Carcinoembryonic antigen (CEA)-related cell adhesion molecules are co-expressed in the human lung and their expression can be modulated in bronchial epithelial cells by non-typable Haemophilus influenzae, Moraxella catarrhalis, TLR3, and type I and II interferons

Klaile, Esther; Klassert, Tilman E; Scheffrahn, Inka; Müller, Mario M; Heinrich, Annina; Heyl, Kerstin A; Dienemann, Hendrik; Grünewald, Christiane; Bals, Robert; Singer, Bernhard B; Slevogt, Hortense

The up-regulation via viruses and the effects of the inflammatory cytokine IFNγ imply a more general role for CEACAM1 and CEACAM5 in the inflammatory response to infection, and also in the spatial and temporal association between bacterial and viral infections. One of the underlying mechanisms for the colonization of COPD patients by M. catarrhalis and NTHi may consist of the up-regulation of specific host receptors, i.e. CEACAM1, by viral infections, as described for several CEA family receptors [55, 66, 68, 77] . For pathogenic Neisseria it was demonstrated that increased CEACAM expression levels correlated with an increase in bacterial invasion [55, 79] . Once established, M. catarrhalis and NTHi themselves are also able to increase the expression of their receptor CEACAM1. Whether the starting point is a viral or bacterial pathogen, the result is a continual cycle of infection-induced increase in cytokine levels and, subsequently, receptor expression which then promotes bacterial invasion. Since viruses also recruit CEACAMs, elevated CEACAM expression might aid viral infection as well [80, 81] .