Abstract

Alterations of intestinal microbiota play a significant role in the pathogenesis of psoriasis. Dysbiosis may cause disruption of the intestinal barrier, which contributes to immune activation by translocation of microbial antigens and metabolites. Intestinal fatty acid binding protein (I-FABP) serves as a biomarker of enterocyte damage. The aim of this study was to investigate clinical and metabolic factors affecting plasma concentration of I-FABP in patients with psoriasis. Eighty patients with psoriasis and 40 control subjects were enrolled in the study. Serum I-FABP (243.00 (108.88–787.10) vs. 114.38 (51.60–241.60) pg/ml, p < 0.001) and neutrophil to lymphocyte ratio (NLR; 2.59 (1.96–3.09) vs. 1.72 (1.36–47 2.11), p < 0.01) were significantly increased in patients with psoriasis compared to controls. A significant positive correlation was found between I-FABP and body mass index (BMI) (r = 0.82, p < 0.001), Psoriasis Area Severity Index (PASI) (r = 0.78, p < 0.001) and neutrophil to lymphocyte ratio (NLR) (r = 0.24, p < 0.001). Rising quartiles of I-FABP were associated with increasing values of BMI, PASI and NLR. The results of the logistic regression model confirmed an increased risk of higher disease severity with I-FABP concentration – odds ratio 3.34 per 100 pg/mL I-FABP increase. In conclusion, intestinal integrity in patients with psoriasis is affected by obesity, severity of the disease and systemic inflammation. The modulation of gut barrier may represent a new therapeutic approach for psoriasis.

Highlights

  • The gut microbiota refers to the complex community of microorganisms, covering more than 1000 different species of bacteria, viruses, fungi, and protozoa [1]

  • While there is a large number of potential biomarkers of gut permeability, we decided to measure the concentration of Intestinal fatty acid binding protein (I-FABP)

  • Blood concentration of I-FABP is very low in healthy individuals reflecting the physiological turnover rate of enterocytes, whereas it rapidly increases after intestinal epithelial damage [13]

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Summary

Introduction

The gut microbiota refers to the complex community of microorganisms, covering more than 1000 different species of bacteria, viruses, fungi, and protozoa [1]. Microbiota colonizing the human gastrointestinal tract is estimated at 100 trillion microorganisms with around 1:1 microbial to human cells ratio [2]. Alterations in the composition and function of the microbiota, has been implicated in the development and progression of various skin diseases such as psoriasis [3], atopic dermatitis [4], rosacea [5] and systemic sclerosis [6]. The exact mechanism of this crosstalk remains unclear. It may be attributed, at least partially, to increased gut barrier permeability [8]

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