Neutrophils alter epithelial response to Porphyromonas gingivalis in a gingival crevice model

Summary A gingival crevice model (epithelial cell–Porphyromonas gingivalis–neutrophil) was established and used to profile gingipain, matrix metalloproteinase (MMP), MMP mediators [neutrophil gelatinase‐associated lipocalin (NGAL) and tissue inhibitor of metalloproteinases 1 (TIMP‐1)] and cytokine networks. Smoking is the primary environmental risk factor for periodontitis. Therefore, the influence of cigarette smoke extract (CSE) was also monitored in the same model. Porphyromonas gingivalis alone induced low levels of interleukin‐1β and interleukin‐8 from epithelial cells, but high levels of both cytokines were produced on the addition of neutrophils. Exposure to CSE (100 and 1000 ng ml−1 nicotine equivalency) significantly compromised P. gingivalis‐induced cytokine secretion (both P