Acinetobacter species in the skin microbiota protect against allergic sensitization and inflammation - 05/12/14
Abstract |
Background |
The human commensal microbiota interacts in a complex manner with the immune system, and the outcome of these interactions might depend on the immune status of the subject.
Objective |
Previous studies have suggested a strong allergy-protective effect for Gammaproteobacteria. Here we analyze the skin microbiota, allergic sensitization (atopy), and immune function in a cohort of adolescents, as well as the influence of Acinetobacter species on immune responses in vitro and in vivo.
Methods |
The skin microbiota of the study subjects was identified by using 16S rRNA sequencing. PBMCs were analyzed for baseline and allergen-stimulated mRNA expression. In in vitro assays human monocyte-derived dendritic cells and primary keratinocytes were incubated with Acinetobacter lwoffii. Finally, in in vivo experiments mice were injected intradermally with A lwoffii during the sensitization phase of the asthma protocol, followed by readout of inflammatory parameters.
Results |
In healthy subjects, but not in atopic ones, the relative abundance of Acinetobacter species was associated with the expression of anti-inflammatory molecules by PBMCs. Moreover, healthy subjects exhibited a robust balance between anti-inflammatory and TH1/TH2 gene expression, which was related to the composition of the skin microbiota. In cell assays and in a mouse model, Acinetobacter species induced strong TH1 and anti-inflammatory responses by immune cells and skin cells and protected against allergic sensitization and lung inflammation through the skin.
Conclusion |
These results support the hypothesis that skin commensals play an important role in tuning the balance of TH1, TH2, and anti-inflammatory responses to environmental allergens.
Le texte complet de cet article est disponible en PDF.Key words : Atopy, Gammaproteobacteria, Acinetobacter species, PBMC, anti-inflammatory gene expression, dendritic cells, keratinocytes, mouse asthma model
Abbreviations used : ACTB, AHR, DC, FOXP3, GAPDH, moDC, OVA, PE, qPCR, TLR2, Treg
Plan
| The research leading to these results has received funding from the Academy of Finland (grants nos. 138695, 255350, 121025, and 251170), the European Research Council (grant no. 239784), the Jane and Aatos Erkko Foundation, Helsinki University Hospital (HUS) (grant no. 8361), and by the European Union's Seventh Framework Programme FP7/2007-2013 under grant agreements 261366 (MAARS) and 261357 (MeDALL). |
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| Disclosure of potential conflict of interest: This study was funded by the Academy of Finland (grants nos. 138695, 255350, 121025, and 251170), the European Research Council (grant no. 239784), the Jane and Aatos Erkko Foundation, the European Union's Seventh Framework Programme (grant agreements 261366 and 261357), and the Helsinki University Hospital (grant no. 8361). T. Haahtela is on the board of the Global Initiative for Asthma, and has received payment for delivering lectures from OrionPharma and Merck. The rest of the authors declare that they have no relevant conflicts of interest. |
Vol 134 - N° 6
P. 1301 - décembre 2014 Retour au numéro
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