Investigation of the relationship between chronic spontaneous urticaria and gut microbiome DNA

Introduction and Aim: Intestinal microbiome (all of the genetic material of microorganisms) is a large collection of bacteria, viruses, fungi and protozoa in our gastrointestinal (GIS) tract. The beneficial bacteria of intestinal microbiota have many important tasks such as the production of certain vitamins and amino acids, the development and maintenance of the immune system. Dysbiosis can occur if the gut microbiota changes or is damaged for any reason. Various factors such as diet, drugs (antibiotics, proton pump inhibitors, etc.), alcohol and smoking can affect gut microbiota negatively and cause dysbiosis. According to studies, gut dysbiosis is associated with many diseases such as diabetes, hypertension, obesity, autism, inflammatory bowel diseases and depression. Microbiome analyzes were also used to reveal the pathogenesis of some dermatological diseases such as acne vulgaris, psoriasis and atopic dermatitis. In addition to the skin microbiome, gut microbiome has a role in the pathogenesis of dermatological diseases. Chronic urticaria is a dermatologic disease with erythematous, edematous, itchy plaque, sometimes accompanied by angioedema, lasting more than six weeks. It affects almost 1% of the population and approximately 2/3 of these patients form chronic spontaneous urticaria (CSU). Etiologic factors such as drugs, foods, infections, systemic diseases may lead to CSU, or it may also be idiopathic. CSU affects the quality of life seriously in terms of causing sleep disorder and loss of labor. In this study, we aimed to determine the possible relationship between CSU and gut microbiome, regarding the pathogenesis of CSU and to help new diagnosis and treatment approaches. Material and Method: 20 patients with CSU and 10 age and sex matched healthy individuals were included in the present study. Both groups had not used a drug (antibiotics, proton pump inhibitors, etc.) or a probiotic/prebiotic that could affect gut microbiota for at least 4 weeks. After nucleic acid isolation from faecal samples, bacterial 16S ribosomal RNA (rRNA) gene target sequencing was performed with the Illumina MiSeq system using universal bacterial 16S primers (V3-V4). Statistical analyzes (LefSe, alpha and beta diversity) were performed after bioinformatics. The default settings (p <0.05 and LDA score> 2) identified taxa that differed significantly between the groups. Results: The rate of Firmucites/Bacteroidetes in CSU patients was found to be lower than in the healthy control group (0.95 in CSU patients, 1.69 in healthy volunteers). Patients with CSU; Bacteroidetes phylum and Lachnospiraceae, Ruminococcaceae, Clostridiaceae family and Intestinibacter, Megasphaera, Sutterella genus member bacteria were significantly increased (p <0.05 and LDA score> 2). In healthy volunteers, Bifidobacteriaceae, Lachnospiraceae, Ruminococcaceae, Veillonellaceae, Prevotellaceae, Coriobacteriacea family and Clostridiales order and Succinivibrio genus bacteria were found to be statistically significantly higher (p <0.05 and LDA score> 2). There was no significant difference at the alpha diversity between the two groups. Beta diversity analysis showed a difference between the two groups (PC1 maximum variation rate; Bray-Curtis Plot; 22.23%, Bray Curtis Plot (Genus Level); 35.79%). Conclusion: According to the results of series analysis; Bacteroidetes in patients with CSU and Actinobacteria phylum in healthy volunteers were significantly higher and Firmucites/Bacteroidetes ratio was lower in CSU patients. As a result, there is a relationship between CSU disease and gut dysbiosis. Dysbiosis can be considered as an important factor in the pathogenesis of CSU and prebiotic or probiotics may be included in the treatment. In the English literature, only one study is published examining the association of CSU and gut microbiota.