TY  - JOUR
A1  - Halder, Luke D.
A1  - Abdelfatah, Mahmoud A.
A1  - Jo, Emeraldo A. H.
A1  - Jacobsen, Ilse D.
A1  - Westermann, Martin
A1  - Beyersdorf, Niklas
A1  - Lorkowski, Stefan
A1  - Zipfel, Peter F.
A1  - Skerka, Christine
T1  - Factor H binds to extracellular DNA traps released from human blood monocytes in response to Candida albicans
JF  - Frontiers in Immunology
N2  - Upon systemic infection with human pathogenic yeast Candida albicans (C. albicans), human monocytes and polymorph nuclear neutrophilic granulocytes are the first immune cells to respond and come into contact with C. albicans. Monocytes exert immediate candidacidal activity and inhibit germination, mediate phagocytosis, and kill fungal cells. Here, we show that human monocytes spontaneously respond to C. albicans cells via phagocytosis, decondensation of nuclear DNA, and release of this decondensed DNA in the form of extracellular traps (called monocytic extracellular traps: MoETs). Both subtypes of monocytes (CD14\(^{++}\)CD16\(^−\)/CD14\(^+\)CD16\(^+\)) formed MoETs within the first hours upon contact with C. albicans. MoETs were characterized by the presence of citrullinated histone, myeloperoxidase, lactoferrin, and elastase. MoETs were also formed in response to Staphylococcus aureus and Escherichia coli, indicating a general reaction of monocytes to infectious microbes. MoET induction differs from extracellular trap formation in macrophages as MoETs are not triggered by simvastatin, an inhibitor of cholesterol synthesis and inducer of extracellular traps in macrophages. Extracellular traps from both monocytes and neutrophils activate complement and C3b is deposited. However, factor H (FH) binds via C3b to the extracellular DNA, mediates cofactor activity, and inhibits the induction of the inflammatory cytokine interleukin-1 beta in monocytes. Altogether, the results show that human monocytes release extracellular DNA traps in response to C. albicans and that these traps finally bind FH via C3b to presumably support clearance without further inflammation.
KW  - Candida
KW  - monocytes
KW  - DNA traps
KW  - MPO
KW  - factor H
Y1  - 2017
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-181127
VL  - 7
ER  - 
TY  - JOUR
A1  - Stock, Benjamin
A1  - Möckel, Sigrid
A1  - Zander, Christine
A1  - Heinsen, Helmut
A1  - Bohnert, Simone
A1  - Bohnert, Michael
T1  - „Black esophagus“ – zwei Obduktionsfälle mit infektiöser Beteiligung
JF  - Rechtsmedizin
N2  - „Black esophagus“ oder „akute Ösophagusnekrose“ (AÖN) ist eine seltene Erkrankung, die sich makroskopisch durch eine zirkumferente Schwarzverfärbung der Ösophagusmukosa mit abruptem Ende am gastroösophagealen Übergang auszeichnet. Die genaue Pathogenese ist unbekannt; es werden multifaktorielle Einflüsse wie z. B. Säurereflux, Ischämie und verringerte Schutzmechanismen der Mukosa als mögliche Ursachen diskutiert.

Vorgestellt werden 2 Obduktionsfälle, die typische Befunde einer AÖN aufwiesen. Zusätzlich hatten Fall 1 eine Candida-Infektion und Fall 2 eine Appendizitis, sodass eine infektiöse Genese in beiden Fällen eine Rolle gespielt haben könnte.
N2  - Black esophagus, also known as acute esophageal necrosis, is a rare disease characterized by a circumferential black discoloration of the esophageal mucosa with an abrupt stop at the gastroesophageal junction. The exact pathogenesis is unknown, but multifactorial influences, such as acid reflux, ischemia and reduced protective mechanisms of the mucosa are discussed as possible causes.

Two autopsy cases are presented with typical signs of a black esophagus. The first case showed an infection with Candida albicans, the second one died of appendicitis, so in both cases an infectious genesis might have played a role.
T2  - Black esophagus—Two autopsy cases with infectious involvement
KW  - Histopathologie
KW  - Blinddarmentzündung
KW  - Speiseröhre
KW  - Nekrose
KW  - Schleimhaut
KW  - Candida
KW  - Akute Ösophagusnekrose
KW  - Schleimhaut-Ulzera
KW  - Appendizitis
KW  - acute esophageal necrosis
KW  - histopathology
KW  - mucosal ulcers
KW  - appendicitis
KW  - Candida
Y1  - 2023
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-325022
SN  - 0937-9819
VL  - 33
IS  - 3
ER  -