Induction of tumor necrosis factor and interleukin-1 by purified staphylococcal toxic shock syndrome toxin 1 requires the presence of both monocytes and T lymphocytes

See, Raymond H.; Kum, Winnie W. S.; Chang, Alex H.; Goh, Swee Han; Chow, Anthony W.

doi:10.1128/iai.60.7.2612-2618.1992

Cited by 54 publications

(31 citation statements)

References 25 publications

(35 reference statements)

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“…Thus, both cell types are required for an efficient response. A similar requirement for the presence of both monocytes and lymphocytes together has been reported elsewhere for induction of TNF-␣ by SEA (15) and TSST-1 (42). Moreover, incubation of monocytic cell line THP-1 with SEB did not activate TNF-␣ gene expression (31).…”

Section: Discussionsupporting

confidence: 81%

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Production of Tumor Necrosis Factor Alpha in Human T Lymphocytes by Staphylococcal Enterotoxin B Correlates with Toxin-Induced Proliferation and Is Regulated through Protein Kinase C

et al. 1999

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The superantigen staphylococcal enterotoxin B (SEB) simultaneously binds both the major histocompatibility complex (MHC) class II receptor on monocytes and the T-cell receptor (TCR) on T lymphocytes, resulting in a range of cell responses including induction of tumor necrosis factor alpha (TNF-α). In this study, we have used mixed cultures of human peripheral blood monocytes and lymphocytes to investigate biochemical events controlling SEB induction of TNF-α. TNF-α production induced by SEB in mixed cultures is more closely associated with T cells than with monocytes: (i) a TCR-binding-site mutant of SEB (N23F) is less active in TNF-α induction than an MHC class II receptor-binding-site mutant (F44R), and (ii) flow cytometric analysis indicated that SEB induced TNF-α production in T cells but not in monocytes. Pretreatment of cells with inhibitors of signal transduction pathways was employed to further define events in SEB-induced TNF-α production. Neither protein kinase A inhibitors nor two protein tyrosine kinase inhibitors altered SEB-induced TNF-α production. In contrast, SEB induced protein kinase C (PKC) translocation, and pretreatment of cultures with inhibitors of PKC blocked TNF-α induction. Alteration of levels of diacylglycerol (DAG), an activator of PKC, by treatment with inhibitors of phospholipase C or DAG kinase also altered SEB-induced TNF-α production. These data suggest that PKC activation plays a critical role in SEB-induced TNF-α production in human T cells.

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Section: Discussionsupporting

confidence: 81%

“…TNF-␣ induced by superantigen can be produced by both monocytes and T cells (1,15,30). Previous studies have examined the induction of TNF-␣ by SEA, SEB, or TSST-1 (15,30,38,42,43). In this study, we wished to characterize the induction of TNF-␣ by SEB in mixed cultures of human monocytes in the presence of lymphocytes.…”

mentioning

confidence: 99%

Production of Tumor Necrosis Factor Alpha in Human T Lymphocytes by Staphylococcal Enterotoxin B Correlates with Toxin-Induced Proliferation and Is Regulated through Protein Kinase C

et al. 1999

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“…Monokine expression presumably requires participation of bofh T cells and antigen-presenting cells (APC) (See et al, 1992). Purified monocytes stimulated with several superantigens produce little TNF-a or tl-ip in fhe absence of viable T cells or y-interfercn (Kotb, 1993).…”

Section: Interaction With Immune Cellsmentioning

confidence: 99%

Investigation of the role of the disulphide bond in the activity and structure of staphylococcal enterotoxin C1

Hovde

Marr

Hoffmann

et al. 1994

Molecular Microbiology

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The goal of this study was to investigate the role of the disulphide bond of staphylococcal enterotoxin C1 (SEC1) in the structure and activity of the toxin. Mutants unable to form a disulphide bond were generated by substituting alanine or serine for cysteine at positions 93 and/or 110. Although we did not directly investigate the residues between the disulphide linkage, tryptic lability showed that significant native structure in the cystine loop is preserved in the absence of covalent bonding between residues 93 and 110. Since no correlation was observed between the behaviour of these mutants with regard to toxin stability, emesis and T cell proliferation we conclude that SEC1-induced emesis and T cell proliferation are dependent on separate regions of the molecule. The disulphide bond itself is not an absolute requirement for either activity. However, conformation within or adjacent to the loop is important for emesis. Although mutants with alanine substitutions were not emetic, those with serine substitutions retained this activity, suggesting that the disulphide linkage stabilizes a crucial conformation but can be replaced by residues which hydrogen bond.

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“…Like other staphylococcal toxins TSST-1 has numerous immunomodulating effects such as inducing the release of interleukin 1 and the tumour necrosis factor from monocytes (Yokomizo et al 1995). Its mitogen effect on T-lymphocytes results in the release of lymphokines (See et al 1992). When bovine T-lymphocytes are experimentally exposed, TSST-1 acts as a superantigen for bovine immune cells, thus it potentially contributes to the mammary pathology associated with Staph.…”

Section: Introductionmentioning

confidence: 99%

Occurrence and clonal relatedness of sec/tst-gene positive Staphylococcus aureus isolates of quartermilk samples of cows suffering from mastitis

Zschöck¹,

Risse²,

Sommerhäuser³

2004

Lett Appl Microbiol

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Aims: To investigate the prevalence of sec/tst-gene positive Staphylococcus aureus in bovine mastitis and to get information about the clonal relatedness of these clinical isolates. Methods and Results: A total of 533 Staph. aureus strains isolated from bovine mastitic quartermilk samples at 493 randomized dairy farms in Hessia, Germany, from January 1997 until June 1998 were examined for enterotoxin C (sec) gene and toxic shock syndrome toxin (tst) gene by multiplex polymerase chain reaction. Fiftythree (9AE3%) of the strains were sec/tst-gene positive. Phenotypic TSST-1 production was found in all positive strains by reversed passive latex agglutination test. With DNA macrorestriction analysis, sec/tst-gene positive strains were divided into five different macrorestriction types. Type I (10 isolates) and III (40 isolates) were found to be the predominant types in terms of frequency of isolation in the investigated area. These DNA macrorestriction types differed in only two bands in the 500 and 270 bp region. Conclusions: Closely related Staph. aureus strains seem to be responsible for an unusual large proportion of bovine mastitis cases in geographically widely distinct locations. Significance and Impact of the Study: This is one of the first reports about the relatedness of sec/tst-gene positive Staph. aureus clinical isolates from bovine mastitis.

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Induction of tumor necrosis factor and interleukin-1 by purified staphylococcal toxic shock syndrome toxin 1 requires the presence of both monocytes and T lymphocytes

Cited by 54 publications

References 25 publications

Production of Tumor Necrosis Factor Alpha in Human T Lymphocytes by Staphylococcal Enterotoxin B Correlates with Toxin-Induced Proliferation and Is Regulated through Protein Kinase C

Production of Tumor Necrosis Factor Alpha in Human T Lymphocytes by Staphylococcal Enterotoxin B Correlates with Toxin-Induced Proliferation and Is Regulated through Protein Kinase C

Investigation of the role of the disulphide bond in the activity and structure of staphylococcal enterotoxin C1

Occurrence and clonal relatedness of sec/tst-gene positive Staphylococcus aureus isolates of quartermilk samples of cows suffering from mastitis

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