Staphylococcal superantigen-like protein-7 (SSL-7) |
SIgA |
It
enhances the ability to colonize in mucosal environments such as the
nasal passage by binding to SIgA. |
[28] |
Evasion proteins against innate immune |
Target |
Function/ effect on
immune system |
Ref. |
Proteins including extracellular adherence protein (Eap),
collagen-binding protein (Cna) and serine-aspartate repeat protein E
(SdrE) |
C1q in classical pathway, lectin pathway, alternative pathway |
They inhibit the activation of the complement system by blocking these
three pathways. |
[36-38] |
Staphylococcal Protein A (SpA) |
IgG |
It results in the inverted
tagging and blocking of the C1q binding sites, preventing complement
initiation. |
[30] |
|
B cells |
It interferes in B-cells activation and proliferation,
reducing the phagocytosis of MRSA, impeding antibody production and
causing disordered activation, finally leading to the death of the B
cells. |
[44, 45] |
Staphylococcal complement inhibitor (SCIN) |
C3 convertases |
It
binds and stabilizes C3 convertases, interfering with the activation of
the complement system. |
[32] |
Extracellular fibrinogen-binding protein (Efb); its homolog
extracellular complement-binding protein (Ecb) |
C3 |
They prevent C3
from recognition by macrophages. |
[33] |
Second Immunoglobulin-binding protein (Sbi) |
IgG |
It avoids
neutrophil-mediated opsonophagocytosis. |
[46] |
|
C3 |
It binds to complement, leading to the cleavage and consumption
of complement Factor C3. |
[34] |
Factor I |
C3b |
It mediates C3b cleavage to iC3b, inhibiting initiation
of the alternative pathway as well the activation of the terminal
complement cascade. |
[35] |
Staphylokinase (SAK) |
Complement |
It digests IgG and complement. |
[25] |
chemotaxis inhibitory protein of staphylococci (CHIPS) |
C5aR |
It binds
to C5aR to evade complement. |
[29] |
|
FPR1 |
It binds to FPR1 to block the chemotaxis of neutrophils. |
[47] |
Staphylococcal superantigen-like protein-7 (SSL-7) |
C5 |
It
inhibits the opsonization of bacteria by inhibiting the cleavage of C5. |
[31] |
Proteases, e.g., staphopain A (Scp A), aureolysin (Aur) |
Complement |
They degrade complement preventing opsonization and bacteria lysis. |
[30] |
|
Neutrophils |
ScpA inhibits the chemotaxis and activation of
neutrophils. |
[48] |
Staphylococcal superantigen-like 5 (SSL5) |
P-selectin
glycoprotein ligand 1 (PSGL-1) |
It binds to PSGL-1 of sialyl Lewis X,
thus blocking PSGL-1 interaction with the natural ligand P-selectin and
abrogating neutrophil rolling on endothelial cells. |
[39] |
Proteins including extracellular adherence protein (Eap) |
Intercellular
adhesion molecule 1 (ICAM-1) |
It binds to ICAM-1, blocking the
neutrophil recruitment to the infection site. |
[32] |
Staphylococcal complement inhibitor (SCIN), chemotaxis inhibitory
protein of staphylococci (CHIPS) |
Neutrophils |
They impair neutrophil
recruitment as chemotaxis inhibitors. |
[49] |
Nuc |
NETs |
It is a nuclease produced by MRSA to evade NETs. |
[50, 51] |
Panton-Valentine leukocidin (PVL) |
Neutrophils |
It causes neutrophil
lysis at the dose of 0.04 µg/mL. |
[52] |
Phenol-soluble-modulins (PSMs) |
Neutrophils |
They directly kill
neutrophils mainly by disrupting the membrane. |
[41] |