Pneumococcal peptidoglycan-polysaccharides induce the expression of interleukin-8 in airway epithelial cells by way of nuclear factor-kappaB, nuclear factor interleukin-6, or activation protein-1 dependent mechanisms.

Abstract

Cell envelope compounds of bacteria trigger immune and inflammatory reactions by way of chemokines/cytokines. In this study, we demonstrated that pneumococcal peptidoglycan-polysaccharides (PGPS) induced the production of interleukin (IL)-8 by way of nuclear factor (NF)-kappaB, nuclear factor interleukin (NF-IL)6, and activation protein (AP)-1 dependent mechanisms in the human bronchial epithelial cells (NL-20) in a dose- and time-dependent manner in vitro, and the mutation of either the NF-kappaB, NF-IL6, or AP-1 binding sites in the promoter of IL-8 abrogated the IL-8 transcriptional activity. In a similar way, lipopolysaccharides induced the promoter activation of IL-8 in NL-20. However, the PGPS-induced IL-8 promoter activation in rodent middle ear epithelial cells required NF-kappaB and NF-IL6 but not AP-1.