut, heart, vessels, and genitourinary tract. These observations yield a deeper insight into the mechanisms implicated in the pathogenesis of smoke-related diseases, suggesting a role of dysbiosis. We speculate that modulation of the microbiota may help prevent and treat some of these illnesses.

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Section: Discussionmentioning

confidence: 99%

The Impact of Smoking on Microbiota: A Narrative Review

et al. 2023

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“…93 The strongest genetic defects were associated with smoking quantity and nicotine dependence and genome-wide association studies have discovered high-risk single nucleotide polymorphisms close to nicotinic acetylcholine receptor subunits. 205,206 The number of inflammatory bowel disease-associated genes that have been studied and found to be affected by smoking is presented in Table 2. It seems that there is no defined group of genes or cellular pathway, nor process correlating with smoking status.…”

Section: Genetic Polymorphismsmentioning

confidence: 99%

“…Crohn's disease smokers who were of the ATG16L1 T300A genotype, showed significantly shorter time to recurrence after surgery 93 . The strongest genetic defects were associated with smoking quantity and nicotine dependence and genome‐wide association studies have discovered high‐risk single nucleotide polymorphisms close to nicotinic acetylcholine receptor subunits 205,206 . The number of inflammatory bowel disease‐associated genes that have been studied and found to be affected by smoking is presented in Table 2.…”

Section: Introductionmentioning

confidence: 99%

Review article: impact of cigarette smoking on intestinal inflammation—direct and indirect mechanisms

Παπουτσοπουλου

Satsangi

Campbell

et al. 2020

Aliment Pharmacol Ther

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“…We would like to thank Dr. Satsangi and coauthors for their insightful comments and kind reflection on our work in the context of several related findings …”

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confidence: 98%

Editorial: the influence of genetic factors in mediating the effects of tobacco smoke in IBD—Authors’ reply

Lang

Beerenwinkel

Misselwitz

2017

Aliment Pharmacol Ther

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Environmental exposures may influence other established genetic risk loci for IBD and identifying the epigenetic modifications and characterising the pathways involved represent important goals for future research. Some smoking associated variants may act through behavioural alterations such as differences in reward pathways and impulsivity, and future work could look for interactions between these SNPs and IBD mediated by factors such as diet and treatment compliance.The drive for personalised care is central to much current research, and investigations into IBD and smoking are producing promising results such as demonstrating a varying treatment response between smokers and nonsmokers. 8 and clinical phenotype will be equally important. ACKNOWLEDGEMENTSDeclaration of personal interests: None. FUN DING INF ORMATIONJS has served as a speaker for Falk, Ferring UK, and Takeda, and has received research funding from AbbVie. O R C I DA. Adams http://orcid.org/0000-0001-9364-8540 Our goal has been to shed light on potential variant-environment modulations that could be used to identify patient sub-populations with differential risk for severe disease. Our study focused on smoking, and smoking prevalence unfortunately remains high in IBD patients. 7 However, further such relationships will likely exist but may be less obvious to detect. The proposal in the editorial by Adams, Kalla, and Satsangi of diet and treatment compliance are welcome suggestions, though much harder to assess in patients. The hard work, however, will begin when it comes to the validation of these associations and the subsequent application of these findings to patients. 8 ACKNOWLEDGEMENTSThe authors' declarations of personal and financial interests are unchanged from those in the original article. Editorial: hepatocellular carcinoma risk in the era of direct-acting anti-virals-is the case closed?Reig et al first reported a high HCC recurrence rate of 28% among a retrospective cohort of 58 direct-acting-antiviral (DAA)-treated HCCcured patients, 1 with a similar finding from Italy. 2 Does DAA therapy increase HCC recurrence in those "cured" of HCC is the key question rather than development of de novo HCC after HCV SVR. The approach to this question is 3-fold.The first is to standardise the reporting method (use of hazard ratios and Kaplan-Meier graphs). Camma et al re-analysed the Reig data and found that the recurrence rate was actually 13% at 1 year. 3When imaging studies show no evidence of HCC, subclinical HCC cannot be discounted, and in the Reig paper, 7/16 of those with HCC recurrence had abnormal AFP levels at the time of starting

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Editorial: the influence of genetic factors in mediating the effects of tobacco smoke in IBD

Abstract: Linked Content This article is linked to Lang et al papers. To view these articles visit https://doi.org/10.1111/apt.14378 and https://doi.org/10.1111/apt.14447.

Cited by 4 publications

References 8 publications

The Impact of Smoking on Microbiota: A Narrative Review

The Impact of Smoking on Microbiota: A Narrative Review

Review article: impact of cigarette smoking on intestinal inflammation—direct and indirect mechanisms

Editorial: the influence of genetic factors in mediating the effects of tobacco smoke in IBD—Authors’ reply

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