Immunochemical studies on lactate dehydrogenase: Preparation and characterization of anti-M lactate dehydrogenase antiserum: Development of an immunochemical assay for lactate dehydrogenase isoenzymes in human serum

Burd, John F.; Usategui-Gomez, M.; Castro, AL; Mhatre, N.S.; Yeager, Frances M.

doi:10.1016/0009-8981(73)90172-1

Cited by 15 publications

(1 citation statement)

References 12 publications

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“…LDH is a soluble cytoplasmic enzyme that is present in almost all cells and is released into the supernatant when the plasma membrane is damaged (21,22). Indeed, 10 min after treatment with PSMa3, a significant amount of LDH was released from DCs that was comparable with the LDH release of d-toxin, which are known to induce transient pore formation (23) (Fig.…”

Section: /2mentioning

confidence: 92%

PSM Peptides of Staphylococcus aureus Activate the p38–CREB Pathway in Dendritic Cells, Thereby Modulating Cytokine Production and T Cell Priming

Armbruster

Richardson

Schreiner

et al. 2016

The Journal of Immunology

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The challenging human pathogen Staphylococcus aureus has highly efficient immune evasion strategies for causing a wide range of diseases, from skin and soft tissue to life-threatening infections. Phenol-soluble modulin (PSM) peptides are major pathogenicity factors of community-associated methicillin-resistant S. aureus strains. In previous work, we demonstrated that PSMs in combination with TLR2 ligand from S. aureus induce tolerogenic dendritic cells (DCs) characterized by the production of high amounts of IL-10, but no proinflammatory cytokines. This in turn promotes the activation of regulatory T cells while impairing Th1 response; however, the signaling pathways modulated by PSMs remain elusive. In this study, we analyzed the effects of PSMs on signaling pathway modulation downstream of TLR2. TLR2 stimulation in combination with PSMα3 led to increased and prolonged phosphorylation of NF-κB, ERK, p38, and CREB in mouse bone marrow–derived DCs compared with single TLR2 activation. Furthermore, inhibition of p38 and downstream MSK1 prevented IL-10 production, which in turn reduced the capacity of DCs to activate regulatory T cells. Interestingly, the modulation of the signaling pathways by PSMs was independent of the known receptor for PSMs, as shown by experiments with DCs lacking the formyl peptide receptor 2. Instead, PSMs penetrate the cell membrane most likely by transient pore formation. Moreover, colocalization of PSMs and p38 was observed near the plasma membrane in the cytosol, indicating a direct interaction. Thus, PSMs from S. aureus directly modulate the signaling pathway p38–CREB in DCs, thereby impairing cytokine production and in consequence T cell priming to increase the tolerance toward the pathogen.

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Section: /2mentioning

confidence: 92%