Effect of peptidoglycans on erythrocyte survival

Föller, Michael; Biswas, Raja; Mahmud, Hasan; Akel, Ahmad; Shumilina, Ekaterina; Wieder, Thomas; Goetz, Friedrich; Läng, Florian

doi:10.1016/j.ijmm.2008.05.012

Cited by 19 publications

(11 citation statements)

References 75 publications

(64 reference statements)

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“…Similar to the effect of peptidoglycans [13], the effect of Pam3CSK4 is blunted by removal of extracellular Ca 2+ . In polymorphonuclear leukocytes, peptidoglycans have been shown to trigger the arachidonic acid cascade with subsequent formation of prostaglandin E 2 [44].…”

Section: Discussionmentioning

confidence: 78%

“…Eryptosis may be stimulated by bacterial or host sphingomyelinase [5,7] and/or by activation of Ca 2+ -permeable erythrocyte cation channels with subsequent Ca 2+ entry [8][9][10]. Further bacterial components described to stimulate eryptosis include hemolysin from Vibrio parahaemolyticus [11], listeriolysin [12] and peptidoglycans [13]. Phosphatidylserine exposure in erythrocytes could further be elicited by ligation of specific surface antigens, such as glycophorin-C [14], of CD47, 382 the critical RBC antigenic marker that exhibits an inhibitory role in macrophage activation [15], and of the death receptor CD95/Fas [16].…”

Section: Introductionmentioning

confidence: 99%

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Lipopeptides in the Triggering of Erythrocyte Cell Membrane Scrambling

Wang

Mahmud²,

Föller³

et al. 2008

Cell Physiol Biochem

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Sepsis is paralleled by anemia, an effect partially resulting from eryptosis, the suicidal death of erythrocytes. Eryptosis is characterized by cell membrane scrambling with phosphatidylserine exposure at the erythrocyte surface. Pathogen-induced eryptosis may partially result from interaction of bacterial cell wall components such as lipoproteins with the erythrocyte cell membrane. The present study explored, whether the synthetic lipopeptide Pam3CSK4 mimicking the acylated amino terminus of bacterial lipoproteins triggers eryptosis. According to annexin-V-binding in FACS analysis, Pam3CSK4 (1 µg/ml) stimulated phosphatidylserine exposure, an effect significantly blunted in the nominal absence of Ca 2+ . According to Fluo3 fluorescence, Pam3CSK4 increased cytosolic Ca 2+ activity and moderately stimulated erythrocytic ceramide formation, both major triggers of eryptosis. In conclusion, bacterial lipoproteins participate in the stimulation of erythrocyte cell membrane scrambling by bacterial cell wall components. Thus, lipoproteindependent suicidal erythrocyte death may contribute to the pleotropic effects of sepsis.

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Section: Discussionmentioning

confidence: 78%

Section: Introductionmentioning

confidence: 99%

Lipopeptides in the Triggering of Erythrocyte Cell Membrane Scrambling

Wang

Mahmud²,

Föller³

et al. 2008

Cell Physiol Biochem

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“…Several stimuli and diseases trigger eryptosis, including energy depletion, oxidative stress, osmotic shock, cyclosporine, peptidoglycans, prostaglandin E 2 , sepsis, malaria and glucose-6-dehydrogenase-deficiency [22][23][24][25][26][27][28].…”

Section: Discussionmentioning

confidence: 99%

Hemotrophic Mycoplasmas Induce Programmed Cell Death in Red Blood Cells

Felder

Hoelzle

Ritzmann

et al. 2011

Cell Physiol Biochem

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Hemotrophic mycoplasmas (HM) are uncultivable bacteria found on and in the red blood cells (RBCs). The main clinical sign of HM infections is the hemolytic anemia. However, anemia-inducing pathogenesis has not been totally clarified. In this work we used the splenectomized pig as animal model and Mycoplasma suis as a representative for hemotrophic mycoplasmas to study anemia pathogenesis. Eryptosis, i.e. programmed cell death of RBCs, is characterized by cell shrinkage, microvesiculation and phosphatidylserine (PS) exposure on the outer membrane. The eryptosis occurrence and its influence on anemia pathogenesis was observed over the time-course of M. suis infections in pigs using 3 M. suis isolates of differing virulence. All 3 isolates induced eryptosis, but with different characteristics. The occurrence of eryptosis could as well be confirmed in vitro: serum and plasma of an acutely ill pig induced PS exposure on erythrocytes drawn from healthy pigs. Since M. suis is able to induce eryptotic processes it is concluded that eryptosis is one anemia-inducing factor during M. suis infections and, therefore, plays a significant role in the pathogenesis of infectious anemia due to HM infection.

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“…Several anemic conditions are secondary to accelerated eryptosis, such as iron deficiency , sepsis , malaria Koka et al 2008a;Koka et al 2008b), or Wilson's disease . Moreover, eryptosis is triggered by hemin (Gatidis et al 2009), cordycepin (Lui et al 2007), azathioprine (Geiger et al in press), amyloid peptides (Nicolay et al 2007b), lipopeptides , retinoic acid (Niemoeller et al 2008a), peptidoglycan (Foller et al 2009a), amantadine , ciglitazone , methyldopa , lipoproteins , curcumin , amiodarone (Nicolay et al 2007a), anandamide , listeriolysin ), IgA antibodies (Attanasio et al 2007), bismuth (Braun et al 2009), tin (Nguyen et al 2009), mercury (Eisele et al 2006), copper , cadmium (Sopjani et al 2008a), selenium (Sopjani et al 2008b), vanadate , gold ) and arsenic (Mahmud et al 2009). It should be pointed out, that under several of those clinical conditions and toxic effects overt anemia may be prevented by enhanced formation of new erythrocytes.…”

Section: Discussionmentioning

confidence: 99%