Table 1.
Summary of bacterial resistance mechanisms to CAMPs
Mechanism of resistance | Product name/gene | Organism | Virulence of the mutant | Reference |
---|---|---|---|---|
CAMP binding and inactivation | Staphylokinase | S. aureus | ↑ systemic infection | [122, 123] |
SIC | S. pyogenes | ↓ systemic infection | [32] | |
CAMP proteolytic cleavage | V8 protease | S. aureus | ND | [34] |
Aureolysin | S. aureus | ND | [34] | |
ZapA | P. mirabilis | ↓ colonization of urinary tract | [35, 124] | |
Streptopain SpeB | S. pyogenes | ND | [35, 125] | |
Elastase LasA | P. aeruginosa | ↓ chronic infection in rat | [35, 126, 127] | |
Capsular polysaccharides | PIA, PGA | S. epidermidis | ↓virulence | [38–40, 128, 129] |
Capsule synthesis gene cluster | N. meningitidis | ↓virulence | [130–132] | |
K. pneumoniae | ↓ virulence in murine model of pneumonia | [133–135] | ||
Surface charge neutralization | S. aureus |
↓ virulence in mouse, ↓ virulence in rabbit model of endocarditis |
[53, 54, 136] | |
d-alanine modification of teichoic acids | dltABCD | S. pyogenes | ND | [58, 137] |
L. monocytogenes | ↓ mouse model of infection | [55] | ||
L. reuteri | ↓ colonization of mouse | [69] | ||
l-Lysine modification of PG | mprF | S. aureus | ↓ virulence in mouse model of infection | [53, 85, 138] |
↓ virulence rabbit model of endocarditis | ||||
Lipid A modifications Aminoarabinose Ethanolamine | pmrAB, pmrE, pmrFHIJKL pmrC, | S. enterica ser. typhimurium | ↓ virulence in mice | [98, 100, 139, 140] |
Decrease in membrane fluidity | ||||
Modification of lipid A acylation | pagP, pagL, | S. enterica ser. typhimurium | No phenotype | [141, 142] |
Production of carotenoids | crtOPQMN | S. aureus | ↓virulence in subcutaneous abscess model | [143–145] |
Presence of efflux pumps | qacA | S. aureus | ND | [16, 119, 146] |
CAMP expulsion | mtrCDE | N. gonorrhoeae | ↓ virulence in murine model of infection | [117, 147, 148] |
↑ increased virulence, ↓ decreased virulence or virulence attenuated, ND not determined