Janet Wohlers
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Janet Wohlers has a total of 6 co-authors. Here are the top co-authors by number of shared publications:
- Jürgen Hedderich
Institute for Medical Informatics and Statistics, University Clinics Schleswig-Holstein, Campus Kiel, Germany
1 shared publication - Katrin Breucker
University of Kiel, Department of Otorhinolaryngology, Head and Neck Surgery, Arnold-Heller-Straße 14, D-24105 Kiel, Germany
1 shared publication - Martin Laudien
Department of Otorhinolaryngology, Head and Neck Surgery, University of Kiel, Germany.
1 shared publication - Peter Lamprecht
Department of Rheumatology and Clinical Immunology University of Lübeck Lübeck Germany
1 shared publication - Petra Ambrosch
Department of Otorhinolaryngology, Head and Neck Surgery, University Hospital Schleswig-Holstein (UKSH), University of Kiel, 24105 Kiel, Germany
1 shared publication - Rainer Podschun
Institute for Infection Medicine (Head: Prof. Dr. Helmut Fickenscher), University Hospital Schleswig-Holstein, Campus Kiel, Brunswiker Straße 4, 24105 Kiel, Germany
1 shared publication
Latest Publications
- Open Access
- 17 October 2012
- Published by Springer Nature in Arthritis Research & Therapy
- Vol. 14 (5) , R203
Aberrant cytokine pattern of the nasal mucosa in granulomatosis with polyangiitis
Introduction: In granulomatosis with polyangiitis (GPA), a complex autoimmune small-vessel vasculitis frequently associated with chronic necrotizing inflammation of the nasal mucosa, elevated nasal Staphylococcus (S.) aureus carrier rates are a risk factor for relapse. As cytokines are primarily involved in the regulation of defense against potentially pathogenic microorganisms, the aim of this study was to compare healthy individuals and GPA patients with respect to their baseline cytokine expression of nasal epithelial cells (NEC), which form the first barrier against such triggers. The ability of S. aureus to influence the nasal microenvironment's cytokine secretion was assessed by exemplary stimulation experiments. Methods: Baseline expression of 19 cytokines of primary NEC of GPA patients and normal controls (NC) was quantified by a multiplex cytokine assay. Stimulation experiments were performed with supernatants of S. aureus and expression of interleukin-8 was determined by ELISA. Results: In GPA, an altered pattern of baseline cytokine expression with significantly up-regulated G-CSF and reduced interleukin (IL)-8 concentrations was observed. Both NEC of GPA patients and NC responded to stimulation with S. aureus, but GPA patients displayed a significantly lower IL-8 secretion and a diminished dynamic range of response towards the stimulus. Conclusions: The data presented underline the hypothesis of a disturbed epithelial nasal barrier function in GPA. The dysregulated baseline expression of G-CSF and IL-8 and the reduced response to microbial stimulation may facilitate changes in the composition of the nasal flora and favour an imbalanced inflammatory response, which might be relevant for the disease course.
- 17 October 2012
- Published by Springer Nature in Arthritis Research & Therapy
- Vol. 14 (5) , R203
Open AccessAberrant cytokine pattern of the nasal mucosa in granulomatosis with polyangiitis
Introduction: In granulomatosis with polyangiitis (GPA), a complex autoimmune small-vessel vasculitis frequently associated with chronic necrotizing inflammation of the nasal mucosa, elevated nasal Staphylococcus (S.) aureus carrier rates are a risk factor for relapse. As cytokines are primarily involved in the regulation of defense against potentially pathogenic microorganisms, the aim of this study was to compare healthy individuals and GPA patients with respect to their baseline cytokine expression of nasal epithelial cells (NEC), which form the first barrier against such triggers. The ability of S. aureus to influence the nasal microenvironment's cytokine secretion was assessed by exemplary stimulation experiments. Methods: Baseline expression of 19 cytokines of primary NEC of GPA patients and normal controls (NC) was quantified by a multiplex cytokine assay. Stimulation experiments were performed with supernatants of S. aureus and expression of interleukin-8 was determined by ELISA. Results: In GPA, an altered pattern of baseline cytokine expression with significantly up-regulated G-CSF and reduced interleukin (IL)-8 concentrations was observed. Both NEC of GPA patients and NC responded to stimulation with S. aureus, but GPA patients displayed a significantly lower IL-8 secretion and a diminished dynamic range of response towards the stimulus. Conclusions: The data presented underline the hypothesis of a disturbed epithelial nasal barrier function in GPA. The dysregulated baseline expression of G-CSF and IL-8 and the reduced response to microbial stimulation may facilitate changes in the composition of the nasal flora and favour an imbalanced inflammatory response, which might be relevant for the disease course.