Induction of release of tumor necrosis factor from human monocytes by staphylococci and staphylococcal peptidoglycans

Abstract

The role of cytokines in gram-positive infections is still relatively poorly defined. The purpose of this study was to establish whether or not intact staphylococci and purified peptidoglycans and peptidoglycan components derived from staphylococci are capable of stimulating the release of tumor necrosis factor (TNF) by human monocytes. We show here that intact staphylococci and purified peptidoglycans, isolated from three Staphylococcus epidermidis and three S. aureus strains, were indeed able to induce secretion of TNF by human monocytes in a concentration-dependent fashion. TNF release was detected by both enzyme immunoassay and the L929 fibroblast bioassay. In the enzyme immunoassay, a minimal concentration of peptidoglycan of 1 ,ug/ml was required to detect TNF release by monocytes, whereas in the bioassay a peptidoglycan concentration of 10 ,ug/ml was needed to detect a similar amount of TNF release. Peptidoglycan components such as the stem peptide, tetra-and pentaglycine, and muramyl dipeptide were unable to induce TNF release from human monocytes.

Plasma secretory leukocyte protease inhibitor in febrile patients; An indicator of the presence and extent of pulmonary infection

“…2 Difference in SLPI concentration between pneumonia and pyelonephritis (P 0.004) or infection of central airways (P 0.006). 3 Concentrations below detection limit of assay. 4 Difference in TNF-a concentration between pyelonephritis and central airways (P 0.01) or lower respiratory tract infection (P 0.03).…”

Peptidoglycan and teichoic acid from Staphylococcus epidermidis stimulate human monocytes to release tumour necrosis factor-α, interleukin-1β and interleukin-6

“…Teichoic acid (TA), another important cell wall constituent of Gram-positives, consisting of ribitol phosphate polymers, activates complement via the classical pathway [10]. Whole bacteria of S. epidermidis induce PBM to release TNF, IL-1 and IL-6 [6], while PG has been shown to stimulate PBM to TNF release [11]. PG precursors, which are secreted from penicillin-treated Streptococcus faecalis, are also able to trigger PBM to IL-1 production [12].…”

Streptococcus oralis coaggregation receptor polysaccharides induce inflammatory responses in human aortic endothelial cells

“…We used only HAECs to determine the inflammation-inducible effects of S. oralis RPS, and it is uncertain whether the effects are HAEC specific or not. Polysaccharidecontaining bacterial components such as lipopolysaccharide (Tsoyi et al, 2009;Zhang et al, 2011) and peptidoglycan (Timmerman et al, 1993) have been shown to induce inflammatory responses in human cells. These bacterial components are hetero-type complexes of sugars and lipids/proteins.…”