The Experts below are selected from a list of 252 Experts worldwide ranked by ideXlab platform
Hirotaka Kuwata - One of the best experts on this subject based on the ideXlab platform.
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Rothia dentocariosa induces tnf alpha production in a tlr2 dependent manner
Pathogens and Disease, 2014Co-Authors: Hideo Kataoka, Makoto Taniguchi, Haruka Fukamachi, Takafumi Arimoto, Hirobumi Morisaki, Hirotaka KuwataAbstract:Previous work suggested that Rothia dentocariosa is associated with periodontal inflammatory disease. However, little is known about the pathogenicity of this bacterium. To characterize host response to this bacterium, we measured (via ELISA) the amount of TNF-α in the culture supernatant following the stimulation of THP-1 cells (a human acute monocytic leukemia cell line) with R. dentocariosa cells (ATCC14189 and ATCC14190). Exposure to bacterial cells induced the production of TNF-α in a dose-dependent manner. The bacterial induction of TNF-α in THP-1 cells was mediated by the Toll-like receptor 2 (TLR2), as demonstrated by gene-specific knockdown via siRNA, which successfully suppressed TLR2 expression and significantly inhibited the production of TNF-α in the culture supernatant. To confirm the role of TLR2, we examined TLR2-dependent NF-κB activation by R. dentocariosa cells in a distinct cell line. Specifically, HEK293 cells were transiently cotransfected with the human TLR2 gene and an NF-κB-dependent luciferase-encoding reporter gene. The bacterial cells induced NF-κB activation in the transfected HEK293 cells in a dose-dependent manner. In contrast, bacterial cells failed to induce NF-κB activation in cells transfected with pEF6 control vector. Taken together, these results suggest that R. dentocariosa induces host TNF-α production by a TLR2-dependent mechanism.
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Rothia dentocariosa induces TNF‐alpha production in a TLR2‐dependent manner
Pathogens and disease, 2013Co-Authors: Hideo Kataoka, Makoto Taniguchi, Haruka Fukamachi, Takafumi Arimoto, Hirobumi Morisaki, Hirotaka KuwataAbstract:Previous work suggested that Rothia dentocariosa is associated with periodontal inflammatory disease. However, little is known about the pathogenicity of this bacterium. To characterize host response to this bacterium, we measured (via ELISA) the amount of TNF-α in the culture supernatant following the stimulation of THP-1 cells (a human acute monocytic leukemia cell line) with R. dentocariosa cells (ATCC14189 and ATCC14190). Exposure to bacterial cells induced the production of TNF-α in a dose-dependent manner. The bacterial induction of TNF-α in THP-1 cells was mediated by the Toll-like receptor 2 (TLR2), as demonstrated by gene-specific knockdown via siRNA, which successfully suppressed TLR2 expression and significantly inhibited the production of TNF-α in the culture supernatant. To confirm the role of TLR2, we examined TLR2-dependent NF-κB activation by R. dentocariosa cells in a distinct cell line. Specifically, HEK293 cells were transiently cotransfected with the human TLR2 gene and an NF-κB-dependent luciferase-encoding reporter gene. The bacterial cells induced NF-κB activation in the transfected HEK293 cells in a dose-dependent manner. In contrast, bacterial cells failed to induce NF-κB activation in cells transfected with pEF6 control vector. Taken together, these results suggest that R. dentocariosa induces host TNF-α production by a TLR2-dependent mechanism.
Reinhard Zbinden - One of the best experts on this subject based on the ideXlab platform.
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native and prosthetic valve endocarditis caused by Rothia dentocariosa diagnostic and therapeutic considerations
Infection, 1997Co-Authors: D Binder, U Widmer, M Opravil, M Krause, Reinhard ZbindenAbstract:Three cases, one each of native valve, prosthetic valve and composite graft endocarditis caused byRothia dentocariosa are described. The first patient presented with multiple brain abscesses and severe congestive heart failure due to destructive endocarditis with large vegetations on the mitral valve. He died shortly after emergency valve replacement. Gram-positive coccoid rods were identified in the vegetations of the excised mitral valve. The second patient had aR. dentocariosa endocarditis of a prosthetic aortic valve that was treated empirically with netilmicin and teicoplanin, due to an allergy to penicillin. Both antibiotics were replaced according to susceptibility testingin vitro with rifampin and ciprofloxacin, and the endocarditis was cured within 9 weeks. The third patient presented with a circular root abscess of an aortic composite graft that was successfully treated with rifampin and ceftriaxone without surgery. All patients had extensive periodontal disease which was thought to be responsible for hematogenic spread and seeding of the microorganism. The microbiological identification and antibiotic resistance pattern of the isolates, as well as therapeutic implications are discussed.
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Native and prosthetic valve endocarditis caused byRothia dentocariosa: Diagnostic and therapeutic considerations
Infection, 1997Co-Authors: D Binder, U Widmer, M Opravil, M Krause, Reinhard ZbindenAbstract:Three cases, one each of native valve, prosthetic valve and composite graft endocarditis caused by Rothia dentocariosa are described. The first patient presented with multiple brain abscesses and severe congestive heart failure due to destructive endocarditis with large vegetations on the mitral valve. He died shortly after emergency valve replacement. Gram-positive coccoid rods were identified in the vegetations of the excised mitral valve. The second patient had a R. dentocariosa endocarditis of a prosthetic aortic valve that was treated empirically with netilmicin and teicoplanin, due to an allergy to penicillin. Both antibiotics were replaced according to susceptibility testing in vitro with rifampin and ciprofloxacin, and the endocarditis was cured within 9 weeks. The third patient presented with a circular root abscess of an aortic composite graft that was successfully treated with rifampin and ceftriaxone without surgery. All patients had extensive periodontal disease which was thought to be responsible for hematogenic spread and seeding of the microorganism. The microbiological identification and antibiotic resistance pattern of the isolates, as well as therapeutic implications are discussed.
Hideo Kataoka - One of the best experts on this subject based on the ideXlab platform.
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Rothia dentocariosa induces tnf alpha production in a tlr2 dependent manner
Pathogens and Disease, 2014Co-Authors: Hideo Kataoka, Makoto Taniguchi, Haruka Fukamachi, Takafumi Arimoto, Hirobumi Morisaki, Hirotaka KuwataAbstract:Previous work suggested that Rothia dentocariosa is associated with periodontal inflammatory disease. However, little is known about the pathogenicity of this bacterium. To characterize host response to this bacterium, we measured (via ELISA) the amount of TNF-α in the culture supernatant following the stimulation of THP-1 cells (a human acute monocytic leukemia cell line) with R. dentocariosa cells (ATCC14189 and ATCC14190). Exposure to bacterial cells induced the production of TNF-α in a dose-dependent manner. The bacterial induction of TNF-α in THP-1 cells was mediated by the Toll-like receptor 2 (TLR2), as demonstrated by gene-specific knockdown via siRNA, which successfully suppressed TLR2 expression and significantly inhibited the production of TNF-α in the culture supernatant. To confirm the role of TLR2, we examined TLR2-dependent NF-κB activation by R. dentocariosa cells in a distinct cell line. Specifically, HEK293 cells were transiently cotransfected with the human TLR2 gene and an NF-κB-dependent luciferase-encoding reporter gene. The bacterial cells induced NF-κB activation in the transfected HEK293 cells in a dose-dependent manner. In contrast, bacterial cells failed to induce NF-κB activation in cells transfected with pEF6 control vector. Taken together, these results suggest that R. dentocariosa induces host TNF-α production by a TLR2-dependent mechanism.
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Rothia dentocariosa induces TNF‐alpha production in a TLR2‐dependent manner
Pathogens and disease, 2013Co-Authors: Hideo Kataoka, Makoto Taniguchi, Haruka Fukamachi, Takafumi Arimoto, Hirobumi Morisaki, Hirotaka KuwataAbstract:Previous work suggested that Rothia dentocariosa is associated with periodontal inflammatory disease. However, little is known about the pathogenicity of this bacterium. To characterize host response to this bacterium, we measured (via ELISA) the amount of TNF-α in the culture supernatant following the stimulation of THP-1 cells (a human acute monocytic leukemia cell line) with R. dentocariosa cells (ATCC14189 and ATCC14190). Exposure to bacterial cells induced the production of TNF-α in a dose-dependent manner. The bacterial induction of TNF-α in THP-1 cells was mediated by the Toll-like receptor 2 (TLR2), as demonstrated by gene-specific knockdown via siRNA, which successfully suppressed TLR2 expression and significantly inhibited the production of TNF-α in the culture supernatant. To confirm the role of TLR2, we examined TLR2-dependent NF-κB activation by R. dentocariosa cells in a distinct cell line. Specifically, HEK293 cells were transiently cotransfected with the human TLR2 gene and an NF-κB-dependent luciferase-encoding reporter gene. The bacterial cells induced NF-κB activation in the transfected HEK293 cells in a dose-dependent manner. In contrast, bacterial cells failed to induce NF-κB activation in cells transfected with pEF6 control vector. Taken together, these results suggest that R. dentocariosa induces host TNF-α production by a TLR2-dependent mechanism.
D Binder - One of the best experts on this subject based on the ideXlab platform.
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native and prosthetic valve endocarditis caused by Rothia dentocariosa diagnostic and therapeutic considerations
Infection, 1997Co-Authors: D Binder, U Widmer, M Opravil, M Krause, Reinhard ZbindenAbstract:Three cases, one each of native valve, prosthetic valve and composite graft endocarditis caused byRothia dentocariosa are described. The first patient presented with multiple brain abscesses and severe congestive heart failure due to destructive endocarditis with large vegetations on the mitral valve. He died shortly after emergency valve replacement. Gram-positive coccoid rods were identified in the vegetations of the excised mitral valve. The second patient had aR. dentocariosa endocarditis of a prosthetic aortic valve that was treated empirically with netilmicin and teicoplanin, due to an allergy to penicillin. Both antibiotics were replaced according to susceptibility testingin vitro with rifampin and ciprofloxacin, and the endocarditis was cured within 9 weeks. The third patient presented with a circular root abscess of an aortic composite graft that was successfully treated with rifampin and ceftriaxone without surgery. All patients had extensive periodontal disease which was thought to be responsible for hematogenic spread and seeding of the microorganism. The microbiological identification and antibiotic resistance pattern of the isolates, as well as therapeutic implications are discussed.
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Native and prosthetic valve endocarditis caused byRothia dentocariosa: Diagnostic and therapeutic considerations
Infection, 1997Co-Authors: D Binder, U Widmer, M Opravil, M Krause, Reinhard ZbindenAbstract:Three cases, one each of native valve, prosthetic valve and composite graft endocarditis caused by Rothia dentocariosa are described. The first patient presented with multiple brain abscesses and severe congestive heart failure due to destructive endocarditis with large vegetations on the mitral valve. He died shortly after emergency valve replacement. Gram-positive coccoid rods were identified in the vegetations of the excised mitral valve. The second patient had a R. dentocariosa endocarditis of a prosthetic aortic valve that was treated empirically with netilmicin and teicoplanin, due to an allergy to penicillin. Both antibiotics were replaced according to susceptibility testing in vitro with rifampin and ciprofloxacin, and the endocarditis was cured within 9 weeks. The third patient presented with a circular root abscess of an aortic composite graft that was successfully treated with rifampin and ceftriaxone without surgery. All patients had extensive periodontal disease which was thought to be responsible for hematogenic spread and seeding of the microorganism. The microbiological identification and antibiotic resistance pattern of the isolates, as well as therapeutic implications are discussed.
Makoto Taniguchi - One of the best experts on this subject based on the ideXlab platform.
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Rothia dentocariosa induces tnf alpha production in a tlr2 dependent manner
Pathogens and Disease, 2014Co-Authors: Hideo Kataoka, Makoto Taniguchi, Haruka Fukamachi, Takafumi Arimoto, Hirobumi Morisaki, Hirotaka KuwataAbstract:Previous work suggested that Rothia dentocariosa is associated with periodontal inflammatory disease. However, little is known about the pathogenicity of this bacterium. To characterize host response to this bacterium, we measured (via ELISA) the amount of TNF-α in the culture supernatant following the stimulation of THP-1 cells (a human acute monocytic leukemia cell line) with R. dentocariosa cells (ATCC14189 and ATCC14190). Exposure to bacterial cells induced the production of TNF-α in a dose-dependent manner. The bacterial induction of TNF-α in THP-1 cells was mediated by the Toll-like receptor 2 (TLR2), as demonstrated by gene-specific knockdown via siRNA, which successfully suppressed TLR2 expression and significantly inhibited the production of TNF-α in the culture supernatant. To confirm the role of TLR2, we examined TLR2-dependent NF-κB activation by R. dentocariosa cells in a distinct cell line. Specifically, HEK293 cells were transiently cotransfected with the human TLR2 gene and an NF-κB-dependent luciferase-encoding reporter gene. The bacterial cells induced NF-κB activation in the transfected HEK293 cells in a dose-dependent manner. In contrast, bacterial cells failed to induce NF-κB activation in cells transfected with pEF6 control vector. Taken together, these results suggest that R. dentocariosa induces host TNF-α production by a TLR2-dependent mechanism.
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Rothia dentocariosa induces TNF‐alpha production in a TLR2‐dependent manner
Pathogens and disease, 2013Co-Authors: Hideo Kataoka, Makoto Taniguchi, Haruka Fukamachi, Takafumi Arimoto, Hirobumi Morisaki, Hirotaka KuwataAbstract:Previous work suggested that Rothia dentocariosa is associated with periodontal inflammatory disease. However, little is known about the pathogenicity of this bacterium. To characterize host response to this bacterium, we measured (via ELISA) the amount of TNF-α in the culture supernatant following the stimulation of THP-1 cells (a human acute monocytic leukemia cell line) with R. dentocariosa cells (ATCC14189 and ATCC14190). Exposure to bacterial cells induced the production of TNF-α in a dose-dependent manner. The bacterial induction of TNF-α in THP-1 cells was mediated by the Toll-like receptor 2 (TLR2), as demonstrated by gene-specific knockdown via siRNA, which successfully suppressed TLR2 expression and significantly inhibited the production of TNF-α in the culture supernatant. To confirm the role of TLR2, we examined TLR2-dependent NF-κB activation by R. dentocariosa cells in a distinct cell line. Specifically, HEK293 cells were transiently cotransfected with the human TLR2 gene and an NF-κB-dependent luciferase-encoding reporter gene. The bacterial cells induced NF-κB activation in the transfected HEK293 cells in a dose-dependent manner. In contrast, bacterial cells failed to induce NF-κB activation in cells transfected with pEF6 control vector. Taken together, these results suggest that R. dentocariosa induces host TNF-α production by a TLR2-dependent mechanism.
