Harmonisation of Regulatory Oversight in Biotechnology Safety Assessment of Transgenic Organisms in the Environment, Volume 5..

I.1. BACTERIA: PATHOGENICITY FACTORS – 47

the bacteria. Its activity also causes invasion, hence hyaluronidase is also seen as an
invasin (Table 1.2).

Table 1.3. Bacterial proteins that act as immunomodulator

Bacteria/disease Immunomodulator Action Reference

Borrelia burgdorferi/Lyme

disease

OspE Binds factor H McDowell et al. (2004)

Enterococcus faecalis Capsular polysaccharide Resistance to

opsonophagocytic killing

Hancock and Gilmore (2002)

Francisella tularensis/Tularemia? Survive and multiply inside

macrophages

Maier et al. (2007)

Streptococcus pneumoniae PspA Inhibitor of factor B mediating

complement activation and

opsonisation

Tu et al. (1999)

Group A Streptococcus

(S. pyogenes)

Fba Binds factor H and fH-like

protein, contribute to

phagocytosis resistance

Wei et al. (2005)

Streptococci Protein M Alteration of

opsonophagocytosis by

recruitment of factor H

Jarva et al. (2003)

Group B Streptococcus (GBS) Capsule Protects from opsonisation by

C3. ß-protein binds factorH

Rubens et al. (1987);

Jarva et al. (2003)

Group B Streptococcus (GBS) CspA (serine protease-

like)

Evasion of

opsonophagocytosis

Harris et al. (2003)

Lysteria monocytogenes Lysterio-lysin O Evasion of phagosome Schnupf and Portnoy (2007)

Neisseria gonorrhoea Por 1A Binds factor H, C4 bp,

mediates serum resistance

Ram et al. (1998; 2001)

Neisseria meningitides Bind factor H Avoids lysis by complement

system

Schneider et al. (2006)

Staphylococcus aureus Secretes extracellular

adherence protein (EAP)

Binds to Inter-Cellular

Adhesion Molecule (ICAM)-1,

fibrinogen, vitronectin

resulting in the disruption of

the leukocyte recruitment

Athanasopoulos et al. (2006)

Yersinia spp. Yop E, T A, H and Yop J Block phagocytosis and

suppress inflammatory

mediators

Fällman and Gustavsson

(2005)

Yersinia enterocolica YadA Alteration of

opsonophagocytosis by

recruitement of factor H

China et al. (1993)

Kinases

Streptokinase and staphylokinase are produced by streptococci and staphylococci,
respectively. These enzymes convert inactive plasminogen to plasmin which digests
fibrin and prevents clotting of the blood. The relative absence of fibrin in bacterial lesions
allows more rapid diffusion of the bacteria (Gladysheva et al., 2003). Like hyaluronidase,
kinases also cause invasion, and are seen as invasins (Table 1.2).

Sialidases/neuraminidase

Extracellular sialidases or neuraminidases, produced by various pathogens, have the
ability to hydrolyse the sialic acid residues located on many mammalian cell membranes
(Rood, 1998). The neuraminidase produced by Mannheimia haemolytica decreases the
viscosity of respiratory mucus, thus providing the bacteria with greater access to the cell
surface (Zecchinon, Fett and Desmecht, 2005).