Annika Fahlén

Swedish Institute for Communicable Disease Control, Tukholma, Stockholm, Sweden

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Publications (4)11.82 Total impact

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    ABSTRACT: There is a known association between psoriasis and Crohn's disease (CD). Patients with CD are five times more likely to develop psoriasis, and, conversely, patients with psoriasis are more likely to develop CD. Many gastroenterologists now accept that CD is due to a breakdown of immune tolerance to the microbiota of the intestine in genetically susceptible individuals. The microbiota of the skin has recently been investigated in psoriasis. Firmicutes was the commonest phylum, and Streptococcus the commonest genus identified. Beta-haemolytic streptococci have been implicated in both guttate and chronic plaque psoriasis. Furthermore, the innate immune system has been shown to be activated in psoriasis, and many of the genes associated with the disease are concerned with signalling pathways of the innate immune system, notably IL-23 and NFκB. Psoriasis patients also have an increased incidence of periodontitis a disease thought to be due to an abnormal response to normal oral commensals. Based on the similarities between CD and psoriasis, we propose that psoriasis is due to a breakdown of immune tolerance to the microbiota of the skin. In support of this hypothesis we provide evidence for microbiota in the skin, activation of the innate immune system, and genetic abnormalities involving the innate immune system.
    British Journal of Dermatology 03/2013; · 3.76 Impact Factor
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    ABSTRACT: AIM: Necrotizing enterocolitis (NEC) represents one of the gravest complications in premature infants. The suggested role of intestinal microbiota in the development of NEC needs to be elucidated. METHODS: This prospective single centre case-control study applied barcoded pyrosequencing to map the bacterial composition of faecal samples from extremely preterm infants. Ten patients were diagnosed with NEC and matched to healthy controls with regard to sex, gestational age and mode of delivery prior to analysis of the samples. RESULTS: Enterococcus, Bacillales and Enterobacteriaceae dominated the flora. Although not statistically significant, a high relative abundance of Bacillales and Enterobacteriaceae was detected at early time points in patients developing NEC while healthy controls had a microbiota more dominated by Enterococcus. A low diversity of intestinal microbial flora was found without any differences between NEC patients and controls. In 16 healthy controls Firmicutes (Enterococcus and Bacillales) dominated the faecal flora during the first weeks after birth and were then succeeded by Enterobacteriaceae. CONCLUSION: No significant differences in the composition of intestinal microbiota of patients developing NEC were detected; however, some findings need to be scrutinized in subsequent studies. © 2012 The Author(s)/Acta Paediatrica © 2012 Foundation Acta Paediatrica.
    Acta Paediatrica 10/2012; · 1.97 Impact Factor
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    ABSTRACT: Microorganisms have been implicated in the pathogenesis of psoriasis. Previous studies of psoriasis and normal skin have used swabs from the surface rather than skin biopsies. In this study, biopsies were taken from 10 patients with psoriasis and 12 control subjects from unmatched sites. Samples were analysed with massive parallel pyrosequencing on the 454 platform targeting the 16S rRNA gene and the variable regions V3-V4. The samples grouped into 19 phyla, 265 taxon and 652 operational units (OTUs) at 97% identity. A cut-off abundance level was set at 1%. The three most common phyla in both normal and psoriasis skin were Firmicutes (39% psoriasis, 43% normal skin), Proteobacteria (38% psoriasis, 27% normal skin) and Actinobacteria (5% psoriasis, 16% normal skin, p = 0.034). In trunk skin, Proteobacteria were present at significantly higher levels in psoriasis compared to controls (52 vs. 32%, p = 0.0113). The commonest genera were Streptococci in both psoriasis (32%) and normal skin (26%). Staphylococci were less common in psoriasis (5%) than in controls (16%), as were Propionibacteria (psoriasis 0.0001669%, controls 0.0254%). Both Staphylococci and Propionibacteria were significantly lower in psoriasis versus control limb skin (p = 0.051, 0.046, respectively). This study has shown some differences in microbiota between psoriasis and normal skin. Whether these are of primary aetiological significance, or secondary to the altered skin of psoriasis remains to be determined.
    Archives for Dermatological Research 11/2011; 304(1):15-22. · 2.71 Impact Factor
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    ABSTRACT: Patients with severe congenital neutropenia (SCN) often develop periodontitis despite standard medical and dental care. In light of previous findings that mutations in the neutrophil elastase gene, ELANE, are associated with more severe neutropenic phenotypes, we hypothesized an association between the genotype of SCN and development of periodontitis. Fourteen Swedish patients with SCN or cyclic neutropenia harboring different genetic backgrounds were recruited for periodontal examination. Peripheral blood, gingival crevicular fluid (GCF), and subgingival bacterial samples were collected. The levels of cytokines and antibacterial peptides were determined in GCF and plasma by multiplex immunoassay and immunoblotting, respectively. Subgingival bacterial samples were analyzed using 16S rDNA pyrosequencing. ELANE mutations correlated with more severe periodontal status than the HAX1 or unknown mutations in patients with SCN. The subjects with mutant ELANE had higher levels of IL-1β in GCF. Using principal coordinate analysis of the subgingival microbiota, patients with ELANE mutations and reference subjects with periodontitis tended to cluster differently from patients with HAX1 or unknown mutations and non-periodontitis reference subjects. This study demonstrates an association between ELANE mutations in SCN and the development of periodontitis with skewed subgingival microbiota, indicating a potential role of ELANE mutations in the pathogenesis of periodontitis.
    Journal of Clinical Immunology 07/2011; 31(6):936-45. · 3.38 Impact Factor