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Updated: Aug 24, 2026
Polarization and Characterization of M1 and M2 Human Monocyte-Derived Macrophages on Implant Surfaces
Published on: December 6, 2024
Differential gene induction in macrophage-like human cells by two types of Porphyromonas gingivalis: a microarray
Maiko Oshikawa1, Naoyuki Sugano, Ryosuke Koshi
1Nihon University Graduate School of Dentistry, Tokyo, Japan.
Abstract:
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.
Insights
Porphyromonas gingivalis (P.g.) FimA type II (Pg-II) triggers a weaker host immune response than FimA type I (Pg-I). This suggests Pg-II may be less pathogenic, impacting periodontal disease progression.
Area of Science:
- Microbiology
- Immunology
- Genomics
Background:
- FimA clonal variation in Porphyromonas gingivalis (P.g.) is linked to periodontopathogenicity.
- Understanding P.g. virulence factors is crucial for managing periodontal disease.
Purpose of the Study:
- To compare the host gene expression profiles induced by two P.g. FimA types: type I (Pg-I) and type II (Pg-II).
- To elucidate the differential host responses to distinct P.g. FimA variants.
Main Methods:
- Gene expression profiling of U937 macrophage cells infected with Pg-I and Pg-II using microarray analysis.
- Bioinformatics analysis, including hierarchical and K-means clustering, to interpret gene expression patterns.
Main Results:
- Pg-II infection resulted in gene expression patterns similar to uninfected controls, indicating a low host response.
- Pg-I dominance clusters included genes related to cell signaling, communication, receptors, and adhesion.
- Pg-II dominance clusters were less prominent, suggesting suppressed host immune activation.
Conclusions:
- Porphyromonas gingivalis FimA type II induces a significantly lower host gene expression response compared to FimA type I.
- The reduced host response to Pg-II suggests a potentially lower virulence or distinct pathogenic mechanism.
- These findings contribute to understanding the role of FimA variation in P.g. pathogenicity.
