S. aureus Enterotoxin Type B Toxoid

Staphylococci are Gram-positive bacteria. It is widely distributed in nature, and only a few are pathogenic. Among them, Staphylococcus aureus (SA) is the most pathogenic and can secrete more than 33 kinds of Staphylococcus aureus enterotoxins (SE), such as SEA, SEB, SEC, SED, SEE, SEI and enterotoxin G, etc. SEB has the strongest toxicity and stability, is not degraded by trypsin, and affects the body's immune regulation. Under SEB stimulation, myeloid differentiation factor 88 (MyD88) and protein kinase C (PKC) in animal immune cells are phosphorylated, thereby activating IκB kinase (IKK), causing nuclear factor-κB (NF-κB) to gain activity and targets the cell nucleus and mediates the secretion of inflammatory cytokines such as interleukins IL-1, IL-2, IL-6, tumor necrosis factor α (TNF-α), and interferon γ (IFN-γ), triggering inflammation in the body reaction. In addition, SEB can activate signaling cascades mediated by mitogen-activated protein kinases (MAPKs) in immune cells, inducing nuclear activation through p38MAPK, c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase (ERK) pathways. The expression of nuclear factor of activated T cells (NFAT) and activation protein-1 (AP-1) regulates the proliferation, differentiation, apoptosis and other reactions of immune cells.

Figure 1. S. aureus survival strategies during infection.( Source: Liu GY., 2009)

SEB is a single-chain polypeptide and consists of 239 amino acid residues. Its tertiary structure is composed of two domains, which are the N-terminal residues 1 to 120 and contain 3 α-helices and 2 β-sheets. The structural domain of the C-terminal C-terminal residues 127 to 239 contains 2 α-helices, 2 short β-sheets and 2 β-sheets. This special structure determines the thermal stability and acid resistance of SEB. Studies have found that SEB is still active under acidic conditions whether it is boiled at 100°C for 30 minutes, and can resist the hydrolysis of proteases in the gastrointestinal tract. In animals, SEB does not require antigen-presenting cells (APC) processing. Residues 43 to 45, 67, 89, and 115 of the SEBN terminal domain pass through hydrogen bonds, charges, and hydrophobic layers. It can bind unrestrictedly to (MHC) class II molecules on the surface of APC through interactions and other methods; at the same time, the larger domain composed of residues 20, 22, 23, 177 and 210 in SEB, as well as the 60, 90 and A smaller domain consisting of 91 residues, both of which can directly bind to the T cell receptor (TCR) Vβ chain to form the MHCII-SEB-TCR complex structure. This special combination makes it function as a superantigen. A small amount of SEB can activate a large number of T cells and secrete inflammatory cytokines such as IFN-γ and TNF-α.

SEB belongs to the superantigen family. After animal infection, it can induce massive proliferation of T cells and the secretion of cytokines such as IL-1, IL-2, IL-6, TNF-α and IFN-γ, causing various inflammations such as dermatitis and organ damage. The study found that compared with the control group, the degree of proximal small intestinal injury in SA-infected mice was significantly higher than that in the control group. It can be seen that SEB plays an important role in intestinal damage caused by SA infection. SEB can also make animal immune cells unresponsive to antigen stimulation, thereby inducing immune tolerance and affecting the body's normal immune response. Studies have shown that when mice treated with 500ng SEB were then sensitized with Ova, the number of immune cells in the respiratory tract was significantly reduced, and the levels of pro-inflammatory factors were significantly reduced. T cells and effector T cells generated by SEB activation were respectively added to stimulants such as concanavalin, lipopolysaccharide, and IL-2 to co-culture for 3 days. The results showed that the response of T cells to stimulators was significantly inhibited and their proliferation ability was significantly reduced. TM cells that can recognize Ova were co-cultured with APC and SEB. After 14 hours, they were stimulated again with APC with Ova. The TM cells showed obvious unresponsiveness. It can be seen that SEB not only affects the response of normal lymphocytes to antigens, but also inhibits the response of TM to restimulation by antigens, causing the body to develop an immune tolerance response and leading to animal immune system disorders.

S. aureus Toxoid B
Staphylococcal Enterotoxin B Toxoid
SEB Toxoid
Staphylococcal Enterotoxin B Immunogen
SaTox B Toxoid
Staphylococcal Enterotoxin B Antigen
Staphylococcal Enterotoxin B Immunogen