The Experts below are selected from a list of 813 Experts worldwide ranked by ideXlab platform
Jon S. Friedland - One of the best experts on this subject based on the ideXlab platform.
-
regulation of monocyte chemokine and mmp 9 secretion by proinflammatory cytokines in Tuberculous Osteomyelitis
Journal of Leukocyte Biology, 2004Co-Authors: Kathleen M. Wright, Jon S. FriedlandAbstract:Tuberculous Osteomyelitis causes bony destruction as a result of interactions among the pathogen, resident bone cells, and influxing leuko- cytes. Recruitment of monocytes and T cells is critical for antimycobacterial granuloma forma- tion, but little is known about mechanisms regulat- ing this in bone. We investigated the role of tumor necrosis factor (TNF-) and interleukin (IL)-1, key cytokines in granuloma formation, in networks involving human osteoblasts and monocytes. Ex- periments focused on CXC ligand (CXCL)8, CCL2, and matrix metalloproteinase (MMP)-9, human monocyte-derived mediators involved in control of leukocyte influx. TNF- but not IL-1 has a key role stimulating CXCL8 secretion in Mycobacterium tu- berculosis-infected human osteoblast MG-63 cells. Conditioned medium from M. tuberculosis-infected osteoblasts (COBTB) drives CXCL8 and some CCL2 gene expression and secretion from primary human monocytes. IL-1 receptor antagonist and to a lesser extent anti-TNF- inhibited COBTB-in- duced CXCL8 secretion (P<0.01) but did not af- fect gene expression. IL-1 blockade had a compar- atively lesser effect on CCL2 secretion, whereas anti-TNF decreased CCL2 concentrations from 7840 140 to 360 80 pg/ml/4 10 5 cells. Neither proinflammatory mediator affects MMP-9 secretion from COBTB-stimulated human mono- cytes. In summary, in a paracrine network, M. tuberculosis-infected osteoblasts drive high-level CXCL8, comparatively less CCL2, but do not alter MMP-9 secretion from uninfected human mono- cytes. This network is, in part, regulated by IL-1 and TNF-. J. Leukoc. Biol. 75: 000-000; 2004.
-
Regulation of monocyte chemokine and MMP-9 secretion by proinflammatory cytokines in Tuberculous Osteomyelitis.
Journal of Leukocyte Biology, 2004Co-Authors: Kathleen M. Wright, Jon S. FriedlandAbstract:Tuberculous Osteomyelitis causes bony destruction as a result of interactions among the pathogen, resident bone cells, and influxing leuko- cytes. Recruitment of monocytes and T cells is critical for antimycobacterial granuloma forma- tion, but little is known about mechanisms regulat- ing this in bone. We investigated the role of tumor necrosis factor (TNF-) and interleukin (IL)-1, key cytokines in granuloma formation, in networks involving human osteoblasts and monocytes. Ex- periments focused on CXC ligand (CXCL)8, CCL2, and matrix metalloproteinase (MMP)-9, human monocyte-derived mediators involved in control of leukocyte influx. TNF- but not IL-1 has a key role stimulating CXCL8 secretion in Mycobacterium tu- berculosis-infected human osteoblast MG-63 cells. Conditioned medium from M. tuberculosis-infected osteoblasts (COBTB) drives CXCL8 and some CCL2 gene expression and secretion from primary human monocytes. IL-1 receptor antagonist and to a lesser extent anti-TNF- inhibited COBTB-in- duced CXCL8 secretion (P
-
Complex Patterns of Regulation of Chemokine Secretion by T_h2-Cytokines, Dexamethasone, and PGE_2 in Tuberculous Osteomyelitis
Journal of Clinical Immunology, 2003Co-Authors: Kathleen M. Wright, Jon S. FriedlandAbstract:Tuberculous Osteomyelitis is characterized by uncontrolled inflammation leading to bone destruction. Chemokines recruit inflammatory cells but there are no data on the mechanisms limiting cell influx. We investigated the potential down-regulators of chemokine secretion IL-4, IL-10, IL-13, dexamethasone, and PGE_2. IL-10 and IL-13 down-regulate M. tuberculosis -induced IL-8, IP-10, RANTES, and MCP-1 secretion from MG-63 cells by between 48 and 94% ( P < 0.05) but do not inhibit chemokine gene transcription. In contrast, IL-4 augments gene expression and secretion of IP-10 from 12,030 ± 1070 to 24,330 ± 1720 pg/ml/4 × 10^5 cells ( P < 0.01) and RANTES secretion, from 3550 ± 150 to 6930 ± 400 pg/ml/4 × 10^5 cells ( P < 0.01). Dexamethasone and PGE_2 caused a 13-fold down-regulation of secretion of all four chemokines but only dexamethasone inhibits mRNA accumulation. Data from primary osteoblasts were similar. In summary, down-regulation of osteoblastic chemokine secretion was not uniformly observed and the control of chemokine secretion in response to M. tuberculosis is a complex process mediated by pre- and posttranscriptional mechanisms.
-
Complex patterns of regulation of chemokine secretion by Th2-cytokines, dexamethasone, and PGE2 in Tuberculous Osteomyelitis.
Journal of Clinical Immunology, 2003Co-Authors: Kathleen M. Wright, Jon S. FriedlandAbstract:Tuberculous Osteomyelitis is characterized by uncontrolled inflammation leading to bone destruction. Chemokines recruit inflammatory cells but there are no data on the mechanisms limiting cell influx. We investigated the potential down-regulators of chemokine secretion IL-4, IL-10, IL-13, dexamethasone, and PGE2. IL-10 and IL-13 down-regulate M. tuberculosis-induced IL-8, IP-10, RANTES, and MCP-1 secretion from MG-63 cells by between 48 and 94% (P < 0.05) but do not inhibit chemokine gene transcription. In contrast, IL-4 augments gene expression and secretion of IP-10 from 12,030 ± 1070 to 24,330 ± 1720 pg/ml/4 × 105 cells ( P < 0.01) and RANTES secretion, from 3550 ± 150 to 6930 ± 400 pg/ml/4 × 105 cells (P < 0.01). Dexamethasone and PGE2 caused a 13-fold down-regulation of secretion of all four chemokines but only dexamethasone inhibits mRNA accumulation. Data from primary osteoblasts were similar. In summary, down-regulation of osteoblastic chemokine secretion was not uniformly observed and the control of chemokine secretion in response to M. tuberculosis is a complex process mediated by pre- and posttranscriptional mechanisms.
-
Tumor Necrosis Factor-α, Interleukin-6, and Interleukin-8 Secretion and the Acute-Phase Response in Patients with Bacterial and Tuberculous Osteomyelitis
The Journal of Infectious Diseases, 1998Co-Authors: Carlton A. Evans, John Jellis, Sean P. F. Hughes, Daniel G. Remick, Jon S. FriedlandAbstract:Osteomyelitis, or bone infection, is a major worldwide cause of morbidity. Treatment is frequently unsatisfactory, yet little is known about pathogenesis of infection. Plasma tumor necrosis factor (TNF), interleukin (IL)-6, and IL-8 concentrations were measured before and after lipopolysaccharide stimulation of whole blood from patients with bacterial and Tuberculous Osteomyelitis and from controls. Patients with bacterial and Tuberculous Osteomyelitis mounted an acute-phase response and were anemic and febrile. However, plasma IL-6 concentrations were significantly elevated in only Tuberculous Osteomyelitis patients (vs. controls, P < .05). IL-6 concentrations correlated with erythrocyte sedimentation rate, C-reactive protein level, and plasma albumin concentration, all acute-phase markers. There were no other correlations between cytokine concentrations and clinical data. Following ex vivo stimulation, TNF, IL-6, and IL-8 were secreted equally by patients and controls. In summary, Tuberculous Osteomyelitis is characterized by elevated systemic IL-6 concentrations associated with an acute-phase response. For further insight into immunopathology of Osteomyelitis, studies on infected bone are required.
Kathleen M. Wright - One of the best experts on this subject based on the ideXlab platform.
-
2004. Regulation of monocyte chemokine and MMP-9 secretion by proinflammatory cytokines in Tuberculous Osteomyelitis
2016Co-Authors: Kathleen M. Wright, Jon S. FriedlAbstract:Abstract: Tuberculous Osteomyelitis causes bony destruction as a result of interactions among the pathogen, resident bone cells, and influxing leuko-cytes. Recruitment of monocytes and T cells is critical for antimycobacterial granuloma forma-tion, but little is known about mechanisms regulat-ing this in bone. We investigated the role of tumor necrosis factor (TNF-) and interleukin (IL)-1, key cytokines in granuloma formation, in networks involving human osteoblasts and monocytes. Ex-periments focused on CXC ligand (CXCL)8, CCL2, and matrix metalloproteinase (MMP)-9, human monocyte-derived mediators involved in control of leukocyte influx. TNF- but not IL-1 has a key role stimulating CXCL8 secretion in Mycobacterium tu-berculosis-infected human osteoblast MG-63 cells. Conditioned medium from M. tuberculosis-infected osteoblasts (COBTB) drives CXCL8 and some CCL2 gene expression and secretion from primary human monocytes. IL-1 receptor antagonist and to a lesser extent anti-TNF- inhibited COBTB-in-duced CXCL8 secretion (P<0.01) but did not af-fect gene expression. IL-1 blockade had a compar-atively lesser effect on CCL2 secretion, whereas anti-TNF decreased CCL2 concentrations from 7840 140 to 360 80 pg/ml/4 105 cells. Neither proinflammatory mediator affects MMP-9 secretion from COBTB-stimulated human mono-cytes. In summary, in a paracrine network, M. tuberculosis-infected osteoblasts drive high-level CXCL8, comparatively less CCL2, but do not alter MMP-9 secretion from uninfected human mono
-
2004. Regulation of monocyte chemokine and MMP-9 secretion by proinflammatory cytokines in Tuberculous Osteomyelitis
2013Co-Authors: Kathleen M. Wright, Jon S. FriedlAbstract:Abstract: Tuberculous Osteomyelitis causes bony destruction as a result of interactions among the pathogen, resident bone cells, and influxing leukocytes. Recruitment of monocytes and T cells is critical for antimycobacterial granuloma formation, but little is known about mechanisms regulating this in bone. We investigated the role of tumor necrosis factor � (TNF-�) and interleukin (IL)-1, key cytokines in granuloma formation, in networks involving human osteoblasts and monocytes. Experiments focused on CXC ligand (CXCL)8, CCL2, and matrix metalloproteinase (MMP)-9, human monocyte-derived mediators involved in control of leukocyte influx. TNF- � but not IL-1 has a key role stimulating CXCL8 secretion in Mycobacterium tuberculosis-infected human osteoblast MG-63 cells. Conditioned medium from M. tuberculosis-infected osteoblasts (COBTB) drives CXCL8 and some CCL2 gene expression and secretion from primary human monocytes. IL-1 receptor antagonist and to a lesser extent anti-TNF- � inhibited COBTB-induced CXCL8 secretion (P<0.01) but did not affect gene expression. IL-1 blockade had a comparatively lesser effect on CCL2 secretion, whereas anti-TNF decreased CCL2 concentrations from 7840 � 140 to 360 � 80 pg/ml/4 � 10 5 cells. Neither proinflammatory mediator affects MMP-9 secretion from COBTB-stimulated human monocytes. In summary, in a paracrine network, M. tuberculosis-infected osteoblasts drive high-level CXCL8, comparatively less CCL2, but do not alter MMP-9 secretion from uninfected human monocytes
-
regulation of monocyte chemokine and mmp 9 secretion by proinflammatory cytokines in Tuberculous Osteomyelitis
Journal of Leukocyte Biology, 2004Co-Authors: Kathleen M. Wright, Jon S. FriedlandAbstract:Tuberculous Osteomyelitis causes bony destruction as a result of interactions among the pathogen, resident bone cells, and influxing leuko- cytes. Recruitment of monocytes and T cells is critical for antimycobacterial granuloma forma- tion, but little is known about mechanisms regulat- ing this in bone. We investigated the role of tumor necrosis factor (TNF-) and interleukin (IL)-1, key cytokines in granuloma formation, in networks involving human osteoblasts and monocytes. Ex- periments focused on CXC ligand (CXCL)8, CCL2, and matrix metalloproteinase (MMP)-9, human monocyte-derived mediators involved in control of leukocyte influx. TNF- but not IL-1 has a key role stimulating CXCL8 secretion in Mycobacterium tu- berculosis-infected human osteoblast MG-63 cells. Conditioned medium from M. tuberculosis-infected osteoblasts (COBTB) drives CXCL8 and some CCL2 gene expression and secretion from primary human monocytes. IL-1 receptor antagonist and to a lesser extent anti-TNF- inhibited COBTB-in- duced CXCL8 secretion (P<0.01) but did not af- fect gene expression. IL-1 blockade had a compar- atively lesser effect on CCL2 secretion, whereas anti-TNF decreased CCL2 concentrations from 7840 140 to 360 80 pg/ml/4 10 5 cells. Neither proinflammatory mediator affects MMP-9 secretion from COBTB-stimulated human mono- cytes. In summary, in a paracrine network, M. tuberculosis-infected osteoblasts drive high-level CXCL8, comparatively less CCL2, but do not alter MMP-9 secretion from uninfected human mono- cytes. This network is, in part, regulated by IL-1 and TNF-. J. Leukoc. Biol. 75: 000-000; 2004.
-
Regulation of monocyte chemokine and MMP-9 secretion by proinflammatory cytokines in Tuberculous Osteomyelitis.
Journal of Leukocyte Biology, 2004Co-Authors: Kathleen M. Wright, Jon S. FriedlandAbstract:Tuberculous Osteomyelitis causes bony destruction as a result of interactions among the pathogen, resident bone cells, and influxing leuko- cytes. Recruitment of monocytes and T cells is critical for antimycobacterial granuloma forma- tion, but little is known about mechanisms regulat- ing this in bone. We investigated the role of tumor necrosis factor (TNF-) and interleukin (IL)-1, key cytokines in granuloma formation, in networks involving human osteoblasts and monocytes. Ex- periments focused on CXC ligand (CXCL)8, CCL2, and matrix metalloproteinase (MMP)-9, human monocyte-derived mediators involved in control of leukocyte influx. TNF- but not IL-1 has a key role stimulating CXCL8 secretion in Mycobacterium tu- berculosis-infected human osteoblast MG-63 cells. Conditioned medium from M. tuberculosis-infected osteoblasts (COBTB) drives CXCL8 and some CCL2 gene expression and secretion from primary human monocytes. IL-1 receptor antagonist and to a lesser extent anti-TNF- inhibited COBTB-in- duced CXCL8 secretion (P
-
Complex Patterns of Regulation of Chemokine Secretion by T_h2-Cytokines, Dexamethasone, and PGE_2 in Tuberculous Osteomyelitis
Journal of Clinical Immunology, 2003Co-Authors: Kathleen M. Wright, Jon S. FriedlandAbstract:Tuberculous Osteomyelitis is characterized by uncontrolled inflammation leading to bone destruction. Chemokines recruit inflammatory cells but there are no data on the mechanisms limiting cell influx. We investigated the potential down-regulators of chemokine secretion IL-4, IL-10, IL-13, dexamethasone, and PGE_2. IL-10 and IL-13 down-regulate M. tuberculosis -induced IL-8, IP-10, RANTES, and MCP-1 secretion from MG-63 cells by between 48 and 94% ( P < 0.05) but do not inhibit chemokine gene transcription. In contrast, IL-4 augments gene expression and secretion of IP-10 from 12,030 ± 1070 to 24,330 ± 1720 pg/ml/4 × 10^5 cells ( P < 0.01) and RANTES secretion, from 3550 ± 150 to 6930 ± 400 pg/ml/4 × 10^5 cells ( P < 0.01). Dexamethasone and PGE_2 caused a 13-fold down-regulation of secretion of all four chemokines but only dexamethasone inhibits mRNA accumulation. Data from primary osteoblasts were similar. In summary, down-regulation of osteoblastic chemokine secretion was not uniformly observed and the control of chemokine secretion in response to M. tuberculosis is a complex process mediated by pre- and posttranscriptional mechanisms.
Ahmet Erbagci - One of the best experts on this subject based on the ideXlab platform.
-
Tuberculous Osteomyelitis of the lumbosacral region: a spinal epidural abscess with presacral extension
Archives of Orthopaedic and Trauma Surgery, 2004Co-Authors: Orhan Buyukbebeci, Gunhan Karakurum, Akif Gulec, Ahmet ErbagciAbstract:Introduction Tuberculous Osteomyelitis in the lumbosacral region is an uncommon occurrence, and its treatment is not well-defined in the literature, particularly when it is associated with abscess formation. We present the outcome of a patient who had an epidural abscess with presacral extension.
-
Tuberculous Osteomyelitis of the lumbosacral region: a spinal epidural abscess with presacral extension
Archives of Orthopaedic and Trauma Surgery, 2004Co-Authors: Orhan Buyukbebeci, Gunhan Karakurum, Akif Gulec, Ahmet ErbagciAbstract:Introduction Tuberculous Osteomyelitis in the lumbosacral region is an uncommon occurrence, and its treatment is not well-defined in the literature, particularly when it is associated with abscess formation. We present the outcome of a patient who had an epidural abscess with presacral extension. Materials and methods A 30-year-old man had microbiologically confirmed Tuberculous infection of the lumbosacral vertebrae complicated by extensive abscess formation. After a trial of chemotherapy, the infection proved refractory, and the treatment proceeded with abscess drainage through the anterior route. Results Approximately 1 year after surgery, the patient was symptom-free and did not show any significant radiologic changes. Conclusion AntiTuberculous chemotherapy combined with anterior surgery seems to be beneficial in the setting of lumbosacral Osteomyelitis complicated by epidural abscess formation with presacral extension.
Orhan Buyukbebeci - One of the best experts on this subject based on the ideXlab platform.
-
Tuberculous Osteomyelitis of the lumbosacral region: a spinal epidural abscess with presacral extension
Archives of Orthopaedic and Trauma Surgery, 2004Co-Authors: Orhan Buyukbebeci, Gunhan Karakurum, Akif Gulec, Ahmet ErbagciAbstract:Introduction Tuberculous Osteomyelitis in the lumbosacral region is an uncommon occurrence, and its treatment is not well-defined in the literature, particularly when it is associated with abscess formation. We present the outcome of a patient who had an epidural abscess with presacral extension.
-
Tuberculous Osteomyelitis of the lumbosacral region: a spinal epidural abscess with presacral extension
Archives of Orthopaedic and Trauma Surgery, 2004Co-Authors: Orhan Buyukbebeci, Gunhan Karakurum, Akif Gulec, Ahmet ErbagciAbstract:Introduction Tuberculous Osteomyelitis in the lumbosacral region is an uncommon occurrence, and its treatment is not well-defined in the literature, particularly when it is associated with abscess formation. We present the outcome of a patient who had an epidural abscess with presacral extension. Materials and methods A 30-year-old man had microbiologically confirmed Tuberculous infection of the lumbosacral vertebrae complicated by extensive abscess formation. After a trial of chemotherapy, the infection proved refractory, and the treatment proceeded with abscess drainage through the anterior route. Results Approximately 1 year after surgery, the patient was symptom-free and did not show any significant radiologic changes. Conclusion AntiTuberculous chemotherapy combined with anterior surgery seems to be beneficial in the setting of lumbosacral Osteomyelitis complicated by epidural abscess formation with presacral extension.
Sudha Palanimuthu - One of the best experts on this subject based on the ideXlab platform.
-
Primary Tuberculous Osteomyelitis of the mandible: A rare case report.
Dental Research Journal, 2013Co-Authors: J Kannaperuman, Gowri Natarajarathinam, Anusha V. Rao, Sudha PalanimuthuAbstract:Tuberculosis (TB) has become a rare disease in the developed countries but it is still a seriousproblem in developing countries. Incidence of Tuberculous Osteomyelitis of the jaw bones is verylow. This rare incidence is the primary reason that this lesion gets mis‑diagnosed many times. Herewe report the diagnosis, treatment and follow‑up of a case, which is a classical presentation ofTuberculous Osteomyelitis of mandible. Primary Tuberculous Osteomyelitis is a very rare entity butin the recent times, increased incidence of TB as a coinfection of HIV, has posed a big challenge indeveloping countries. If not diagnosed, at the right time, this can lead to serious complications likeinternal organ damage, Tuberculous meningitis etc., Early diagnosis of Tuberculous Osteomyelitis will certainly reduce the morbidity of this disease condition. Key Words: Osteomyelitis mandible, primary tuberculosis , Tuberculous Osteomyelitis
-
Primary Tuberculous Osteomyelitis of the mandible: A rare case report
Wolters Kluwer Medknow Publications, 2013Co-Authors: J Kannaperuman, Gowri Natarajarathinam, Anusha V. Rao, Sudha PalanimuthuAbstract:Tuberculosis (TB) has become a rare disease in the developed countries but it is still a serious problem in developing countries. Incidence of Tuberculous Osteomyelitis of the jaw bones is very low. This rare incidence is the primary reason that this lesion gets mis-diagnosed many times. Here we report the diagnosis, treatment and follow-up of a case, which is a classical presentation of Tuberculous Osteomyelitis of mandible. Primary Tuberculous Osteomyelitis is a very rare entity but in the recent times, increased incidence of TB as a coinfection of HIV, has posed a big challenge in developing countries. If not diagnosed, at the right time, this can lead to serious complications like internal organ damage, Tuberculous meningitis etc., Early diagnosis of Tuberculous Osteomyelitis will certainly reduce the morbidity of this disease condition
