Besides receptor polymorphisms, several other scenarios may lead to increased bacterial ligand binding to CEACAMs. Both Nm and Hi CEACAM-binding ligands (Opa and P5) are known to undergo antigenic variation. Thus, in any population, antigenic/structural variants are present and may be selected for during the course of host colonization and subsequent pathogenesis (Virji et al., 1996a; Duim et al., 1997; Meyers et al., 2003) . The receptor repertoire and subtypes may select bacteria capable of binding with high affinity. As mentioned above, upregulation of receptor expression on target cells may also increase bacterial binding affinity. In such cases, high affinity interactions result in cellular invasion, whereas lower affinity or load of bacteria may not proceed beyond surface adhesion (Tran Van Nhieu and Isberg, 1993; Bradley et al., 2005) . The expression of CEACAMs on normal epithelia of the respiratory tract has been reported, which would allow bacterial attachment and possible subsequent penetration into these tissues (Tsutsumi et al., 1990; Virji, 2001) . Following exposure to cytokines such as IFN-g or TNF-a, CEACAM expression by colonic carcinoma cells has been shown to increase (Fahlgren et al., 2003) . In addition, certain viral infections have also been shown to upregulate CEACAM1 expression in several epithelial cell lines (Avadhanula et al., 2006) . Increased cytokine levels following viral infection could lead to increased CEACAM expression and bacterial association with respiratory epithelia and subsequent invasion of deeper tissue by these organisms. Such a situation may explain the epidemiological association of increased incidence of Nm and Hi infections following certain viral infections (Cartwright et al., 1991; Takala et al., 1993) .