TY  - JOUR
A1  - Boeckel, Hannah
A1  - Karsten, Christian M.
A1  - Göpel, Wolfgang
A1  - Herting, Egbert
A1  - Rupp, Jan
A1  - Härtel, Christoph
A1  - Hartz, Annika
T1  - Increased expression of anaphylatoxin C5a-receptor-1 in neutrophils and natural killer cells of preterm infants
JF  - International Journal of Molecular Sciences
N2  - Preterm infants are susceptible to infection and their defense against pathogens relies largely on innate immunity. The role of the complement system for the immunological vulnerability of preterm infants is less understood. Anaphylatoxin C5a and its receptors C5aR1 and -2 are known to be involved in sepsis pathogenesis, with C5aR1 mainly exerting pro-inflammatory effects. Our explorative study aimed to determine age-dependent changes in the expression of C5aR1 and C5aR2 in neonatal immune cell subsets. Via flow cytometry, we analyzed the expression pattern of C5a receptors on immune cells isolated from peripheral blood of preterm infants (n = 32) compared to those of their mothers (n = 25). Term infants and healthy adults served as controls. Preterm infants had a higher intracellular expression of C5aR1 on neutrophils than control individuals. We also found a higher expression of C5aR1 on NK cells, particularly on the cytotoxic CD56\(^{dim}\) subset and the CD56\(^-\) subset. Immune phenotyping of other leukocyte subpopulations revealed no gestational-age-related differences for the expression of and C5aR2. Elevated expression of C5aR1 on neutrophils and NK cells in preterm infants may contribute to the phenomenon of “immunoparalysis” caused by complement activation or to sustained hyper-inflammatory states. Further functional analyses are needed to elucidate the underlying mechanisms.
KW  - preterm infants
KW  - C5a
KW  - C5aR1
KW  - neutrophils
KW  - NK cells
KW  - innate immunity
KW  - sepsis
Y1  - 2023
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-321196
SN  - 1422-0067
VL  - 24
IS  - 12
ER  - 
TY  - JOUR
A1  - Hampf, Chantal
A1  - Scherf-Clavel, Maike
A1  - Weiß, Carolin
A1  - Klüpfel, Catherina
A1  - Stonawski, Saskia
A1  - Hommers, Leif
A1  - Lichter, Katharina
A1  - Erhardt-Lehmann, Angelika
A1  - Unterecker, Stefan
A1  - Domschke, Katharina
A1  - Kittel-Schneider, Sarah
A1  - Menke, Andreas
A1  - Deckert, Jürgen
A1  - Weber, Heike
T1  - Effects of anxious depression on antidepressant treatment response
JF  - International Journal of Molecular Sciences
N2  - Anxious depression represents a subtype of major depressive disorder and is associated with increased suicidality, severity, chronicity and lower treatment response. Only a few studies have investigated the differences between anxious depressed (aMDD) and non-anxious depressed (naMDD) patients regarding treatment dosage, serum-concentration and drug-specific treatment response. In our naturalistic and prospective study, we investigated whether the effectiveness of therapy including antidepressants (SSRI, SNRI, NaSSA, tricyclics and combinations) in aMDD patients differs significantly from that in naMDD patients. In a sample of 346 patients, we calculated the anxiety somatization factor (ASF) and defined treatment response as a reduction (≥50%) in the Hamilton Depression Rating Scale (HDRS)-21 score after 7 weeks of pharmacological treatment. We did not observe an association between therapy response and the baseline ASF-scores, or differences in therapy outcomes between aMDD and naMDD patients. However, non-responders had higher ASF-scores, and at week 7 aMDD patients displayed a worse therapy outcome than naMDD patients. In subgroup analyses for different antidepressant drugs, venlafaxine-treated aMDD patients showed a significantly worse outcome at week 7. Future prospective, randomized-controlled studies should address the question of a worse therapy outcome in aMDD patients for different psychopharmaceuticals individually.
KW  - pharmacotherapy
KW  - depressive disorder
KW  - anxious depression
KW  - anxiety
KW  - therapy response
Y1  - 2023
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-355801
SN  - 1422-0067
VL  - 24
IS  - 24
ER  -