Opposing Effects of Smoking in Ulcerative Colitis and Crohnʼs Disease May Be Explained by Differential Effects on Dendritic Cells

Ueno, Aito; Jijon, Humberto; Traves, Suzanne L.; Chan, Ronald; Ford, Kim; Beck, Paul L.; Iacucci, Marietta; Gasia, Miriam Fort; Barkema, Herman W.; Panaccione, Remo; Kaplan, Gilaad G.; Proud, David; Ghosh, Subrata

doi:10.1097/mib.0000000000000018

Cited by 33 publications

(29 citation statements)

References 26 publications

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“…chemical- vs. pathogen-induced colitis) to trigger intestinal damage, as smoking by itself does not result in spontaneous enterocolitis in most animal models (70). Nonetheless, in vitro application of cigarette extract on patient-derived dendritic cells showed that it increased the prevalence of Foxp3+ CD4 T cells in UC whereas it skewed toward Th1 subset in CD (71), suggesting a possible differential effect in immune cells in CD vs. UC. One possible scenario is that to trigger/aggravate IBD requires combinations of specific sets of genes and smoking exposure, thereby explaining the seemingly different effects in patients from different ethnic groups.…”

Section: Identifying Environmental Factorsmentioning

confidence: 99%

Genetics and Pathogenesis of Inflammatory Bowel Disease

Liu

Stappenbeck

2016

Annu. Rev. Pathol. Mech. Dis.

231

156

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We are currently in an exciting time where our understanding of genetic underpinnings of inflammatory bowel disease (IBD) has undergone a revolution, based in large part by novel genotyping and sequencing technologies. With >160 susceptible loci identified for IBD, the goals now are to understand at a fundamental level, the function of these susceptibility alleles. Clinical relevance of how these susceptible genes shape the development of IBD is also a high priority. The main challenge is to understand how the environment and microbiome play a role in triggering disease in genetically susceptible individual, as the interactions may be complex. To advance the field, novel in vitro and mouse models that are designed to interrogate complex genetics and be able to functionally test hypotheses are needed. Ultimately, the goal of genetics studies will be to translate genetics to the patients with IBD and improve their care.

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Section: Identifying Environmental Factorsmentioning

confidence: 99%

Genetics and Pathogenesis of Inflammatory Bowel Disease

Liu

Stappenbeck

2016

Annu. Rev. Pathol. Mech. Dis.

231

156

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“…To date, the exact mechanisms which underlie the differential effects of CS on CD and UC remain a matter of debate. For example, it has been suggested that differential DC responses to CS between CD and UC may play a role [139]. Another study suggests that CS induces barrier dysfunction in the ileum, but not in the colon [140].…”

Section: Impact Of Cs On Trp Channels In the Gut?mentioning

confidence: 99%

Transient Receptor Potential Channels in Intestinal Inflammation: What Is the Impact of Cigarette Smoking?

Allais

Smet²,

Verschuere³

et al. 2016

Pathobiology

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Inflammatory bowel disease (IBD) is characterized by severe gastrointestinal inflammation and results from a complex interplay between genetic and environmental factors. IBD includes two prominent subtypes: Crohn's disease (CD) and ulcerative colitis (UC). One of the main risk factors for the development of CD is cigarette smoking, while UC is rather a disease of ex-smokers. To date, many of the mechanisms underlying the immune imbalance in IBD and the involvement of cigarette smoke (CS) are incompletely understood. Transient receptor potential (TRP) proteins are non-selective cation channels that, upon activation, lead to plasma membrane depolarization and, in general, to Ca²⁺ influx. TRP channels of the ankyrin and vanilloid family, expressed by sensory neurons in the central and enteric nervous systems, have been extensively studied in the context of intestinal inflammation. Moreover, recent advances made on the role of non-neuronal expressed TRP channels shed light on the involvement of epithelial cells in inflammatory processes. This review focuses on how CS may impact TRP channel function in intestinal inflammation. Firstly, we discuss the current knowledge on neuronal TRP channels, known to be linked to IBD, in health, immune homeostasis and intestinal inflammation. Subsequently, we address how TRP channels are activated by CS and its components in other organ systems and also hypothesize on the potential implications for CS-mediated TRP channel activation in gut inflammation.

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“…Similarly, the same investigators demonstrated that smokers with CD had significantly lower IL-10 (anti-inflammatory)/IL-12 (pro-inflammatory) ratios than non-smokers or smokers with UC. As suggested in some reports, the differential signalling of dendritic cells from CD (Th1-like) and UC patients exposed to cigarette smoke extract (CSE) in vitro could play a role in the opposing responses of cigarette smoke exposure, that is, a Th1-like response in CD, with increased Foxp3-positive CD4 T cells [121].…”

Section: Immune Regulationmentioning

confidence: 99%

Animal Inhalation Models to Investigate Modulation of Inflammatory Bowel Diseases

Sasso¹,

Schlage²,

Phillips³

et al. 2018

Experimental Animal Models of Human Diseases - An Effective Therapeutic Strategy

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Inflammatory bowel diseases (IBDs) comprise primarily two disease manifestations, ulcerative colitis (UC) and Crohn's disease (CD), each with distinctive clinical and pathological features. Environmental and clinical factors strongly affect the development and clinical outcomes of IBDs. Among environmental factors, cigarette smoke (CS) is considered the most important risk factor for CD, while it attenuates the disease course of UC. Various animal models have been used to assess the impact of CS on intestinal pathophysiology. This chapter examines the suitability of animal inhalation/smoke exposure models for assessing the contrary effects of CS on UC and CD. It presents an updated literature review of IBD mouse models and a description of possible mechanisms relevant to relationships between IBD and smoking. In addition, it summarises various technical inhalation approaches, in the context of mouse disease models of IBD.

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Opposing Effects of Smoking in Ulcerative Colitis and Crohnʼs Disease May Be Explained by Differential Effects on Dendritic Cells

Cited by 33 publications

References 26 publications

Genetics and Pathogenesis of Inflammatory Bowel Disease

Genetics and Pathogenesis of Inflammatory Bowel Disease

Transient Receptor Potential Channels in Intestinal Inflammation: What Is the Impact of Cigarette Smoking?

Animal Inhalation Models to Investigate Modulation of Inflammatory Bowel Diseases

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