Several studies have provided clinical evidence that FimA clonal variation may contribute to the periodontopathogenicity of Porphyromonas gingivalis (P.g.). We studied the gene expression profiling of the macrophage-like human cell line U937 after infection of two types of P.g. (fimA type I; Pg-I and fimA type II; Pg-II) using microarray. Of 1088 genes examined, 394 genes were detectable. Bioinformatics algorithms were used to analyze the detectable genes. Hierarchical clustering analysis showed that gene expression patterns of Pg-II and the control (no infection) were grouped together. K-means clustering grouped 79 genes into Pg-II dominance and 88 genes into Pg-I dominance. A large number of genes related to cell signaling, extracellular communication proteins, cell receptors (by ligands), protein turnover and cell adhesion receptors/proteins were grouped into clusters of Pg-I dominance. Our results indicate that compared with Pg-I, Pg-II induces a low host response as measured by its weak induction of gene expression.