Is Psoriasis Treatment a Risk Factor for Inflammatory Bowel Disease?

Nehring, Piotr; Przybyłkowski, Adam

doi:10.1007/s40290-020-00340-1

Cited by 10 publications

(6 citation statements)

References 52 publications

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“…Psoriasis is a complex immune-mediated skin disease, which can also manifest as joint inflammation [ 58 ]. Psoriatic patients have a higher risk of comorbidities such as cardiovascular disease, inflammatory bowel disease, and nonalcoholic fatty liver disease [ 59 – 61 ]. There is a close link between this multifaceted disease and inflammasome activation; for example, an unbiased sequencing approach revealed inflammasome signaling as the highest differentially expressed pathway in psoriasis patients, whereby inflammasome activation was correlated with disease severity [ 62 ].…”

Section: Resultsmentioning

confidence: 99%

Causal Biological Network Model for Inflammasome Signaling Applied for Interpreting Transcriptomic Changes in Various Inflammatory States

Yepiskoposyan

Peitsch

Talikka

2022

International Journal of Inflammation

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Virtually any stressor that alters the cellular homeostatic state may result in an inflammatory response. As a critical component of innate immunity, inflammasomes play a prominent role in the inflammatory response. The information on inflammasome biology is rapidly growing, thus creating the need for structuring it into a model that can help visualize and enhance the understanding of underlying biological processes. Causal biological network (CBN) models provide predictive power for novel disease mechanisms and treatment outcomes. We assembled the available literature information on inflammasome activation into the CBN model and scored it with publicly available transcriptomic datasets that address viral infection of the lungs, osteo- and rheumatoid arthritis, psoriasis, and aging. The scoring inferred pathway activation leading to NLRP3 inflammasome activation in these diverse conditions, demonstrating that the CBN model provides a platform for interpreting transcriptomic data in the context of inflammasome activation.

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Section: Resultsmentioning

confidence: 99%

Causal Biological Network Model for Inflammasome Signaling Applied for Interpreting Transcriptomic Changes in Various Inflammatory States

Yepiskoposyan

Peitsch

Talikka

2022

International Journal of Inflammation

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“…In addition, Genome Wide Association Studies (GWAS) uncovered that IBD and psoriasis share 4 susceptibility loci, which contain several shared genes involved in innate and adaptive immunity ( Skroza et al., 2013 ). The link between the two diseases has been further strengthened by the finding that they can appear to each other as paradoxical treatment-related adverse events ( Lolli et al., 2015 ; Vlachos et al., 2016 ; Nehring and Przybyłkowski, 2020 ). As mentioned earlier, IBD patients develop multiple types of skin manifestations and patients receiving anti-TNF therapy often suffer from skin adverse events.…”

Section: Discussionmentioning

confidence: 99%

Skin microbiota signature distinguishes IBD patients and reflects skin adverse events during anti-TNF therapy

Reiss

Rob²,

Kolář³

et al. 2023

Front. Cell. Infect. Microbiol.

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Crohn’s disease (CD) and ulcerative colitis (UC) are two forms of inflammatory bowel disease (IBD), where the role of gut but not skin dysbiosis is well recognized. Inhibitors of TNF have been successful in IBD treatment, but up to a quarter of patients suffer from unpredictable skin adverse events (SkAE). For this purpose, we analyzed temporal dynamics of skin microbiota and serum markers of inflammation and epithelial barrier integrity during anti-TNF therapy and SkAE manifestation in IBD patients. We observed that the skin microbiota signature of IBD patients differs markedly from healthy subjects. In particular, the skin microbiota of CD patients differs significantly from that of UC patients and healthy subjects, mainly in the retroauricular crease. In addition, we showed that anti-TNF-related SkAE are associated with specific shifts in skin microbiota profile and with a decrease in serum levels of L-FABP and I-FABP in IBD patients. For the first time, we showed that shifts in microbial composition in IBD patients are not limited to the gut and that skin microbiota and serum markers of the epithelium barrier may be suitable markers of SkAE during anti-TNF therapy.

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“…Some of these biologic agents, such as secukinumab and brodalimumab, were included to treat moderate-to-severe CD, with no significant effectiveness compared to controls [34]. However, some studies evidenced that some biologics (e.g., anti-IL17 and the anti-TNF molecules) used for the treatment of psoriasis increased the risk of IBD [35][36][37][38][39], whereas the use of other biological drugs for psoriasis, such as the anti-IL23/IL39 antibodies (guselkumab, tildrakizumab, risankizumab) and anti-IL12/IL-23 inhibitor (ustekinumab), were not associated with the development of IBD [40].…”

Section: Introductionmentioning

confidence: 99%

The Gut Microbiome in Psoriasis and Crohn’s Disease: Is Its Perturbation a Common Denominator for Their Pathogenesis?

Francesco

Caruso

2022

Vaccines

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Psoriasis and inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn’s disease (CD), are interlinked. In fact, the prevalence of IBD is higher in patients with psoriasis, with a risk of ulcerative colitis of 1.6-times higher than in the general population. Analogously, patients with psoriasis have a greater risk of developing IBD. Furthermore, they share some clinical features and pathogenic mechanisms. Both are chronic inflammatory diseases with a relapsing-remitting condition that persists for the patient’s whole life and exhibit increased permeability of the mucosal barrier of skin and gut, allowing an increased interaction of pathogens with inflammatory receptors of the immune cells. A key element in the pathogenesis of these diseases is represented by the microbiota; in particular, the gut microbiota is an important driver of CD pathogenesis, while in psoriasis changes in gut and skin microbiota have been described without a defined pathogenic function. Furthermore, genetic predispositions or environmental factors contribute to disease manifestation, with a central role attributed to the immune responses and, in particular, to a dysregulated role played by T helper 17 cells both in psoriasis and IBD. The purpose of this review was to summarize present information about the links between psoriasis, inflammatory bowel disease, in particular Crohn’s disease, and changes in gut and/or skin microbiome.

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Is Psoriasis Treatment a Risk Factor for Inflammatory Bowel Disease?

Cited by 10 publications

References 52 publications

Causal Biological Network Model for Inflammasome Signaling Applied for Interpreting Transcriptomic Changes in Various Inflammatory States

Causal Biological Network Model for Inflammasome Signaling Applied for Interpreting Transcriptomic Changes in Various Inflammatory States

Skin microbiota signature distinguishes IBD patients and reflects skin adverse events during anti-TNF therapy

The Gut Microbiome in Psoriasis and Crohn’s Disease: Is Its Perturbation a Common Denominator for Their Pathogenesis?

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