However, by modulating the immune status throughout the body [8], an inflammogenic gut microbial community in atopic subjects could significantly contribute to the severity of the disease. In this perspective we performed a pilot case–control study of the atopy-associated dysbiosis of the intestinal microbiota in atopic children. Since from birth to weaning the infant intestinal microbiota is an extremely CSF-1R inhibitor dynamic entity, which continuously fluctuates

in response to factors of environmental and endogenous origin [22], we enrolled children aged > 2 years, characterized by a relatively stable adult-like intestinal microbial community [23]. In particular, the faecal microbiota of 19 atopic children and 12 healthy controls aged 4–14 years was characterized by means of the previously developed phylogenetic microarray platform High Taxonomic Fingerprint (HTF)-Microbi.Array [24] and quantitative PCR (qPCR). Integrated click here of an additional probe pair for Akkermansia muciniphila, the HTF-Microbi.Array platform detects up to 31 intestinal bacterial groups and covers up to 95% of the human intestinal microbiota [25]. For our study faeces were selected since they represent the only realistic and reliable sample for a non-invasive study of the human intestinal microbiota. Methods Subjects enrolled and

study groups We enrolled 19 children (referred as atopics throughout the paper) Cell Penetrating Peptide with clinical diagnosis of allergy (rhinitis, asthma, grass pollen sensitization, allergic atopic dermatitis, oral allergy syndrome, cow’s milk allergy) and encountering all the following criteria: (i) delivered naturally at term, (ii) breast fed for at least 3 months, (iii) aged

between 4 and 14 years, (iv) no acute diseases for at least 2 weeks, (v) no Tipifarnib datasheet antibiotic treatment in the last 3 months. In particular, 17 children presented allergic rhinitis, in 4 cases associated with asthma. Atopic dermatitis was observed in 8 cases of which 6 associated with rhinitis and inhalant sensitization and 1 with food allergy (Table 1). During the visit the children underwent a clinical evaluation and skin prick test for main food or inhalant allergens. Total and specific IgE determination was performed when clinically necessary. Fresh stool samples were collected within 3 days. As controls, 12 non-allergic children who encountered the same criteria above described but without family history of atopy were enrolled. All the children were routinely followed by the Paediatric Oncology and Haematology Unit Lalla Seràgnoli, Sant’Orsola-Malpighi Hospital, University of Bologna. Parents provided a written informed consent. Approval by the Ethics Committee of the Sant’Orsola-Malpighi Hospital was not needed for this study.