Superantigen Immune Stimulation Evokes Epithelial Monocyte Chemoattractant Protein 1 and RANTES Production

Abstract

Bacterial superantigens (SAgs) have been implicated in inflammatory disease, and SAg-treated mice have increased jejunal T cells. Here we show that T84 cells (a human epithelial cell line) display increased MCP-1 and RANTES mRNA expression and protein production in response to conditioned medium from Staphylococcus aureus enterotoxin B (SEB; a model SAg)-activated immune cells. Also, MCP-1 and RANTES mRNAs were increased in jejunal enterocytes isolated from SEB-treated mice. We suggest that T-cell recruitment to the gut following SAg immune activation could be partially due to epithelium-derived chemokines.

Staphylococcus aureus enterotoxin B augments granulocyte migration and survival via airway epithelial cell activation

“…However, CXCR3‐expression is also found on eosinophils (28) and neutrophils (29), in particular in inflammatory microenvironments. Furthermore, increased levels of RANTES and MCP‐1 – both chemoattractant for mononuclear cells – after SEB stimulation are in line with previous data (23), and increased levels of G‐CSF – causing granulocyte proliferation and differentiation – are reported after S. aureus stimulation of epithelial cells (30). Pretreatment of HNEC with IFNgamma has resulted in increased levels of IL‐8 upon SEB stimulation (20).…”

“…Previous studies using either SEB or S. aureus itself confirm the role of the innate immune activation through epithelial cells secreting cytokines and chemokines, which lead to a secondary influx of inflammatory cells (23, 25–27). However, this is the first study evaluating the effect of the prototypic staphylococcal superantigen SEB on a highly purified human nasal epithelial cell population.…”

“…The airway epithelium not only is a physiological barrier, but also is actively involved in the immune response as a major source of inflammatory cytokines and mediators (21), relevant to the ongoing inflammatory responses dominated, among other features, by abundant granulocytes. Activated epithelial cells are potent sources of haematopoietic cytokines such as granulocyte (‐macrophage) colony stimulating factor [G (M)‐CSF], and chemokines like regulated upon activation normal T cell expressed and secreted (RANTES), eotaxin, monokine induced by interferon‐γ (MIG), interferon‐inducible protein‐10 (IP‐10), interleukin (IL)‐8 (22), and monocyte chemoattractant protein 1 (MCP‐1) (23).…”

Differential Regulation of Chemokine Secretion in Tuberculous and Staphylococcal Osteomyelitis

“…S. aureus ‐induced MCP‐1 secretion is delayed and 10‐fold less than that induced by M. tuberculosis . MCP‐1 secretion is dependent on bacterial invasion, although heat‐killed staphylococci do induce chemokine secretion, possibly via liberation of heat‐stable toxins (20,46) . This study and another recent report (47) describe chemokine secretion at reduced levels in the presence of nonviable bacteria although whether this is a consequence of decreased internalization of either M. tuberculosis or S. aureus was not investigated.…”

Staphylococcus aureusand its food poisoning toxins: characterization and outbreak investigation

“…The activation of T84 cells (a human epithelial cell line) by SAgs induces the production of (1) monocyte chemoattractant protein 1 (MCP-1) and (2) regulated on activation normal T-cell expressed and secreted protein (RANTES). These chemokines promote the recruitment of immune mononuclear cells, which may explain the role of the SAgs in the pathogenesis of inflammatory gastrointestinal diseases (Jedrzkiewicz et al, 1999). In addition, both SEA and SEB bind to intestinal myofibroblasts with MHC class II molecules (Pinchuk et al, 2007).…”