Table 1.

Host pressures and bacterial factors to counteract them

Host pressure	Bacterial countering factor
Anionic mucus prevents bacterial binding to epithelial surface	Polysaccharide capsule repels mucus; neuraminidases degrade mucus
Transporters limit free carbon on the mucosal surface	Glycosidases liberate carbon sources for uptake by carbon transporters; bacteria induce inflammation to promote secretion of substrates such as sialylated mucins
Lipocalin-2 binds siderophores	Nonsiderophore mechanisms obtain iron; nonenterobactin siderophores resist lipocalin-2 binding
Actively increases toxic zinc while limiting manganese	Zinc/manganese transporters
Mucociliary flow clears bacteria mechanically	Attach to host cells and tissues
Opsonophagocytosis	Antiphagocytic polysaccharide capsule
Mucosal secreted IgA1	IgA1 protease
Humoral immunity	Evade antibodies through antigenic variation
Recognizes bacterial LPS	Mask LPS with the host mimic ChoP
Neutrophil influx	Polysaccharide capsule, toxins
Inflammatory response to colonization	Exploit host responses to drive transmission
Hosts a diverse beneficial commensal flora	Displace or compete with host microbiota
TLR-mediated epithelial opening allows immune cell infiltration	Exploit epithelial opening to promote invasion and persistence
Specialized M cells sample lumen for antigens	Enter through M cells as portal for invasion
Creates microniches with opposing selective pressures	Phenotypic or phase variation generates diversity within a bacterial population

Abbreviations: ChoP, phosphorylcholine; LPS, lipopolysaccharide; TLR, Toll-like receptor.