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Category: Food Microbiology
Staphylococcus aureus, Page 1 of 2
< Previous page | Next page > /docserver/preview/fulltext/10.1128/9781555819972/9781555819965.ch21-1.gif /docserver/preview/fulltext/10.1128/9781555819972/9781555819965.ch21-2.gifAbstract:
Staphylococcal enterotoxins (SEs) are causative agents of staphylococcal food poisoning (SFP). Advances in genome sequencing and recent monkey feeding assays have continuously expanded the list of SEs expressed by Staphylococcus aureus and other staphylococci. Although the implementation of Hazard Analysis and Critical Control Points systems and active foodborne illness outbreak surveillance programs have greatly reduced SFP, most instances of SFP are attributable to improper food handling practices in the retail industry. Additional knowledge of the molecular aspects of staphylococcal survival and growth, SE production in food, and the molecular mechanism of emesis caused by SEs will enable further development of effective ways to prevent SFP. In addition to emetic activity, all SEs have superantigenic properties that modulate host immune responses to cause toxic shock syndrome, as well as causing transient immunosuppression by inducing regulatory T cells. These suggest that the harmful effects of SEs are not merely emesis to allow S. aureus to exit the host but also immunosuppression to survive in and persistently colonize its many human and animal hosts.
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Alignment of primary sequences of mature SEs and SEl proteins in the current literature. Sequence alignment and output were conducted using the ClustalW program ( 177 ). The secondary structure was aligned to SEA ( 66 ).
Neighbor-joining tree based on the sequences of currently known SEs, SEl proteins, and TSST-1. This tree was created with the clustering feature of ClustalW using MEGA 4.0.1 software ( 178 ).
Interactions between APCs and T cells facilitated by conventional Ags and SAgs. The binding of SAg with TCR-MHCII triggers activation of signaling cascades through Lck-dependent and Lck-independent pathways, leading to the activation of transcriptional factors that induce T-cell proliferation, cytokine production, and proinflammation. TGFβR, transforming growth factor beta receptor; PLCγ, phospholipase Cγ; ERK, extracellular signal-regulated kinase; JNK, Jun N-terminal protein kinase; NFAT, nuclear factor of activated T cells; PI3K, phosphatidylinositol 3-kinase; mTOR, the mechanistic target of rapamycin; AKT, protein kinase B.
(A) Schematic diagrams of SEA, SEB, SEC2, and TSST-1 crystal structures. Domain 1 contains highly conserved, low-affinity binding sites for TCR Vβ and MHCII at generic sites. (B) Hypothetical model of the MHCII-SEC3-TCR complex based on modeling predicted from the crystal structures of the SEC3-HLA-DR1 and SEC3-Vβ complexes.
Comparison of the cysteine loop and adjacent sequences between highly emetic and weakly emetic SEs in the monkey feeding assay.
Regulation of SE expression by the agr locus and other interacting regulatory genes and gene products (not drawn to scale) in S. aureus. The blue arrow indicates activation, and the red line indicates inhibition. A letter “P” in a red dot indicates phosphorylation.