Tumour necrosis factor-alpha (TNFα) and interleukin-10 are crucial mediators in post-operative systemic inflammatory response and determine the occurrence of complications after major abdominal surgery

Dimopoulou, Ioanna; Armaganidis, Apostolos; Douka, Evangelia; Mavrou, Irini; Augustatou, C; Kopterides, Petros; Lyberopoulos, Panagiotis; Tzanela, Marinella; Orfanos, Stylianos E.; Pelekanou, Emilia; Kostopanagiotou, Georgia; Macheras, Anastasios; Giamarellos‐Bourboulis, Evangelos J.

doi:10.1016/j.cyto.2007.02.023

Cited by 55 publications

(45 citation statements)

References 11 publications

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“…26 One study indicated that the tumor necrosis factor-a/IL-10 quote predicted the occurrence of postoperative complications. 27 Ugras et al 28 investigated the role of peritoneal cytokine levels in developing anastomotic leakage after colorectal surgery. It was found that the peritoneal cytokine levels of IL-6, IL-10, and tumor necrosis factor-a can be an additional diagnostic tool that can support the early prediction of anastomotic leakage (AL) in colorectal surgery.…”

Section: Discussionmentioning

confidence: 99%

Surgical Stress Response After Colorectal Resection

Andersson

Ansari

Nordén

et al. 2013

International Surgery

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The human body's response to surgery is correlated with the extent of tissue damage. The aim of the present study was to, over time, map out parameters concerning inflammation, metabolism, nutrition, breathing function, muscle strength, and well-being in elective colorectal surgery. Eighteen patients were prospectively included: colon resection (n ¼ 9) and rectum resection/amputation (n ¼ 9). Postoperative interleukin 10 (IL-10) rose more in the rectum surgery group on day 0 (P ¼ 0.007) and day 3 (P ¼ 0.025). Furthermore, significant differences between groups were detected regarding albumin, prealbumin, and total iron-binding capacity (TIBC). For albumin and TIBC, this difference was seen even on day 7. C-reactive protein, IL-6, IL-8, glucose, cortisol, insulin, pain, fatigue, nausea, grip strength, and forced expiratory volume in 1 second did not show any differences. No correlation was revealed between measured parameters and postoperative complications. Postoperative levels of IL-10, albumin, prealbumin, and TIBC may be used as determinants of surgical stress after colorectal surgery.

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Section: Discussionmentioning

confidence: 99%

Surgical Stress Response After Colorectal Resection

Andersson

Ansari

Nordén

et al. 2013

International Surgery

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Section: Introductionmentioning

confidence: 99%

“…[4][5][6] These observations suggest the transition from inflammatory to immunosuppressive macrophages may be critical to control initial inflammatory responses and prevent lethal septic shock. 4,7,8 However, the molecular mechanism by which this transition is achieved remains poorly understood.In the present work, we examine the role that endogenous CD39 and adenosine triphosphate (ATP) play in regulating the macrophage inflammatory response. Recently, extracellular ATP (eATP) has been characterized as a "danger signal" that can promote inflammation through P2X7-dependent activation of the NLRP3 inflammasome, leading to IL-1b production.…”

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confidence: 99%

“…Third, there is currently a paucity of studies investigating how ATP and CD39 influence inflammasome-independent responses, such as TNF-a production. 4,8,22 Finally, the specific contribution of CD39 The online version of this article contains a data supplement.The publication costs of this article were defrayed in part by page charge payment. Therefore, and solely to indicate this fact, this article is hereby marked "advertisement" in accordance with 18 USC section 1734.…”

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confidence: 99%

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TLR stimulation initiates a CD39-based autoregulatory mechanism that limits macrophage inflammatory responses

Cohen

Briggs

Marino

et al. 2013

Blood

125

140

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• TLR-stimulated macrophages synthesize, release, and hydrolyze ATP via CD39 to regulate their own activation state.• The loss of macrophage CD39 prevents regulatory macrophage development and leads to lethal inflammatory responses and septic shock in mice.Sepsis is a highly fatal disease caused by an initial hyperinflammatory response followed by a state of profound immunosuppression. Although it is well appreciated that the initial production of proinflammatory cytokines by macrophages accompanies the onset of sepsis, it remains unclear what causes the transition to an immunosuppressive state. In this study, we reveal that macrophages themselves are key regulators of this transition and that the surface enzyme CD39 plays a critical role in self-limiting the activation process. We demonstrate that Toll-like receptor (TLR)-stimulated macrophages modulate their activation state by increasing the synthesis and secretion of adenosine triphosphate (ATP). This endogenous ATP is paradoxically immunosuppressive due to its rapid catabolism into adenosine by CD39. Macrophages lacking CD39 are unable to transition to a regulatory state and consequently continue to produce inflammatory cytokines. The importance of this transition is demonstrated in a mouse model of sepsis, where small numbers of CD39-deficient macrophages were sufficient to induce lethal endotoxic shock. Thus, these data implicate CD39 as a key "molecular switch" that allows macrophages to self-limit their activation state. We propose that therapeutics targeting the release and hydrolysis of ATP by macrophages may represent new ways to treat inflammatory diseases. (Blood. 2013;122(11):1935-1945 IntroductionFailure to control inflammatory macrophage activation responses can lead to pathological diseases, best exemplified by sepsis. Despite our growing understanding of its pathogenesis, sepsis continues to affect more than 200 000 people annually in the United States, with a mortality rate as high as 50%.1,2 The severe pathology associated with sepsis occurs in response to the hyperproduction of macrophagederived inflammatory cytokines, which can lead to vascular and tissue destruction, multiple organ failure, shock, and death.3 Intriguingly, macrophages isolated from late-stage septic individuals exhibit the phenotype of immunosuppressive, regulatory macrophages, expressing high levels of the anti-inflammatory cytokine interleukin-10 (IL-10) and low levels of tumor necrosis factor a (TNF-a) and IL-12. [4][5][6] These observations suggest the transition from inflammatory to immunosuppressive macrophages may be critical to control initial inflammatory responses and prevent lethal septic shock. 4,7,8 However, the molecular mechanism by which this transition is achieved remains poorly understood.In the present work, we examine the role that endogenous CD39 and adenosine triphosphate (ATP) play in regulating the macrophage inflammatory response. Recently, extracellular ATP (eATP) has been characterized as a "danger signal" that can promote inflammation through ...

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“…Systemic inflammatory response syndrome (SIRS) following major abdominal surgery is characterized by complex alterations in cytokine concentrations, and the balance between tumor necrosis factor (TNF)-α and IL-10 may be related to the occurrence of postoperative complications [21] . Wu et al reported that small intestinal ischemia reperfusion increased mucosal inflammatory modulator IL-6 concentration and inhibited anti-inflammatory cytokine IL-10 synthesis [22] .…”

Section: Discussionmentioning

confidence: 99%

Direct hemoperfusion with a polymyxin B-immobilized cartridge in intestinal warm ischemia reperfusion

Sato¹,

Oshima²,

Arakawa³

et al. 2008

WJG

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AIM:To investigate the effectiveness of direct hemoperfusion with polymyxin B-immobilized fibers (DHP-PMX therapy) on warm ischemia-reperfusion (I/R) injury of the small intestine. METHODS:The proximal jejunum and distal ileum of mongrel dogs were resected. Warm ischemia was performed by clamping the superior mesenteric artery (SMA) and vein (SMV) for 2 h. Blood flow to the proximal small intestine was restored 1 h after reperfusion, and the distal small intestine was used as a stoma. The experiment was discontinued 6 h after reperfusion. The dogs were divided into two groups: the DHP-PMX group (n = 6, DHP-PMX was performed for 180 min; from 10 min prior to reperfusion to 170 min after reperfusion) and the control group (n = 5). The rate pressure product (RPP), SMA blood flow, mucosal tissue blood flow, and intramucosal pH (pHi) were compared between the two groups. The serum interleukin (IL)-10 levels measured 170 min after reperfusion were also compared. RESULTS: The RPP at 6 h after reperfusion was significantly higher in the PMX group than in the control group (12 174 ± 1832 mmHg/min vs 8929 ± 1797 mmHg/min, P < 0.05). The recovery rates of the SMA blood flow at 1 and 6 h after reperfusion were significantly better in the PMX group than in the control group (61% ± 7% vs 44% ± 4%, P < 0.05, and 59% ± 5% vs 35% ± 5%, P < 0.05, respectively).The recovery rate of the mucosal tissue blood flow and the pHi levels at 6 h after reperfusion were significantly higher in the PMX group (61% ± 8% vs 31% ± 3%, P < 0.05 and 7.91 ± 0.06 vs 7.69 ± 0.08, P < 0.05, respectively). In addition, the serum IL-10 levels just before DHP-PMX removal were significantly higher in the PMX group than in the control group (1 569 ± 253 pg/mL vs 211 ± 40 pg/mL, P < 0.05).

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Tumour necrosis factor-alpha (TNFα) and interleukin-10 are crucial mediators in post-operative systemic inflammatory response and determine the occurrence of complications after major abdominal surgery

Cited by 55 publications

References 11 publications

Surgical Stress Response After Colorectal Resection

Surgical Stress Response After Colorectal Resection

TLR stimulation initiates a CD39-based autoregulatory mechanism that limits macrophage inflammatory responses

Direct hemoperfusion with a polymyxin B-immobilized cartridge in intestinal warm ischemia reperfusion

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