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Hyporesponsiveness of natural killer cells and impaired inflammatory responses in critically ill patients.

ABSTRACT: To investigate natural killer (NK) cell activity, circulating cytokine level and peripheral blood mononuclear cell (PBMC) cytokine production status in critically ill patients.Blood samples were collected <24 h after admission from 24 intensive care unit (ICU) patients and 24 age-, sex-, and body mass index (BMI)-matched healthy controls. Serum cytokine concentrations and cytokine production by PBMCs and lipopolysaccharide (LPS)-stimulated PBMCs were measured.The ICU group showed lower NK cell activity than the controls under all conditions and an absence of interferon (IFN)-?. After adjusting for triglycerides, LDL- and HDL-cholesterol, and glucose, the ICU group exhibited lower serum levels of albumin and interleukin (IL)-12 and higher leukocyte counts and hs-CRP and IL-6 levels than the controls. Non-stimulated PBMCs from ICU patients secreted significantly greater amounts of IL-6 and IL-1? than the controls; however, the production of IL-6, TNF-? and IL-1? in response to LPS stimulation was significantly lower in the ICU group.Significant reductions in NK cell activity and serum IL-12 level, an absence of serum IFN-?, and decreased cytokine production from LPS-stimulated PBMCs indicate the hyporesponsiveness of NK cells and an impaired early phase inflammatory response in critically ill patients (ClinicalTrials.gov NCT02565589 :). Retrospectively registered; October 1, 2015.

SUBMITTER: Kim M

PROVIDER: S-EPMC5723033 | biostudies-literature | 2017 Dec

REPOSITORIES: biostudies-literature

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Hyporesponsiveness of natural killer cells and impaired inflammatory responses in critically ill patients.

Kim Minkyung M Kim Minjoo M Jeong Hana H Chae Jey Sook JS Kim Young Sam YS Lee Jae Gil JG Cho Younsoo Y Lee Jong Ho JH

BMC immunology 20171208 1

<h4>Background</h4>To investigate natural killer (NK) cell activity, circulating cytokine level and peripheral blood mononuclear cell (PBMC) cytokine production status in critically ill patients.<h4>Methods</h4>Blood samples were collected <24 h after admission from 24 intensive care unit (ICU) patients and 24 age-, sex-, and body mass index (BMI)-matched healthy controls. Serum cytokine concentrations and cytokine production by PBMCs and lipopolysaccharide (LPS)-stimulated PBMCs were measured.< ...[more]

PMID: 29221433

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Project description:ObjectiveSystemic juvenile idiopathic arthritis (sJIA) is characterized by fever, arthritis, rash, hepatosplenomegaly, and macrophage activation syndrome; however, its pathogenesis is still unclear. Elevated serum interleukin (IL)-18 concentrations and decreased natural killer (NK) cell activity are characteristic of active disease; thus, we examined IL-18 signaling in NK cells from sJIA.MethodsWe analyzed mitogen-activated protein kinase (MAPK) p38 and nuclear factor κ light chain enhancer of activated B cells (NFκB) p65 phosphorylation in NK cells after in vitro recombinant IL-18 (rIL-18) stimulation in 31 patients with sJIA. Associations between clinical features, serum IL-18, and phosphorylation intensity were analyzed. Furthermore, we investigated the effects of high IL-18 concentrations on phosphorylation in NK cells.ResultsPatients were divided according to their disease activity: systemic features (n = 8), chronic arthritis (n = 7), remission on medication (n = 10), and remission off medication (n = 6). MAPK p38 and NFκB p65 phosphorylation intensity were the highest in healthy controls, followed by remission off medication, remission on medication (vs. control; MAPK p38, P < 0.01; NFκB p65, P < 0.05), chronic arthritis (P < 0.001, P < 0.001), and systemic features (P < 0.001, P < 0.001). The systemic features group showed a complete defect in phosphorylation. Serum IL-18 was the highest in the systemic features group followed by chronic arthritis, remission on medication (P < 0.01), remission off medication (P < 0.01), and healthy controls (P < 0.01). Phosphorylation intensity was negatively correlated with serum IL-18 (MAPK p38, r2 = 0.42; NFκB p65, r2 = 0.54). Furthermore, healthy control NK cells were cultured with rIL-18; impaired phosphorylation was reproduced in vitro.ConclusionImpaired IL-18 signaling in NK cells correlated with disease activity in sJIA. High serum IL-18 exposure induces impaired MAPK and NFκB phosphorylation in NK cells.

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Hyporesponsiveness of natural killer cells and impaired inflammatory responses in critically ill patients.

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Hyporesponsiveness of natural killer cells and impaired inflammatory responses in critically ill patients.

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