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Berlin Brandenburg

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  • 1
    Language: English
    In: Respiratory Research, July 8, 2010, Vol.11, p.93
    Description: Background Legionella pneumophila is an important causative agent of severe pneumonia in humans. Human alveolar epithelium and macrophages are effective barriers for inhaled microorganisms and actively participate in the initiation of innate host defense. The beta defensin-3 (hBD-3), an antimicrobial peptide is an important component of the innate immune response of the human lung. Therefore we hypothesize that hBD-3 might be important for immune defense towards L. pneumophila. Methods We investigated the effects of L. pneumophila and different TLR agonists on pulmonary cells in regard to hBD-3 expression by ELISA. Furthermore, siRNA-mediated inhibition of TLRs as well as chemical inhibition of potential downstream signaling molecules was used for functional analysis. Results L. pneumophila induced release of hBD-3 in pulmonary epithelium and alveolar macrophages. A similar response was observed when epithelial cells were treated with different TLR agonists. Inhibition of TLR2, TLR5, and TLR9 expression led to a decreased hBD-3 expression. Furthermore expression of hBD-3 was mediated through a JNK dependent activation of AP-1 (c-Jun) but appeared to be independent of NF-[kappa]B. Additionally, we demonstrate that hBD-3 elicited a strong antimicrobial effect on L. pneumophila replication. Conclusions Taken together, human pulmonary cells produce hBD-3 upon L. pneumophila infection via a TLR-JNK-AP-1-dependent pathway which may contribute to an efficient innate immune defense.
    Keywords: Cellular Proteins -- Health Aspects ; Cellular Proteins -- Research ; Immune Response -- Health Aspects ; Immune Response -- Research ; Legionnaires' Disease -- Causes Of ; Legionnaires' Disease -- Drug Therapy ; Legionnaires' Disease -- Research
    ISSN: 1465-9921
    Source: Cengage Learning, Inc.
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  • 2
    Language: English
    In: Respiratory Research, July 8, 2010, Vol.11, p.93
    Description: Background Legionella pneumophila is an important causative agent of severe pneumonia in humans. Human alveolar epithelium and macrophages are effective barriers for inhaled microorganisms and actively participate in the initiation of innate host defense. The beta defensin-3 (hBD-3), an antimicrobial peptide is an important component of the innate immune response of the human lung. Therefore we hypothesize that hBD-3 might be important for immune defense towards L. pneumophila. Methods We investigated the effects of L. pneumophila and different TLR agonists on pulmonary cells in regard to hBD-3 expression by ELISA. Furthermore, siRNA-mediated inhibition of TLRs as well as chemical inhibition of potential downstream signaling molecules was used for functional analysis. Results L. pneumophila induced release of hBD-3 in pulmonary epithelium and alveolar macrophages. A similar response was observed when epithelial cells were treated with different TLR agonists. Inhibition of TLR2, TLR5, and TLR9 expression led to a decreased hBD-3 expression. Furthermore expression of hBD-3 was mediated through a JNK dependent activation of AP-1 (c-Jun) but appeared to be independent of NF-[kappa]B. Additionally, we demonstrate that hBD-3 elicited a strong antimicrobial effect on L. pneumophila replication. Conclusions Taken together, human pulmonary cells produce hBD-3 upon L. pneumophila infection via a TLR-JNK-AP-1-dependent pathway which may contribute to an efficient innate immune defense.
    Keywords: Cellular Proteins -- Health Aspects ; Cellular Proteins -- Research ; Immune Response -- Health Aspects ; Immune Response -- Research ; Legionnaires' Disease -- Causes Of ; Legionnaires' Disease -- Drug Therapy ; Legionnaires' Disease -- Research
    ISSN: 1465-9921
    Source: Cengage Learning, Inc.
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  • 3
    Language: English
    In: Respiratory Research, 01 July 2010, Vol.11(1), p.93
    Description: Abstract Background Legionella pneumophila is an important causative agent of severe pneumonia in humans. Human alveolar epithelium and macrophages are effective barriers for inhaled microorganisms and actively participate in the initiation of innate host defense. The beta defensin-3 (hBD-3), an antimicrobial peptide is an important component of the innate immune response of the human lung. Therefore we hypothesize that hBD-3 might be important for immune defense towards L. pneumophila. Methods We investigated the effects of L. pneumophila and different TLR agonists on pulmonary cells in regard to hBD-3 expression by ELISA. Furthermore, siRNA-mediated inhibition of TLRs as well as chemical inhibition of potential downstream signaling molecules was used for functional analysis. Results L. pneumophila induced release of hBD-3 in pulmonary epithelium and alveolar macrophages. A similar response was observed when epithelial cells were treated with different TLR agonists. Inhibition of TLR2, TLR5, and TLR9 expression led to a decreased hBD-3 expression. Furthermore expression of hBD-3 was mediated through a JNK dependent activation of AP-1 (c-Jun) but appeared to be independent of NF-κB. Additionally, we demonstrate that hBD-3 elicited a strong antimicrobial effect on L. pneumophila replication. Conclusions Taken together, human pulmonary cells produce hBD-3 upon L. pneumophila infection via a TLR-JNK-AP-1-dependent pathway which may contribute to an efficient innate immune defense.
    Keywords: Medicine
    ISSN: 1465-9921
    E-ISSN: 1465-993X
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  • 4
    Language: English
    In: The American Journal of Physiology, Jan, 2007, Vol.292(1), p.L267(11)
    Description: Legionella pneumophila causes community- and hospital-acquired pneumonia. Lung airway and alveolar epithelial cells comprise an important barrier against airborne pathogens. Cyclooxygenase (COX) and microsomal [PGE.sub.2] synthase-1 (mPGES-1)-derived prostaglandins like prostaglandin [E.sub.2] ([PGE.sub.2]) are considered as important regulators of lung function. Herein we tested the hypothesis that L. pneumophila induced COX-2 and mPGES-l-dependent [PGE.sub.2] production in pulmonary epithelial cells. Legionella induced the release of [PGE.sub.2] in primary human small airway epithelial cells and A549 cells. This was accompanied by an increased expression of COX-2 and mPGES-1 as well as an increased [PLA.sub.2] activity in infected cells. Deletion of the type IV secretion system Dot/Icm did not impair Legionella-related COX-2 expression or [PGE.sub.2] release in A549 cells. L. pneumophila induced the degradation of I[kappa]B[alpha] and activated NF-[kappa]B. Inhibition of IKK blocked L. pneumophila-induced [PGE.sub.2] release and COX-2 expression. We noted activation of p38 and p42/44 MAP kinase in Legionella-infected A549 cells. Moreover, membrane translocation and activation of PKC[alpha] was observed in infected cells. PKC[alpha] and p38 and p42/44 MAP kinase inhibitors reduced PGE2 release and COX-2 expression. In summary, PKC[alpha] and p38 and p42/44 MAP kinase controlled COX-2 expression and subsequent PGE2 release by Legionella-infected lung epithelial cells. These pathways may significantly contribute to the host response in Legionnaires' disease. alveolar epithelium; protein kinase C; prostaglandin [E.sub.2]; cyclooxygenase-2; phospholipase [A.sub.2]; microsomal [PGE.sub.2] synthase-1; mitogenactivated protein kinase
    Keywords: Macrophages -- Research ; Protein Kinases -- Research ; Prostaglandins -- Research
    ISSN: 0002-9513
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  • 5
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, 2009, Vol.29(3), pp.380-386
    Description: OBJECTIVE—: Activation of the endothelium by oxidized low-density lipoprotein (oxLDL) has been implicated in the development of atherosclerosis. Histone modifications impact on the transcriptional activity state of genes. We tested the hypothesis that oxLDL-induced inflammatory gene expression is regulated by histone modifications and experienced the effect of statins on these alterations. METHODS AND RESULTS—: OxLDL-related interleukin-8 (IL-8) and monocyte-chemoattractant protein-1 (MCP-1) secretion in endothelial cells was reduced by statins but enhanced by histone deacetylase inhibitors. OxLDL induced lectin-like oxidized LDL receptor-1 (LOX-1) and extracellular regulated kinases (ERK1/2)-dependent acetylation of histone H3 and H4 as well as phosphorylation of histone H3, both globally and on the promoters of il8 and mcp1. Pretreatment of oxLDL-exposed cells with statins reduced the above mentioned histone modification, as well as recruitment of CREB binding protein (CBP) 300, NF-κB, and of RNA polymerase II but prevented loss of binding of histone deacetylase (HDAC)-1 and -2 at the il8 and mcp1 gene promoters. OxLDL reduced HDAC1 and 2 expression, and statins partly restored global HDAC-activity. Statin-related effects were reverted with mevalonate. In situ experiments indicated decreased expression of HDAC2 in endothelial cells in atherosclerotic plaques of human coronary arteries. CONCLUSIONS—: Histone modifications seem to play an important role in atherosclerosis.
    Keywords: Medicine;
    ISSN: 1079-5642
    E-ISSN: 15244636
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  • 6
    Language: English
    In: American journal of physiology. Lung cellular and molecular physiology, January 2007, Vol.292(1), pp.L267-77
    Description: Legionella pneumophila causes community- and hospital-acquired pneumonia. Lung airway and alveolar epithelial cells comprise an important barrier against airborne pathogens. Cyclooxygenase (COX) and microsomal PGE(2) synthase-1 (mPGES-1)-derived prostaglandins like prostaglandin E(2) (PGE(2)) are considered as important regulators of lung function. Herein we tested the hypothesis that L. pneumophila induced COX-2 and mPGES-1-dependent PGE(2) production in pulmonary epithelial cells. Legionella induced the release of PGE(2) in primary human small airway epithelial cells and A549 cells. This was accompanied by an increased expression of COX-2 and mPGES-1 as well as an increased PLA(2) activity in infected cells. Deletion of the type IV secretion system Dot/Icm did not impair Legionella-related COX-2 expression or PGE(2) release in A549 cells. L. pneumophila induced the degradation of IkappaBalpha and activated NF-kappaB. Inhibition of IKK blocked L. pneumophila-induced PGE(2) release and COX-2 expression. We noted activation of p38 and p42/44 MAP kinase in Legionella-infected A549 cells. Moreover, membrane translocation and activation of PKCalpha was observed in infected cells. PKCalpha and p38 and p42/44 MAP kinase inhibitors reduced PGE(2) release and COX-2 expression. In summary, PKCalpha and p38 and p42/44 MAP kinase controlled COX-2 expression and subsequent PGE(2) release by Legionella-infected lung epithelial cells. These pathways may significantly contribute to the host response in Legionnaires' disease.
    Keywords: Cyclooxygenase 2 -- Metabolism ; Extracellular Signal-Regulated MAP Kinases -- Metabolism ; Legionella Pneumophila -- Pathogenicity ; Lung -- Metabolism ; Membrane Proteins -- Metabolism ; Nf-Kappa B -- Metabolism ; Protein Kinase C-Alpha -- Metabolism
    ISSN: 1040-0605
    E-ISSN: 15221504
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  • 7
    Language: English
    Description: Background: Legionella pneumophila is an important causative agent of severe pneumonia in humans. Human alveolar epithelium and macrophages are effective barriers for inhaled microorganisms and actively participate in the initiation of innate host defense. The beta defensin-3 (hBD-3), an antimicrobial peptide is an important component of the innate immune response of the human lung. Therefore we hypothesize that hBD-3 might be important for immune defense towards L. pneumophila. Methods: We investigated the effects of L. pneumophila and different TLR agonists on pulmonary cells in regard to hBD-3 expression by ELISA. Furthermore, siRNA-mediated inhibition of TLRs as well as chemical inhibition of potential downstream signaling molecules was used for functional analysis. Results: L. pneumophila induced release of hBD-3 in pulmonary epithelium and alveolar macrophages. A similar response was observed when epithelial cells were treated with different TLR agonists. Inhibition of TLR2, TLR5, and TLR9 expression led to a decreased hBD-3 expression. Furthermore expression of hBD-3 was mediated through a JNK dependent activation of AP-1 (c-Jun) but appeared to be independent of NF-κB. Additionally, we demonstrate that hBD-3 elicited a strong antimicrobial effect on L. pneumophila replication. Conclusions: Taken together, human pulmonary cells produce hBD-3 upon L. pneumophila infection via a TLR-JNK-AP-...
    Keywords: Humans ; Cultured ; Time Factors ; Epithelial Cells/Microbiology ; Legionella Pneumophila/Immunology ; Nf-Kappa B/Metabolism ; Transcription Factor Ap-1/Metabolism ; Legionella Pneumophila/Growth & Development ; Recombinant Proteins/Metabolism ; Cells ; Epithelial Cells/Immunology ; Epithelial Cells/Metabolism ; Immunity ; Innate ; Legionella Pneumophila/Pathogenicity ; Map Kinase Kinase 4/Metabolism ; Macrophages ; Alveolar/Immunology ; Alveolar/Metabolism ; Alveolar/Microbiology ; Respiratory Mucosa/Immunology ; Respiratory Mucosa/Metabolism ; Respiratory Mucosa/Microbiology ; Signal Transduction ; Toll-Like Receptors/Metabolism ; Up-Regulation ; Beta-Defensins/Metabolism ; Medizin
    Source: DataCite
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