Epidemiological Study and Classification of ICU Infections, Using the Carrier State Criterion

A high level of cholesterol is associated with obesity, cardiovascular diseases and atherosclerosis. Immune response in atherosclerosis is mediated by chemokines which attract monocytes, leading to the innate immune response characterised by the production of cytokines. The immunoregulatory cytokines are an important bridge between innate and adductive immunity. TH1 cytokines are involved as effector T cells in inflammatory response, while TH2 cytokines can be anti-inflammatory such as IL-10 and IL-4. It is well known that statins enhance the production of TH2 cytokines whereas the secretion of TH1 cytokines is suppressed. For this purpose, we studied the significance of anti-inflammatory effect and suppression of inflammation by statins. In this paper we revisited the role of cholesterol and cytokines IL-18, IL-10, IL-12, TNF-α, interferon-γ, and chemokines in inflammatory diseases.

Section: Statinsmentioning

confidence: 99%

Cholesterol, Cytokines and Diseases

Saggini

Anogeianaki

Maccauro

et al. 2011

“…Polyethylene debris determines an articular inflammatory reaction induced by macrophages and histiocytes (33)(34)(35)(36)(37). Synovial inflammation causes osteoclastic bone resorption with a consequent peri-prosthetic osteolysis and implant loosening (38)(39)(40)(41)(42)(43).…”

Section: Discussionmentioning

confidence: 99%

Metallosis following Knee Arthroplasty: A Histological and Immunohistochemical Study

Panni

Vasso

Cerciello

et al. 2011

Metallosis represents a rare and severe complication of knee replacement surgery. It is caused by the infiltration and accumulation of metallic debris into the peri-prosthetic structures, deriving from friction between metallic prosthetic components. In knee arthroplasty, this event generally occurs as a result of polyethylene wear of the tibial or metal-back patellar component. The real incidence of metallosis is still unknown, although it seems to be more frequent in hip than in knee arthroplasty. The metallic debris induces a massive release of cytokines from inflammatory cells, making a revision necessary whenever osteolysis and loosening of the prosthesis occur. We report four patients who underwent revision of their knee arthroplasty because of severe metallosis. In one of these patients, polyethylene wear had determined friction between the metal-back patellar component and the anterior portion of the femoral component. In the remaining three cases, metallosis was caused by friction between the femoral and tibial prosthetic metal surfaces, resulting from full-thickness wear of the ti~ial polyethylene. T lymphocytes were activated by metal particles present in periprosthetic membranes. In all patients, one-stage revision was necessary, with rapid pain disappearance and a complete functional recovery of the knee joint. Metallosis represents a rare and dangerous complication of total knee arthroplasty (TKA). It is characterized by the infiltration and accumulation of metal debris into the peri-prosthetic structures, including bone and soft tissues (1-3). The debris derives from friction among metal prosthetic surfaces, mainly due to the wear of the tibial and/or the metal-backed patellar polyethylene component. Metallosis seems to be more frequent in hip replacement, being the result of the metal-on-metal coupling (4). The exact incidence of metallosis following TKA is unknown. Chang et al. reported an overall 5.3% incidence of metallosis in 418 total hip arthroplasties (5); Ollivere et al. reported a 3.1% rate of metallosis-related failure at five years in 463 primary metal-on-metal hip resurfacing arthroplasties (6). Metallosis has also been described in shoulder arthroplasty (7-13).The presence of intra-articular metallic debris can be detected by x-ray imaging, this condition being an indication for early revision (1,3,5). Furthermore, metallosis can cause peri-prosthetic osteolysis, as the consequence of the release of cytokines from the inflammatory cells, inducing pain and implant loosening (14-19): this condition makes implant revision essential in order to prevent further bone loss.All orthopaedic implants are heading towards

“…Neovascularization arising from the artery 's vasa vasorum contributes to lesion progression in many ways (39)(40)(41)(42). It provides another portal for leukocyte entry into established atherosclerotic lesions (43)(44)(45)(46). In addition, these fragile neovessels can favor focal intraplaque hemorrhage that provides a mechanism for the discontinuous increments seen in plaque growth.…”

mentioning

confidence: 99%

Atherosclerosis: A Classic Inflammatory Disease

Anogeianaki

Angelucci

Cianchetti³

et al. 2011

Atherosclerosis is an inflammatory disease due to a diet high in saturated fat, hypercholesterolemia, obesity, hypoglycemia, etc. mainly mediated by the infiltration of macrophage and T cells into the vascular wall. Once the endothelial is damaged monocytes penetrate the tissue and are transformed in scavenger cells. Upon stimulation of Th1 cells, a group of cytokines is released and contributes to the inflammatory response of atherosclerotic tissue. When macrophages proliferate they amplify inflammatory response through the secretion of growth factors and cytokines such as TNF and IL-1. In addition, chemokines such as RANTES and other C-C chemokines are generated, and matrix metalloprotinease 9 (MMP-9) are produced by activated monocytes. However, the immune system in atherosclerosis still remains unclear. Here, in this study we revisited the inter-relationship between atherosclerosis and inflammation.