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  1. AU="Song, Xiao-yu R"
  2. AU="Abounader, Roger"
  3. AU="van Sterkenburg, M A J A"
  4. AU="Sayed Masoud Hosseini"
  5. AU="Pathania, Deepak"
  6. AU=Xu Yuzhong AU=Xu Yuzhong
  7. AU="Mehmood, Huzaifa"
  8. AU="Etcheverry, Amandine"
  9. AU="Sein, Andrea M"
  10. AU="Vo, Thi-Phi-Giao"
  11. AU="Allan, Alasdair"
  12. AU="Thurlow, Lance R"
  13. AU="Lum, Krystal"
  14. AU="Wilms, Miriam"
  15. AU="Russell, Michael H"
  16. AU="Bedoya-Arias, Hugo A"
  17. AU="Hijri, Mohamed"
  18. AU="Priscilla Gates"
  19. AU="Reiber, Matthew"
  20. AU="Bauer-Rowe, Khristian E"
  21. AU="Tanner, Martin E"
  22. AU="Creech, Gardner S"
  23. AU="José P. Oliveira-Filho"
  24. AU="Munt, Jennifer E"
  25. AU="Whiley, Phillip J"
  26. AU="V.Sudhir, "
  27. AU="Chatow, Lior"
  28. AU=Xue Zhe
  29. AU="Peter D. Yurchenco"
  30. AU="Várbíró, Gábor"
  31. AU="Sheleg, Dmitriy"
  32. AU="Panzirer, David"

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  1. Artikel: Anti-tumor necrosis factor-alpha treatment activates Borrelia burgdorferi spirochetes 4 weeks after ceftriaxone treatment in C3H/He mice.

    Yrjänäinen, Heta / Hytönen, Jukka / Song, Xiao-yu R / Oksi, Jarmo / Hartiala, Kaija / Viljanen, Matti K

    The Journal of infectious diseases

    2007  Band 195, Heft 10, Seite(n) 1489–1496

    Abstract: Background: The effect of anti-tumor necrosis factor (TNF)-alpha treatment in Borrelia burgdorferi-infected and ceftriaxone-treated C3H/He mice was evaluated.: Methods: Mice were infected with B. garinii A218 or B. burgdorferi sensu stricto N40. At 2 ...

    Abstract Background: The effect of anti-tumor necrosis factor (TNF)-alpha treatment in Borrelia burgdorferi-infected and ceftriaxone-treated C3H/He mice was evaluated.
    Methods: Mice were infected with B. garinii A218 or B. burgdorferi sensu stricto N40. At 2 weeks of infection, one group was treated simultaneously with ceftriaxone and anti-TNF-alpha, whereas another received ceftriaxone at 2 weeks and anti-TNF-alpha 4 weeks later. One group received ceftriaxone treatment only. Infected and noninfected control groups were sham treated.
    Results: At 14 weeks of infection, B. burgdorferi could not be detected by cultivation or by polymerase chain reaction in tissue samples of any mouse treated with ceftriaxone only. However, spirochetes grew from the tissue samples of one-third of the mice treated with anti-TNF-alpha simultaneously or 4 weeks after ceftriaxone. These activated spirochetes showed ceftriaxone sensitivity rates, plasmid profiles, and virulence rates similar to those of bacteria used to infect the mice. All infected control mice and mice given anti-TNF-alpha only were culture positive.
    Conclusions: This report shows that, after ceftriaxone treatment for 5 days, a portion of B. burgdorferi-infected mice still have live spirochetes in their body, which are activated by anti-TNF-alpha treatment.
    Mesh-Begriff(e) Animals ; Anti-Bacterial Agents/therapeutic use ; Antibodies/therapeutic use ; Borrelia burgdorferi/drug effects ; Borrelia burgdorferi/pathogenicity ; Borrelia burgdorferi/physiology ; Borrelia burgdorferi Group/drug effects ; Borrelia burgdorferi Group/isolation & purification ; Ceftriaxone/adverse effects ; Ceftriaxone/therapeutic use ; Disease Models, Animal ; Immunoglobulin G/therapeutic use ; Joint Diseases/chemically induced ; Joint Diseases/prevention & control ; Kinetics ; Lyme Disease/drug therapy ; Mice ; Mice, Inbred C3H ; Rats ; Spirochaetales/drug effects ; Tumor Necrosis Factor-alpha/antagonists & inhibitors ; Tumor Necrosis Factor-alpha/immunology
    Chemische Substanzen Anti-Bacterial Agents ; Antibodies ; Immunoglobulin G ; Tumor Necrosis Factor-alpha ; Ceftriaxone (75J73V1629)
    Sprache Englisch
    Erscheinungsdatum 2007-05-15
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3019-3
    ISSN 1537-6613 ; 0022-1899
    ISSN (online) 1537-6613
    ISSN 0022-1899
    DOI 10.1086/513873
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel: Anti-interleukin-6 monoclonal antibody inhibits autoimmune responses in a murine model of systemic lupus erythematosus.

    Liang, Bailin / Gardner, Debra B / Griswold, Don E / Bugelski, Peter J / Song, Xiao Yu R

    Immunology

    2006  Band 119, Heft 3, Seite(n) 296–305

    Abstract: Systemic lupus erythematosus (SLE) is an autoimmune disease resulting from dysregulation of the immune system. Interleukin-6 (IL-6) is a multifunctional cytokine produced by macrophages, monocytes and T and B cells. It stimulates B-cell differentiation/ ... ...

    Abstract Systemic lupus erythematosus (SLE) is an autoimmune disease resulting from dysregulation of the immune system. Interleukin-6 (IL-6) is a multifunctional cytokine produced by macrophages, monocytes and T and B cells. It stimulates B-cell differentiation/maturation, immunoglobulin secretion, and T-cell functions. Elevated levels of IL-6 in serum, urine and renal glomeruli were detected in patients with active SLE and in murine models of SLE. Our study investigated the role of IL-6 in an SLE-like disease in New Zealand Black/White (NZB/W) F1 mice by administration of an anti-murine IL-6 monoclonal antibody (mAb). Intraperitoneal administration of the anti-IL-6 mAb suppressed the production of anti-dsDNA autoantibody. B-cell proliferation induced by anti-IgM and anti-CD40 was lower in the anti-IL-6 mAb-treated mice, ex vivo studies demonstrated that anti-IL-6 mAb treatment inhibited anti-dsDNA production. Anti-CD3-induced T-cell proliferation and mixed lymphocyte reactions were inhibited by anti-IL-6 mAb treatment, indicating a partial down-regulation of T cells. Histological analysis showed that treatment with anti-IL-6 mAb prevented the development of severe kidney disease. These results suggest that treatment with anti-IL-6 mAb has a beneficial effect on autoimmunity in murine SLE and that autoreactive B cells may be the primary target for anti-IL-6 mAb treatment; its effect on autoreactive T cells is also indicated.
    Mesh-Begriff(e) Animals ; Antibodies, Antinuclear/biosynthesis ; Antibodies, Monoclonal/therapeutic use ; Autoimmune Diseases/blood ; Autoimmune Diseases/immunology ; Autoimmune Diseases/therapy ; B-Lymphocytes/immunology ; DNA/immunology ; Disease Models, Animal ; Disease Progression ; Interleukin-6/antagonists & inhibitors ; Interleukin-6/blood ; Interleukin-6/immunology ; Lupus Erythematosus, Systemic/blood ; Lupus Erythematosus, Systemic/immunology ; Lupus Erythematosus, Systemic/therapy ; Lupus Nephritis/immunology ; Lupus Nephritis/pathology ; Lupus Nephritis/prevention & control ; Lymphocyte Activation/immunology ; Mice ; Mice, Inbred NZB ; STAT3 Transcription Factor/metabolism ; Serum Amyloid A Protein/analysis ; Severity of Illness Index ; T-Lymphocyte Subsets/immunology
    Chemische Substanzen Antibodies, Antinuclear ; Antibodies, Monoclonal ; Interleukin-6 ; STAT3 Transcription Factor ; Serum Amyloid A Protein ; Stat3 protein, mouse ; DNA (9007-49-2)
    Sprache Englisch
    Erscheinungsdatum 2006-11
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 80124-0
    ISSN 1365-2567 ; 0019-2805 ; 0953-4954
    ISSN (online) 1365-2567
    ISSN 0019-2805 ; 0953-4954
    DOI 10.1111/j.1365-2567.2006.02433.x
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Coming of age: anti-cytokine therapies.

    Song, Xiao-yu R / Torphy, Theodore J / Griswold, Don E / Shealy, David

    Molecular interventions

    2002  Band 2, Heft 1, Seite(n) 36–46

    Abstract: Although cytokines are critical in maintaining normal physiology, excessive production of these proteins can lead to pathological consequences. Inhibitors of cytokine production or action are therefore widely investigated as potential therapeutic agents ... ...

    Abstract Although cytokines are critical in maintaining normal physiology, excessive production of these proteins can lead to pathological consequences. Inhibitors of cytokine production or action are therefore widely investigated as potential therapeutic agents in a variety of immune and inflammatory diseases. Indeed, the successful application of inhibitors of tumor necrosis factor-alpha in rheumatoid arthritis and Crohn's disease heralds the great therapeutic potential of biopharmaceutical agents to counteract cytokine activities. Emerging opportunities for new therapeutics, as well as the challenges we face in their use and development, are described in this review.
    Mesh-Begriff(e) Animals ; Cytokines/antagonists & inhibitors ; Humans ; Immune System Diseases/drug therapy ; Immunologic Factors/pharmacology ; Immunologic Factors/therapeutic use ; Inflammation/drug therapy
    Chemische Substanzen Cytokines ; Immunologic Factors
    Sprache Englisch
    Erscheinungsdatum 2002-02
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2108819-6
    ISSN 1543-2548 ; 1534-0384
    ISSN (online) 1543-2548
    ISSN 1534-0384
    DOI 10.1124/mi.2.1.36
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel: Tumor necrosis factor-alpha neutralization reduced cerebral edema through inhibition of matrix metalloproteinase production after transient focal cerebral ischemia.

    Hosomi, Naohisa / Ban, Camelia R / Naya, Takayuki / Takahashi, Tsutomu / Guo, Peng / Song, Xiao-yu R / Kohno, Masakazu

    Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism

    2005  Band 25, Heft 8, Seite(n) 959–967

    Abstract: After focal cerebral ischemia, tumor necrosis factor-alpha deteriorates cerebral edema and survival rate. Therefore, tumor necrosis factor-alpha neutralization could reduce cerebral microvascular permeability in acute cerebral ischemia. Left middle ... ...

    Abstract After focal cerebral ischemia, tumor necrosis factor-alpha deteriorates cerebral edema and survival rate. Therefore, tumor necrosis factor-alpha neutralization could reduce cerebral microvascular permeability in acute cerebral ischemia. Left middle cerebral artery occlusion for 120 mins followed by reperfusion was performed with the thread method under halothane anesthesia in Sprague-Dawley rats. Antirat tumor necrosis factor-alpha neutralizing monoclonal antibody with a rat IgG Fc portion (15 mg/kg) was infused intravenously right after reperfusion. Stroke index score, infarct volume, cerebral specific gravity, and the endogenous expression of tumor necrosis factor-alpha, matrix metalloproteinase (MMP)-2, MMP-9, and membrane type 1-MMP in the brain tissue were quantified in the ischemic and matched contralateral nonischemic hemisphere. In the antitumor necrosis factor-alpha neutralizing antibody-treated rats, infarct volume was significantly reduced (P=0.014, n=7; respectively), and cerebral specific gravity was dramatically increased in the cortex and caudate putamen (P<0.001, n=7; respectively) in association with a reduction in MMP-9 and membrane type 1-MMP upregulation. Tumor necrosis factor-alpha in the brain tissue was significantly elevated in the ischemic hemisphere 6 h after reperfusion in the nonspecific IgG-treated rats (P=0.021, n=7) and was decreased in the antitumor necrosis factor-alpha neutralizing antibody-treated rats (P=0.001, n=7). Postreperfusion treatment with antirat tumor necrosis factor-alpha neutralizing antibody reduced brain infarct volume and cerebral edema, which is likely mediated by a reduction in MMP upregulation.
    Mesh-Begriff(e) Animals ; Antibodies, Blocking/pharmacology ; Antibodies, Monoclonal/pharmacology ; Blood Pressure/drug effects ; Brain Chemistry ; Brain Edema/drug therapy ; Brain Edema/enzymology ; Brain Edema/pathology ; Brain Ischemia/enzymology ; Cerebral Infarction/enzymology ; Cerebral Infarction/pathology ; Male ; Matrix Metalloproteinase 1/metabolism ; Matrix Metalloproteinase 2/metabolism ; Matrix Metalloproteinase 9/metabolism ; Matrix Metalloproteinases/biosynthesis ; Rats ; Rats, Sprague-Dawley ; Specific Gravity ; Stroke/enzymology ; Stroke/pathology ; Tumor Necrosis Factor-alpha/antagonists & inhibitors
    Chemische Substanzen Antibodies, Blocking ; Antibodies, Monoclonal ; Tumor Necrosis Factor-alpha ; Matrix Metalloproteinases (EC 3.4.24.-) ; Matrix Metalloproteinase 2 (EC 3.4.24.24) ; Matrix Metalloproteinase 9 (EC 3.4.24.35) ; Matrix Metalloproteinase 1 (EC 3.4.24.7)
    Sprache Englisch
    Erscheinungsdatum 2005-08
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 604628-9
    ISSN 1559-7016 ; 0271-678X
    ISSN (online) 1559-7016
    ISSN 0271-678X
    DOI 10.1038/sj.jcbfm.9600086
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel: Effects of 2 different anti-tumor necrosis factor-alpha agents in a primate model of subcutaneous abscess formation.

    Song, Xiao-yu R / Fox, Floyd / Gallo, Mary Ann / Rosenberg, Amy / Jordan, Robert / Shealy, David / Wagner, Carrie

    The Journal of infectious diseases

    2002  Band 185, Heft 2, Seite(n) 204–213

    Abstract: Tumor necrosis factor (TNF)-alpha exerts both physiologic and pathologic effects in response to infection, conferring the benefit of host defense against infection at the risk of eliciting severe pathology if the response is excessive or inappropriate. ... ...

    Abstract Tumor necrosis factor (TNF)-alpha exerts both physiologic and pathologic effects in response to infection, conferring the benefit of host defense against infection at the risk of eliciting severe pathology if the response is excessive or inappropriate. In the present study, the effects of an anti-TNF-alpha monoclonal antibody (MAb) and a TNF-alpha receptor construct (p75-Fc) were compared with that of saline in a primate model of subcutaneous abscess induced with Staphylococcus aureus. Intravenous administration of anti-TNF-alpha MAb delayed the onset and reduced the incidence and the severity of abscess formation in response to inoculation with S. aureus at concentrations of 10(9) and 10(10) cfu/mL, compared with administration of saline. In contrast, no improvement in abscess formation was observed in animals treated with p75-Fc. These results supply initial evidence that anti-TNF-alpha MAb, unlike p75-Fc, provides a beneficial effect in this abscess model.
    Mesh-Begriff(e) Abscess/drug therapy ; Animals ; Antibodies, Monoclonal/immunology ; Antibodies, Monoclonal/therapeutic use ; Etanercept ; Female ; Immunoglobulin G/therapeutic use ; Interleukin-12/biosynthesis ; Interleukin-12/blood ; Interleukin-8/blood ; Macaca mulatta ; Male ; Receptors, Tumor Necrosis Factor/therapeutic use ; Skin Diseases, Bacterial/drug therapy ; Tumor Necrosis Factor-alpha/antagonists & inhibitors
    Chemische Substanzen Antibodies, Monoclonal ; Immunoglobulin G ; Interleukin-8 ; Receptors, Tumor Necrosis Factor ; Tumor Necrosis Factor-alpha ; Interleukin-12 (187348-17-0) ; Etanercept (OP401G7OJC)
    Sprache Englisch
    Erscheinungsdatum 2002-01-15
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 3019-3
    ISSN 1537-6613 ; 0022-1899
    ISSN (online) 1537-6613
    ISSN 0022-1899
    DOI 10.1086/338451
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel: PGE2 and IL-6 production by fibroblasts in response to titanium wear debris particles is mediated through a Cox-2 dependent pathway.

    Bukata, Susan V / Gelinas, Jill / Wei, Xiaochao / Rosier, Randy N / Puzas, J Edward / Zhang, Xinping / Schwarz, Edward M / Song, Xiao-yu R / Griswold, Don E / O'Keefe, Regis J

    Journal of orthopaedic research : official publication of the Orthopaedic Research Society

    2004  Band 22, Heft 1, Seite(n) 6–12

    Abstract: Aseptic loosening of orthopaedic implants is precipitated by wear debris-induced osteolysis. Central to this process are the pro-inflammatory mediators that are produced in response to wear by the fibroblastic cells, which comprise the majority of ... ...

    Abstract Aseptic loosening of orthopaedic implants is precipitated by wear debris-induced osteolysis. Central to this process are the pro-inflammatory mediators that are produced in response to wear by the fibroblastic cells, which comprise the majority of periprosthetic membranes. Since this pro-inflammatory cascade is mediated by a plethora of factors with redundant functions, it is imperative to establish a hierarchy. Two well-known fibroblast derived pro-inflammatory factors that stimulate wear debris-induced osteoclastic resorption are prostaglandin E2 (PGE2) and IL-6. However, their relationship to each other in this process is poorly defined. Here we show immunohistochemistry of retrieval membranes indicating that COX-2 is the principal cyclooxygenase responsible for PGE2 production in fibroblasts around failed implants. We also performed in vitro experiments with fibroblasts derived from wild-type (WT), COX-1 (-/-) and COX-2 (-/-) mice, which demonstrated that COX-2 is required for Ti wear debris-induced PGE2 production. Interestingly, COX-2 was also required for IL-6 production in these assays, which could be rescued by the addition of exogenous PGE2 (10(-6) M). Pharmacology studies that utilized the COX-1 selective inhibitor SC 560, the COX-2 selective inhibitor celecoxib, and the nonselective COX inhibitor indomethacin confirmed these results. Taken together, these results indicate that selective inhibition of prostaglandin signaling could favorably impact aseptic loosening beyond its direct effects on PGE2 synthesis, in that it inhibits downstream pro-inflammatory/pro-osteoclastic cytokine production.
    Mesh-Begriff(e) Animals ; Cell Line ; Cyclooxygenase 2 ; Dinoprostone/metabolism ; Fibroblasts/cytology ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; In Vitro Techniques ; Interleukin-6/metabolism ; Isoenzymes/genetics ; Isoenzymes/metabolism ; Mice ; Mice, Inbred CBA ; Osteolysis ; Prostaglandin-Endoperoxide Synthases/genetics ; Prostaglandin-Endoperoxide Synthases/metabolism ; Prosthesis Failure ; Titanium/pharmacology
    Chemische Substanzen Interleukin-6 ; Isoenzymes ; Titanium (D1JT611TNE) ; Cyclooxygenase 2 (EC 1.14.99.1) ; Prostaglandin-Endoperoxide Synthases (EC 1.14.99.1) ; Dinoprostone (K7Q1JQR04M)
    Sprache Englisch
    Erscheinungsdatum 2004-01
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 605542-4
    ISSN 1554-527X ; 0736-0266
    ISSN (online) 1554-527X
    ISSN 0736-0266
    DOI 10.1016/S0736-0266(03)00153-0
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel: Anti-TNF-alpha antibody allows healing of joint damage in polyarthritic transgenic mice.

    Shealy, David J / Wooley, Paul H / Emmell, Eva / Volk, Amy / Rosenberg, Amy / Treacy, George / Wagner, Carrie L / Mayton, Lois / Griswold, Don E / Song, Xiao-Yu R

    Arthritis research

    2002  Band 4, Heft 5, Seite(n) R7

    Abstract: Anti-tumor-necrosis-factor-alpha (TNF-alpha) monoclonal antibody was used to treat Tg197 transgenic mice, which constitutively produce human TNF-alpha (hTNF-alpha) and develop a progressive polyarthritic disease. Treatment of both young (7- or 8-week-old) ...

    Abstract Anti-tumor-necrosis-factor-alpha (TNF-alpha) monoclonal antibody was used to treat Tg197 transgenic mice, which constitutively produce human TNF-alpha (hTNF-alpha) and develop a progressive polyarthritic disease. Treatment of both young (7- or 8-week-old) and aged (27- or 28-week-old) mice commenced when at least two limbs showed signs of moderate to severe arthritis. The therapeutic efficacy of anti-TNF-alpha antibody was assessed using various pathological indicators of disease progression. The clinical severity of arthritis in Tg197 mice was significantly reduced after anti-TNF-alpha treatment in comparison with saline-treated mice and in comparison with baseline assessments in both young and aged mice. The treatment with anti-TNF-alpha prevented loss of body weight. Inflammatory pathways as reflected by elevated circulating hTNF-alpha and local expression of various proinflammatory mediators were all diminished by anti-TNF-alpha treatment, confirming a critical role of hTNF-alpha in this model of progressive polyarthritis. More importantly, the amelioration of the disease was associated with reversal of existing structural damage, including synovitis and periosteal bone erosions evident on histology. Repair of cartilage was age dependent: reversal of cartilage degradation after anti-TNF-alpha treatment was observed in young mice but not in aged mice.
    Mesh-Begriff(e) Animals ; Antibodies, Monoclonal/therapeutic use ; Arthritis, Rheumatoid/metabolism ; Arthritis, Rheumatoid/pathology ; Arthritis, Rheumatoid/therapy ; Chemokines/genetics ; Chemokines/metabolism ; Disease Models, Animal ; Enzyme-Linked Immunosorbent Assay ; Forearm/pathology ; Heterozygote ; Hindlimb/pathology ; Joints/drug effects ; Joints/pathology ; Mice ; Mice, Transgenic ; RNA, Messenger/metabolism ; Tumor Necrosis Factor-alpha/analysis ; Tumor Necrosis Factor-alpha/immunology
    Chemische Substanzen Antibodies, Monoclonal ; Chemokines ; RNA, Messenger ; Tumor Necrosis Factor-alpha
    Sprache Englisch
    Erscheinungsdatum 2002
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 2007393-8
    ISSN 1465-9913 ; 1465-9905
    ISSN (online) 1465-9913
    ISSN 1465-9905
    DOI 10.1186/ar430
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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