Claudia Weidler
University of Regensburg
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Featured researches published by Claudia Weidler.
Arthritis Research & Therapy | 2005
Martin Schmidt; Claudia Weidler; Heidrun Naumann; Sven Anders; Jürgen Schölmerich; Rainer H. Straub
In synovial cells of patients with osteoarthritis (OA) and rheumatoid arthritis (RA), conversion products of major anti-inflammatory androgens are as yet unknown but may be proinflammatory. Therefore, therapy with androgens in RA could be a problem. This study was carried out in order to compare conversion products of androgens in RA and OA synoviocytes. In 26 OA and 24 RA patients, androgen conversion in synovial cells was investigated using radiolabeled substrates and analysis by thin-layer chromatography and HPLC. Aromatase expression was studied by immunohistochemistry. Dehydroepiandrosterone (DHEA) was converted into androstenediol, androstenedione (ASD), 16αOH-DHEA, 7αOH-DHEA, testosterone, estrone (E1), estradiol (E2), estriol (E3), and 16αOH-testosterone (similar in OA and RA). Surprisingly, levels of E2, E3, and 16α-hydroxylated steroids were as high as levels of testosterone. In RA and OA, 5α-dihydrotestosterone increased conversion of DHEA into testosterone but not into estrogens. The second androgen, ASD, was converted into 5α-dihydro-ASD, testosterone, and negligible amounts of E1, E2, E3, or 16αOH-testosterone. 5α-dihydro-ASD levels were higher in RA than OA. The third androgen, testosterone, was converted into ASD, 5α-dihydro-ASD, 5α-dihydrotestosterone, and negligible quantities of E1 and E2. 5α-dihydrotestosterone was higher in RA than OA. ASD and testosterone nearly completely blocked aromatization of androgens. In addition, density of aromatase-positive cells and concentration of released E2, E3, and free testosterone from superfused synovial tissue was similar in RA and OA but estrogens were markedly higher than free testosterone. In conclusion, ASD and testosterone might be favorable anti-inflammatory compounds because they decrease aromatization and increase anti-inflammatory 5α-reduced androgens. In contrast, DHEA did not block aromatization but yielded high levels of estrogens and proproliferative 16α-hydroxylated steroids. Androgens were differentially converted to pro- and anti-inflammatory steroid hormones via diverse pathways.
Annals of the New York Academy of Sciences | 2006
Heidrun Naumann; Claudia Weidler; Martina Schellenberg; Sven Anders; Rainer H. Straub
Abstract: The incidence of autoimmune diseases is higher in females than in males. In both sexes, adrenal hormones, that is, glucocorticoids, dehydroepiandrosterone (DHEA), and androgens, are inadequately low in patients when compared to healthy controls. Hormonally active androgens are anti‐inflammatory, whereas estrogens are pro‐inflammatory. Therefore, the mechanisms responsible for the alterations of steroid profiles in inflammation are of major interest. The local metabolism of androgens and estrogens may determine whether a given steroid profile found in a subjects blood results in suppression or promotion of inflammation. The steroid metabolism in mixed synovial cells, fibroblasts, macrophages, and monocytes was assessed. Major focus was on cells from patients with rheumatoid arthritis (RA), while cells from patients with osteoarthritis served as controls. Enzymes directly or indirectly involved in local sex steroid metabolism in RA are: DHEA‐sulfatase, 3β‐hydroxysteroid dehydrogenase, 17β‐hydroxysteroid dehydrogenase, and aromatase (CYP19), which are required for the synthesis of sex steroids from precursors, 5α‐reductase and 16α‐hydroxylase, which can be involved either in the generation of more active steroids or in the pathways leading to depletion of active hormones, and 3α‐reductase and 7α‐hydroxylase (CYP7B), which unidirectionally are involved in the depletion of active hormones. Androgens inhibit aromatization in synovial cells when their concentration is sufficiently high. As large amounts of estrogens are formed in synovial tissue, there may be a relative lack of androgens. Production of 5α‐reduced androgens should increase the local anti‐inflammatory activity; however, it also opens a pathway for the inactivation of androgens. The data discussed here suggest that therapy of RA patients may benefit from the use of nonaromatizable androgens and/or the use of aromatase inhibitors.
The Journal of Infectious Diseases | 2005
Rainer H. Straub; Georg Pongratz; Claudia Weidler; Hans-Jörg Linde; Carsten J. Kirschning; Thomas Glück; Jürgen Schölmerich; Werner Falk
The sympathetic nervous system is intensely activated during bacteremia, but its immediate influence on the bacterial tissue burden remains unclear. We demonstrate that prior ablation of the sympathetic nervous system decreases this dissemination of Pseudomonas aeruginosa or Escherichia coli through a mechanism of increased secretion of peritoneal tumor necrosis factor, improved phagocytic response of peritoneal cells, and increased influx of monocytes into the peritoneal cavity. When gram-positive Staphylococcus aureus strains were used, sympathectomy increased the bacterial tissue burden, which was caused by a reduction in corticosterone tonus, and decreased both interleukin-4 secretion from peritoneal cells and the influx of lymphocytes into the peritoneal cavity. In both models, the peritoneal wall was the critical border for systemic infection. These results show the dual role of the sympathetic nervous system in sepsis. It can be favorable or unfavorable, depending on the innate immune effector mechanisms necessary to overcome infection.
Arthritis & Rheumatism | 2012
Torsten Lowin; Claudia Weidler; Zsuzsa Jenei-Lanzl; Silvia Capellino; Christoph Baerwald; Frank Buttgereit; Rainer H. Straub
OBJECTIVE Proliferating pannus is in many aspects similar to placental tissue. Both fibroblast-rich tissues have high vascularity, and tissue from patients with rheumatoid arthritis (RA) and patients with osteoarthritis (OA) demonstrates conversion of androgenic prehormones to downstream estrogens. We undertook this study to investigate similarities between proliferating pannus and placental tissue by focusing on angiogenic placenta growth factor 1 (PlGF-1) in patients with OA and patients with RA. METHODS We used immunohistochemistry to study the presence of PlGF-1, its synovial distribution, and the PlGF-1-expressing synovial cell type. The relationship between PlGF-1 and conversion of the biologically inactive placental prehormone dehydroepiandrosterone sulfate (DHEAS) to the biologically active dehydroepiandrosterone (DHEA) was investigated in mixed synovial cells. The effects of DHEA on PlGF-1 expression were studied by intracellular fluorescence-activated cell sorting analysis. RESULTS PlGF-1-positive cells were detected in the lining and sublining areas in patients with RA and patients with OA, and cellular density was similar. Double staining revealed that PlGF-1-positive cells were macrophages. In RA and OA, the density of PlGF-1-positive cells correlated positively with the density of macrophages and the density of type IV collagen-positive vessels. The supernatant concentration of (3) H-DHEA after conversion from (3) H-DHEAS and the density of aromatase-positive cells were positively correlated with the density of PlGF-1-positive cells only in OA. Low DHEA concentrations (≤10(-9) M) had stimulatory effects on PlGF-1 when compared to serum concentrations (10(-8) M to 10(-7) M) in the monocytic cell line THP-1 and in primary mixed synovial cells. CONCLUSION PlGF-1 functions similarly in inflamed synovium and in the placenta. It is related to vessel formation and, in OA patients, to androgen/estrogen conversion. Evolutionarily conserved functions of PlGF-1 for placental phenomena are obviously also present in synovial inflammation.
Brain Behavior and Immunity | 2006
Silvia Capellino; Claudia Weidler; Sven Anders; Christoph Baerwald; Frank Buttgereit; Rainer H. Straub
ference was particularly evident in female patients of both disease groups. In addition, in patients with RA, we detected CGA-positive synovial cells in the inflamed tissue which were significantly increased as compared to control tissue of patients with osteoarthritis. In conclusion, this study demonstrates a marked increase of serum levels of CGA. The origin of CGA is probably the adrenal gland but inflamed tissue CGA-positive cells might also contribute to elevated serum levels. In summary, increased CGA levels are another indication for an activated sympathetic nervous system.
Arthritis & Rheumatism | 2004
Luitpold E. Miller; Claudia Weidler; Werner Falk; Peter Angele; Jens Schaumburger; Jürgen Schölmerich; Rainer H. Straub
Arthritis & Rheumatism | 2005
Martin Schmidt; Claudia Weidler; Heidrun Naumann; Sven Anders; Jürgen Schölmerich; Rainer H. Straub
The Journal of Rheumatology | 2004
Claudia Weidler; Peter Härle; Joerg Schedel; Martin Schmidt; Jürgen Schölmerich; Rainer H. Straub
The Journal of Rheumatology | 2005
Rainer H. Straub; Peter Härle; Fabiola Atzeni; Claudia Weidler; Maurizio Cutolo; Piercarlo Sarzi-Puttini
Arthritis & Rheumatism | 2005
Claudia Weidler; Sona Struharova; Bernhard Ugele; Jürgen Schölmerich; Rainer H. Straub