10 research outputs found

    Is monocyte chemotactic protein 1 elevated in aseptic loosening of TKA? A pilot study

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    Item does not contain fulltextBACKGROUND: Failure of TKA from aseptic loosening is a growing concern, as TKA is performed with increasing frequency. Loosening is multifactorial and may be associated with elevated inflammatory cytokines in addition to biomechanical failure. QUESTIONS/PURPOSES: We asked whether proinflammatory cytokines and chemokines are elevated in synovial fluid from patients undergoing revision surgery as compared to those with osteoarthritis (OA) or rheumatoid arthritis (RA). METHODS: We obtained synovial fluid samples from 20 patients: six with aseptic loosening of TKA (all with bone loss), 10 with primary OA, and four with RA. A panel of cytokines/chemokines was screened using a SearchLight((R)) Array (Pierce Biotechnology, Rockford, IL, USA) in one revision sample. Using these data, we assayed the synovial fluids for monocyte chemotactic protein 1 (MCP-1) by ELISA. RESULTS: We observed an increase in synovial MCP-1 levels in samples from patients planned for TKA revision compared to those with OA or RA. In patients undergoing revision arthroplasty, the mean (+/- SD) MCP-1 concentration was 21,233 +/- 18,966 pg/mL (range, 1550-50,657 pg/mL; n = 6). In patients with OA, the mean MCP-1 level was 3012 +/- 3321 pg/mL. In patients with RA, the mean MCP-1 concentration was 690 +/- 561 pg/mL. CONCLUSIONS: All patients undergoing revision TKA showed elevated concentrations of MCP-1 compared to patients with OA and RA, suggesting MCP-1 may serve as a potential marker or predictor of bone loss in patients undergoing revision surgery. CLINICAL RELEVANCE: MCP-1 may be a novel biomarker in patients showing early symptoms of aseptic loosening of TKA

    Interleukin-17-induced Protein Lipocalin 2 Is Dispensable For Immunity To Oral Candidiasis

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    Oropharyngeal candidiasis (OPC; thrush) is an opportunistic fungal infection caused by the commensal microbe Candida albicans. Immunity to OPC is strongly dependent on CD4+ T cells, particularly those of the Th17 subset. Interleukin-17 (IL-17) deficiency in mice or humans leads to chronic mucocutaneous candidiasis, but the specific downstream mechanisms of IL-17- mediated host defense remain unclear. Lipocalin 2 (Lcn2; 24p3; neutrophil gelatinase-associated lipocalin [NGAL]) is an antimicrobial host defense factor produced in response to inflammatory cytokines, particularly IL-17. Lcn2 plays a key role in preventing iron acquisition by bacteria that use catecholate-type siderophores, and lipocalin 2-/- mice are highly susceptible to infection by Escherichia coli and Klebsiella pneumoniae. The role of Lcn2 in mediating immunity to fungi is poorly defined. Accordingly, in this study, we evaluated the role of Lcn2 in immunity to oral infection with C. albicans. Lcn2 is strongly upregulated following oral infection with C. albicans, and its expression is almost entirely abrogated in mice with defective IL-17 signaling (IL-17RA-/- or Act1-/- mice). However, Lcn2-/- mice were completely resistant to OPC, comparably to wild-type (WT) mice. Moreover, Lcn2 deficiency mediated protection from OPC induced by steroid immunosuppression. Therefore, despite its potent regulation during C. albicans infection, Lcn2 is not required for immunity to mucosal candidiasis. © 2014, American Society for Microbiology.82310301035Fidel Jr., P.L., Candida-host interactions in HIV disease: implications for oropharyngeal candidiasis (2011) Adv. Dent. Res., 23, pp. 45-49. , http://dx.doi.org/10.1177/0022034511399284Glocker, E., Grimbacher, B., Chronic mucocutaneous candidiasis and congenital susceptibility to Candida (2010) Curr. Opin. Allergy Clin. 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