Tumour Necrosis Factor: Implications for Surgical Patients

Khalil, Alizan Abdul; Hall, John C.; Aziz, Faieza Abdul; Price, Patricia

doi:10.1111/j.1445-2197.2006.03921.x

Cited by 16 publications

(11 citation statements)

References 83 publications

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“…TNF is a mediator in the normal inXammatory pathway [6] and has bactericidal properties [7]. A previous study found that patients requiring revision of total joint replacement due to sepsis had higher levels of serum TNF-alpha compared to those undergoing aseptic revision arthroplasty [8].…”

Section: Introductionmentioning

confidence: 99%

Should anti-TNF therapy be discontinued in rheumatoid arthritis patients undergoing elective orthopaedic surgery? A systematic review of the evidence

et al. 2011

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Anti-tumour necrosis factor (TNF) therapies have revolutionized the management of rheumatoid arthritis (RA). A high proportion of RA patients are now established users of anti-TNF agents. Unfortunately, many RA patients with longstanding disease still require elective orthopaedic procedures. Published studies on the influence of TNF antagonist on infection rates in RA patients undergoing surgery are conflicting. However, national registries of RA patients on anti-TNF reported an increased risk of infection. The risk of anti-TNF-related infection is highest at the start of treatment with frequent involvement of the skin and subcutaneous tissue. Infection at these sites could negatively influence the healing of surgical wound. Current guidelines suggest that treatment with biologics should be discontinued prior to surgery. Patients with established disease are more likely to flare compared to those with early disease on stopping treatment. Consequently, TNF blockers need to be reinstated promptly after surgery to avoid the risk of RA flare.

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Section: Introductionmentioning

confidence: 99%

Should anti-TNF therapy be discontinued in rheumatoid arthritis patients undergoing elective orthopaedic surgery? A systematic review of the evidence

et al. 2011

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“…Ассоциация uPar с α5β1 индуцирует в интегрине появление дополни-тельного сайта для фибронектина в дополне-ние к связывающему rgd-сайту. недавно на uPar был идентифицирован сайт связывания с α5β1 во втором домене (130)(131)(132)(133)(134)(135)(136)(137)(138)(139)(140)(141)(142) [49].…”

Section: сигнализация урокиназыunclassified

“…ВкМ -внеклеточный матрикс Biochemistry aNd BiotechNology for moderN mediciNe с ее уровнем в контрольной группе, в то время как нанесение тканевого активатора плазми-ногена подобного эффекта не оказывало [130]. фактор некроза опухолей-α (tNf-α), выраба-тываемый моноцитами/макрофагами, нейтро-филами, а также структурными компонентами сосудистой стенки (гладкомышечными клет-ками и фиб робластами), является важным по-средником развития воспаления и вызывает образование и секрецию провоспалительных факторов (интерлейкин-10, кортикостероиды, простагландины) [131].…”

Section: рис 8 схема механизмов способствующих пролиферации клетокunclassified

Role of multidomain structure of urokinase in regulation of growth and remodeling of vessels

Ткачук¹

2013

Ukr.Biochem.J.

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“…If levels of this key regulator of the inflammatory response are too low, an inadequate immune response occurs. Conversely, if levels of TNFα are elevated in the absence of infection then chronic inflammation can develop (Guicciardi and Gores 2009; Khalil et al, 2006; Silke 2011; Goetz et al, 2004). TNFα is produced predominantly by lymphocytes and monocytes/macrophages (Khalil et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Flame retardants, hexabromocyclododecane (HCBD) and tetrabromobisphenol a (TBBPA), alter secretion of tumor necrosis factor alpha (TNFα) from human immune cells

Yasmin

Whalen

2018

Arch Toxicol

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Hexabromocyclododecane (HBCD) and tetrabromobisphenol A (TBBPA) are flame retardants, used in a variety of applications, which contaminate the environment and are found in human blood. HBCD and TBBPA have been shown to alter the tumor killing function of natural killer (NK) lymphocytes and the secretion of the inflammatory cytokines interferon gamma (IFNγ) and interleukin 1 beta (IL-1β). The current study examined the effects of HBCD and TBBPA on secretion of the critical pro-inflammatory cytokine tumor necrosis factor alpha (TNFα) from human immune cells. Preparations of human immune cells that ranged in complexity were studied to determine if the effects of the compounds were consistent as the composition of the cell preparation became more heterogeneous. Cell preparations studied were: NK cells, monocyte-depleted (MD) peripheral blood mononuclear cells (PBMCs), and PBMCs. Exposure of NK cells to higher concentrations of HBCD (5 and 2.5 µM) caused decreased secretion of TNFα. However, when the cell preparation contained T lymphocytes (MD-PBMCs and PBMCs) these same concentrations of HBCD increased TNFα secretion as did nearly all other concentrations. This suggests that HBCD's ability to increase TNFα secretion from immune cells was dependent on the presence of T lymphocytes. In contrast, exposures to TBBPA decreased the secretion of TNFα from all immune cell preparations regardless of the composition of the cell preparation. Further, HBCD-induced increases in TNFα secretion utilized the p38 MARK pathway. Thus, both HBCD and TBBPA may have the capacity to disrupt the inflammatory response with HBCD having the potential to cause chronic inflammation.

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Tumour Necrosis Factor: Implications for Surgical Patients

Cited by 16 publications

References 83 publications

Should anti-TNF therapy be discontinued in rheumatoid arthritis patients undergoing elective orthopaedic surgery? A systematic review of the evidence

Should anti-TNF therapy be discontinued in rheumatoid arthritis patients undergoing elective orthopaedic surgery? A systematic review of the evidence

Role of multidomain structure of urokinase in regulation of growth and remodeling of vessels

Flame retardants, hexabromocyclododecane (HCBD) and tetrabromobisphenol a (TBBPA), alter secretion of tumor necrosis factor alpha (TNFα) from human immune cells

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