Surgical trauma: hyperinflammation versus immunosuppression?

Menger, Michael D.; Vollmar, Brigitte

doi:10.1007/s00423-004-0472-0

Cited by 213 publications

(176 citation statements)

References 101 publications

(56 reference statements)

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“…The immunosuppressive effects of surgical and anesthetic intervention include impaired T cell proliferation (39), decreased natural killer cell cytotoxicity (43), and altered phagocytic cell function (5,23). After surgery, the imbalance between pro-and anti-inflammatory cytokines released by monocytes and macrophages may promote dysfunction of innate cellular immunity and increased susceptibility to infection (35,59). Phagocytosis by alveolar macrophages or neutrophils is decreased during and after major surgery (28).…”

mentioning

confidence: 99%

Propofol inhibits pressure-stimulated macrophage phagocytosis via the GABA_A receptor and dysregulation of p130cas phosphorylation

Shiratsuchi

Kouatli

et al. 2009

American Journal of Physiology-Cell Physiology

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Surgical stress and anesthesia result in systemic immunosuppression. Propofol, a commonly used anesthetic agent, alters immune cell functions. Previously, we demonstrated that extracellular pressure increases macrophage phagocytosis. We hypothesized that propofol might influence pressure-induced macrophage phagocytosis in monocytes from patients undergoing surgery. Pressure (20 mmHg above ambient pressure) augmented phagocytosis in monocytes from non-propofol-anesthetized patients but reduced phagocytosis in monocytes from propofol-anesthetized patients. In vitro, propofol stimulated phagocytosis but reversed pressure-induced phagocytosis in THP-1 macrophages and monocytes from healthy volunteers. The GABAA receptor antagonists picrotoxin and SR-95531 did not affect basal THP-1 phagocytosis or prevent pressure-stimulated phagocytosis. However, picrotoxin and SR-95531 negated the inhibitory effect of pressure in propofol-treated cells without altering propofol-induced phagocytosis. Phosphorylation of the adaptor protein p130cas was inversely related to phagocytosis: it was inhibited by pressure or propofol but increased by pressure + propofol compared with propofol alone. Reduction of p130cas by small interfering RNA in THP-1 macrophages increased basal phagocytosis and prevented pressure and propofol effects. In conclusion, propofol may alter macrophage responses to pressure via the GABAA receptor and p130cas, whereas pressure also acts via p130cas but independently of GABAA receptors. p130cas may be an important target for modulation of macrophage function in anesthetized patients.

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confidence: 99%

Propofol inhibits pressure-stimulated macrophage phagocytosis via the GABA_A receptor and dysregulation of p130cas phosphorylation

Shiratsuchi

Kouatli

et al. 2009

American Journal of Physiology-Cell Physiology

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“…Surgery has long been known to suppress immune function [1][2][3][4][5][6]. Human Leukocyte Antigen-DR (HLA-DR), one of the Major Histocompatibility Complex class-II proteins expressed on monocytes, macrophages and dendritic cells, is a crucial molecule for the presentation of antigen to lymphocytes and the initiation of adaptive immune responses [7,8].…”

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confidence: 99%

HLA‐DR expression and differential trafficking of monocyte subsets following low to intermediate risk surgery*

et al. 2009

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SummaryReduced HLA-DR expression on monocytes has been suggested as a predictive marker of immunosuppression following very high risk surgery, but there are few reports in lower risk surgery. In 32 patients undergoing low to intermediate risk surgery, blood samples were analysed by flow cytometry for HLA-DR expression and numbers in both CD14 high and CD14 low CD16+ monocyte subsets. The numbers of CD14high monocytes increased at 24 h (mean (SD), 5.0 (2.2) vs 7.6 (3.9) · 10 5 cells.ml )1 ; p < 0.01) while CD14 low CD16+ monocytes decreased (0.68 (0.36) vs 0.44 (0.36) · 10 5 cells.ml; p < 0.01). HLA-DR expression was significantly reduced in both subsets by 24 h (mean (SD) fluorescent intensity 440 (310) vs 160 (130) for CD14 high and 1000 (410) vs 560 (380) for CD14 low CD16+ subsets; p < 0.01). This reduction of monocyte HLA-DR expression 24 h following lower risk surgery raises questions about the purported clinical utility of this biomarker as an early predictor of postoperative complications. Our results also suggest that surgery induces significant trafficking (i.e. mobilisation, margination and extravasation) of monocyte subsets, and that monocyte HLA-DR depression is the result of a down-regulatory phenomenon (decreased protein expression on each cell) rather than the differential trafficking of monocyte subsets.

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“…These are the leading causes of death in middle and late phases of hemorrhagic shock. These conditions are thought to result from hyperinflammation or immunodepression (Menger and Vollmar, 2004;Moore et al, 2004;2006;Brøchner and Toft, 2009).…”

Section: Introductionmentioning

confidence: 99%

Immune recovery after fluid resuscitation in rats with severe hemorrhagic shock

Feng

Jiang

et al. 2017

J. Zhejiang Univ. Sci. B

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Abstract:Objective: To investigate the effects of resuscitation with normal saline (NS), hypertonic saline (HTS), and hydroxyethyl starch (HES) on regulatory T cells (Tregs), helper T 1 (Th1)/Th2 and cytotoxic T 1 (Tc1)/Tc2 profiles in the treatment of hemorrhagic shock. Methods: Rats subjected to severe hemorrhagic shock were resuscitated for 30 min with NS (n=8), HTS (n=8), or HES (n=8); sham (n=8) and naive control (n=8) groups were used for comparison. Following fluid resuscitation, the whole shed blood was reinfused for 30 min, and the rats were observed with continuous hemodynamic monitoring for 120 min. CD4 + CD25 + Foxp3 + Treg proportions, Th1/Th2 and Tc1/Tc2 profiles in spleen were analyzed by three-color flow cytometry. Results: The proportion of CD4 + CD25 + Foxp3 + Tregs and ratios of Th1/Th2 and Tc1/Tc2 did not differ among control, sham, and HTS groups, but were significantly lower in NS and HES groups (both P<0.05 vs. sham); NS and HES levels were similar. The level of Tc1 was significantly increased in HTS (P<0.05 vs. sham), and levels of Tc2 were increased in NS, HES, and HTS groups compared to sham (all P<0.05), but did not differ from each other. Conclusions: HTS resuscitation has a greater impact on immune system recovery than NS or HES by preserving the proportion of Tregs and maintaining the balance between Th1/Th2 and Tc1/Tc2 cells in the spleen. Thus, HTS resuscitation provides potential immunomodulatory activity in the early stage after hemorrhagic shock.

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Surgical trauma: hyperinflammation versus immunosuppression?

Abstract: When drawing up the therapeutic regimen the physician should not consider hyperinflammation versus immunosuppression, but hyperinflammation and immunosuppression, aiming at restoring an appropriate mediator- and immune cell-associated balance.

Cited by 213 publications

References 101 publications

Propofol inhibits pressure-stimulated macrophage phagocytosis via the GABA_A receptor and dysregulation of p130cas phosphorylation

Propofol inhibits pressure-stimulated macrophage phagocytosis via the GABA_A receptor and dysregulation of p130cas phosphorylation

HLA‐DR expression and differential trafficking of monocyte subsets following low to intermediate risk surgery*

Immune recovery after fluid resuscitation in rats with severe hemorrhagic shock

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Surgical trauma: hyperinflammation versus immunosuppression?

Abstract: When drawing up the therapeutic regimen the physician should not consider hyperinflammation versus immunosuppression, but hyperinflammation and immunosuppression, aiming at restoring an appropriate mediator- and immune cell-associated balance.

Cited by 213 publications

References 101 publications

Propofol inhibits pressure-stimulated macrophage phagocytosis via the GABAA receptor and dysregulation of p130cas phosphorylation

Propofol inhibits pressure-stimulated macrophage phagocytosis via the GABAA receptor and dysregulation of p130cas phosphorylation

HLA‐DR expression and differential trafficking of monocyte subsets following low to intermediate risk surgery*

Immune recovery after fluid resuscitation in rats with severe hemorrhagic shock

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Propofol inhibits pressure-stimulated macrophage phagocytosis via the GABA_A receptor and dysregulation of p130cas phosphorylation

Propofol inhibits pressure-stimulated macrophage phagocytosis via the GABA_A receptor and dysregulation of p130cas phosphorylation