TY - JOUR
T1 - Proinflammatory gene expression in mouse ST2 cell line in response to infection by Porphyromonas gingivalis
AU - Ohno, Takashi
AU - Okahashi, Nobuo
AU - Kawai, Shinji
AU - Kato, Takahiro
AU - Inaba, Hiroaki
AU - Shibata, Yasuko
AU - Morisaki, Ichijiro
AU - Abiko, Yoshimitsu
AU - Amano, Atsuo
N1 - Funding Information:
We thank Dr. Koji Nakayama (Nagasaki University Graduate School of Biomedical Sciences) for providing the mutant strains of P. gingivalis. We also thank Asayo Imaoka (Nihon University School of Dentistry at Matsudo) for the expert support with the microarray analysis. This work was a part of the 21st Century COE program entitled “Origination of Frontier BioDentistry” at Osaka University Graduate School of Dentistry supported by the Ministry of Education, Culture, Sports, Science and Technology of Japan, and also supported by an Academic Frontier Project for Private Universities Matching Fund (2001–2005) and a grant-in-aid for Scientific Research (#A1–16209063) from Ministry of Education, Culture, Sports, Science and Technology.
PY - 2006/4
Y1 - 2006/4
N2 - Porphyromonas gingivalis is a predominant periodontal pathogen, whose infection causes inflammatory responses in periodontal tissue and alveolar bone resorption. Various virulence factors of this pathogen modulate host innate immune responses. It has been reported that gingipains degrade a wide variety of host cell proteins, and fimbriae are involved in bacterial adhesion to and invasion of host cells. In the present study, we profiled ST2 stromal cell gene expression following infection with the viable P. gingivalis strain ATCC33277 as well as with its gingipain- and fimbriae-deficient mutants, using microarray technology and quantitative real-time polymerase chain reaction. Using a mouse array of about 20,000 genes, we found that infection with the wild strain elicited a significant upregulation (greater than 2-fold) of expression of about 360 genes in ST2 cells, which included the chemokines CCL2, CCL5, and CXCL10, and other proinflammatory proteins such as interleukin-6 (IL-6) and matrix metalloproteinase-13 (MMP-13). Further, infection with the gingipain-deficient mutant elicited a reduced expression of the CXCL10, IL-6 and MMP-13 genes, suggesting that gingipains play an important role in inducing the expression of those genes following P. gingivalis infection. On the other hand, the pattern of global gene expression induced by the fimbriae-deficient mutant was similar to that by the wild strain. These results suggest that P. gingivalis infection induces gene expression of a wide variety of proinflammatory proteins in stromal cells/osteoblasts, and gingipains may be involved in inducing several of the proinflammatory factors.
AB - Porphyromonas gingivalis is a predominant periodontal pathogen, whose infection causes inflammatory responses in periodontal tissue and alveolar bone resorption. Various virulence factors of this pathogen modulate host innate immune responses. It has been reported that gingipains degrade a wide variety of host cell proteins, and fimbriae are involved in bacterial adhesion to and invasion of host cells. In the present study, we profiled ST2 stromal cell gene expression following infection with the viable P. gingivalis strain ATCC33277 as well as with its gingipain- and fimbriae-deficient mutants, using microarray technology and quantitative real-time polymerase chain reaction. Using a mouse array of about 20,000 genes, we found that infection with the wild strain elicited a significant upregulation (greater than 2-fold) of expression of about 360 genes in ST2 cells, which included the chemokines CCL2, CCL5, and CXCL10, and other proinflammatory proteins such as interleukin-6 (IL-6) and matrix metalloproteinase-13 (MMP-13). Further, infection with the gingipain-deficient mutant elicited a reduced expression of the CXCL10, IL-6 and MMP-13 genes, suggesting that gingipains play an important role in inducing the expression of those genes following P. gingivalis infection. On the other hand, the pattern of global gene expression induced by the fimbriae-deficient mutant was similar to that by the wild strain. These results suggest that P. gingivalis infection induces gene expression of a wide variety of proinflammatory proteins in stromal cells/osteoblasts, and gingipains may be involved in inducing several of the proinflammatory factors.
KW - Gene expression
KW - Inflammation
KW - Microarray
KW - Osteoblast
KW - Periodontitis
KW - Porphyromonas gingivalis
KW - Stromal cell
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U2 - 10.1016/j.micinf.2005.10.021
DO - 10.1016/j.micinf.2005.10.021
M3 - Article
C2 - 16476562
AN - SCOPUS:33646146468
VL - 8
SP - 1025
EP - 1034
JO - Microbes and Infection
JF - Microbes and Infection
SN - 1286-4579
IS - 4
ER -