Sepsis and serum cytokine concentrations

Damas, Pierre; Canivet, Jean-Luc; Groote, Donat De; Vrindts, Y; Albert, Adelin; Franchimont, P; Lamy, Maurice

doi:10.1097/00003246-199703000-00006

Cited by 221 publications

(134 citation statements)

References 39 publications

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“…However, the mechanisms by which C5a is regulated in sepsis remain unclear. Proinflammatory cytokines contribute to an overwhelming inflammatory immune response in the early phase of sepsis, whereas anti-inflammatory cytokines are involved in the late-phase immune response [6,18,19]. Based on these findings, it is conceivable that the cytokine network interacts with the complement system in regulating immune responses in sepsis.…”

Section: Introductionmentioning

confidence: 99%

IFN‐γ‐producing NKT cells exacerbate sepsis by enhancing C5a generation via IL‐10‐mediated inhibition of CD55 expression on neutrophils

Kim

Ahn

et al. 2014

Eur J Immunol

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A role for NKT cells has been implicated in sepsis, but the mechanism by which NKT cells contribute to sepsis remains unclear. Here, we examined WT and NKT-cell-deficient mice of C57BL/6 background during cecal ligation and puncture-induced sepsis. The levels of C5a, IFN-γ, and IL-10 were higher in the serum and peritoneal fluid of WT mice than in those of CD1d −/− mice, while the mortality rate was lower in CD1d −/− mice than in WT mice. C5a blockade decreased mortality of WT mice during sepsis, whereas it did not alter that of CD1d −/− mice. As assessed by intracellular staining, NKT cells expressed IFN-γ, while neutrophils expressed IL-10. Upon coculture, IL-10-deficient NKT cells enhanced IL-10 production by WT, but not IFN-γR-deficient, neutrophils. Meanwhile, CD1d −/− mice exhibited high CD55 expression on neutrophils during sepsis, whereas those cells from WT mice expressed minimal levels of CD55. Recombinant IL-10 administration into CD1d −/− mice reduced CD55 expression on neutrophils. Furthermore, adoptive transfer of sorted WT, but not IFN-γ-deficient, NKT cells into CD1d −/− mice suppressed CD55 expression on neutrophils, but increased IL-10 and C5a levels. Taken together, IFN-γ-producing NKT cells enhance C5a generation via IL-10-mediated inhibition of CD55 expression on neutrophils, thereby exacerbating sepsis.Keywords: C5a r IFN-γ r Neutrophils r NKT cell r Sepsis Additional supporting information may be found in the online version of this article at the publisher's web-site IntroductionNKT cells are a distinct T-cell subset characterized by the expression of natural killer receptors and semi-invariant TCRs. These cells recognize glycolipids presented by CD1d, an MHC class I-like Correspondence: Dr. Doo Hyun Chung e-mail: doohyun@snu.ac.kr protein expressed by APCs [1]. During bacterial infection, TCRs on NKT cells directly recognize glycolipids derived from certain Gramnegative bacterial membranes [2,3] and can be activated by innate cytokines secreted by dendritic cells that have been activated by microorganisms [2,4]. Furthermore, LPS-mediated engagement of TLR4 directly activates NKT cells in terms of differential * These authors contributed equally to this work. Eur. J. Immunol. 2014Immunol. . 44: 2025Immunol. -2035 cytokine production, thereby regulating immune diseases [5]. These findings suggest that NKT cells, activated during immune responses against bacteria, regulate bacteria-mediated pathologic processes such as sepsis. Sepsis is a complex inflammatory dysregulation that causes multiple organ dysfunction and coagulopathy, often resulting in death [6,7]. Several studies have demonstrated that NKT cells promote LPS-or cecal ligation and puncture (CLP)-induced sepsis in mice through the production of . Consistent with these findings, two independent studies have demonstrated that treatment of C57BL/6 mice with anti-CD1d antibody enhances survival rates during CLP-induced sepsis [11,12], suggesting that NKT-cell-mediated promotion of sepsis depends on an interaction between CD1d and TCR...

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Section: Introductionmentioning

confidence: 99%

IFN‐γ‐producing NKT cells exacerbate sepsis by enhancing C5a generation via IL‐10‐mediated inhibition of CD55 expression on neutrophils

Kim

Ahn

et al. 2014

Eur J Immunol

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“…Traditionally, it is envisioned as an uncontrolled systemic inflammatory response, including a "cytokine storm" (29). IL-1␤, TNF-␣, and IL-6 are some major proinflammatory cytokines associated with sepsis (15,52), and high cytokine concentrations have been shown to correlate with disease severity (17,18,23). A number of efforts have therefore been made in reducing cytokine actions in sepsis, but such efforts have mostly been unsuccessful in reducing mortality.…”

mentioning

confidence: 99%

Acute reactive oxygen species (ROS)-dependent effects of IL-1β, TNF-α, and IL-6 on the glomerular filtration barrier (GFB) in vivo

Sverrisson

Axelsson

Rippe

et al. 2015

American Journal of Physiology-Renal Physiology

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“…Peripheral blood mononuclear cells play a prominent role in the innate immune response, and can increase during critical illness (12). In the circulation, they may participate in both inflammatory and coagulation cascades, releasing mediators with autocrine and paracrine effects, and activating additional monocytes and endothelial cells (1,13). Assessing the identity and functional capabilities of PBMCs mobilized during critical illness can lead to the development of unique prognostic biomarkers, thereby advancing our understanding of ALI and the pathophysiology of severe sepsis.…”

mentioning

confidence: 99%

Acute Lung Injury but Not Sepsis Is Associated with Increased Colony Formation by Peripheral Blood Mononuclear Cells

Burnham¹,

Mealer²,

Gaydos³

et al. 2010

Am J Respir Cell Mol Biol

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Acute lung injury (ALI) and severe sepsis are common critical illnesses associated with the mobilization of bone marrow-derived cells into the circulation. By identifying and determining these cells' functional characteristics, unique prognostic biomarkers can be developed to help investigators understand the mechanisms underlying the pathophysiology of these disorders. We previously demonstrated an increased colony-forming unit (CFU) ability of circulating peripheral blood mononuclear cells (PBMCs) in patients with ALI, compared with healthy control subjects, that also correlated with improved survival. Here we hypothesized that the increased CFUs in ALI are associated with lung injury, and therefore ALI will result in an increased number of CFUs compared with patients exhibiting severe sepsis. To test this, blood was collected from 80 patients (63 with ALI, and 17 with severe sepsis) within 72 hours of diagnosis, and from 5 healthy control subjects. A CFU assay was performed on isolated PBMCs. Lung injury scores and the need for mechanical ventilation were greater in patients with ALI than in patients with severe sepsis (P , 0.0001 for each). CFU numbers were highest in patients with ALI compared with patients manifesting severe sepsis or control subjects (median CFU number [25-75% quartiles] of 61 Our findings suggest that increased colony-forming ability by PBMCs in ALI results from lung injury, independent of sepsis and mechanical ventilation. Factors contributing to colony formation by PBMCs in ALI, and the role PBMCs play in its pathogenesis remain to be fully established.

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Sepsis and serum cytokine concentrations

Abstract: According to the profiles of the cytokines, septic shock patients do not represent a homogeneous population. These profiles should be described in order to distinguish between patients, and the profiles may be useful to identify those patients susceptible to new therapies.

Cited by 221 publications

References 39 publications

IFN‐γ‐producing NKT cells exacerbate sepsis by enhancing C5a generation via IL‐10‐mediated inhibition of CD55 expression on neutrophils

IFN‐γ‐producing NKT cells exacerbate sepsis by enhancing C5a generation via IL‐10‐mediated inhibition of CD55 expression on neutrophils

Acute reactive oxygen species (ROS)-dependent effects of IL-1β, TNF-α, and IL-6 on the glomerular filtration barrier (GFB) in vivo

Acute Lung Injury but Not Sepsis Is Associated with Increased Colony Formation by Peripheral Blood Mononuclear Cells

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