Interleukin-6 at discharge predicts all-cause mortality in patients with sepsis

Naffaa, Mohammad E.; Makhoul, Badira F.; Tobia, Amjad; Kaplan, Marielle; Aronson, Doron; Saliba, Walid; Azzam, Zaher S.

doi:10.1016/j.ajem.2013.06.011

Cited by 23 publications

(18 citation statements)

References 14 publications

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“…First, we tested whether CD28 or TNF neutralization affected serum IL-6 levels since increased IL-6 correlates with decreased survival not only in models of sepsis but also in septic patients (48–51). Both, CTLA4-Ig and anti-TNF significantly reduced serum IL-6 compared to the IgG controls, with anti-TNF being even more effective in decreasing IL-6 than CTLA4-Ig (Fig.…”

Section: Resultsmentioning

confidence: 99%

TNF and CD28 Signaling Play Unique but Complementary Roles in the Systemic Recruitment of Innate Immune Cells after Staphylococcus aureus Enterotoxin A Inhalation

Svedova

Tsurutani

Liu

et al. 2016

The Journal of Immunology

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Staphylococcus aureus enterotoxins cause debilitating systemic inflammatory responses, but how they spread systemically and trigger inflammatory cascade is unclear. Here, we showed in mice that after inhalation, Staphylococcus aureus enterotoxin A rapidly entered the bloodstream and induced T cells to orchestrate systemic recruitment of inflammatory monocytes and neutrophils. To study the mechanism used by specific T cells that mediate this process, a systems approach revealed inducible and non-inducible pathways as potential targets. It was found that TNF caused neutrophil entry into the peripheral blood, while CD28 signaling, but not TNF, was needed for chemotaxis of inflammatory monocytes into blood and lymphoid tissue. However, both pathways triggered local recruitment of neutrophils into lymph nodes. Thus, our findings revealed a dual mechanism of monocyte and neutrophil recruitment by T cells relying on overlapping and non-overlapping roles for the non-inducible costimulatory receptor CD28 and the inflammatory cytokine TNF. During sepsis, there might be clinical value in inhibiting CD28 signaling to decrease T cell-mediated inflammation and recruitment of innate cells while retaining bioactive TNF to foster neutrophil circulation.

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Section: Resultsmentioning

confidence: 99%

TNF and CD28 Signaling Play Unique but Complementary Roles in the Systemic Recruitment of Innate Immune Cells after Staphylococcus aureus Enterotoxin A Inhalation

Svedova

Tsurutani

Liu

et al. 2016

The Journal of Immunology

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“…Interleukin-6 is a proinflammatory cytokine involved in the initial innate cell immune response to infection [34]. There are several SNPs found in the promoter region of IL-6 [18].…”

Section: Discussionmentioning

confidence: 99%

Association of tumor necrosis factor α −308G/A and interleukin-6 −174G/C gene polymorphism with pneumonia-induced sepsis

Feng

Mao

Pang

et al. 2015

Journal of Critical Care

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“…Inconsistent levels of IL-6 have also been observed during pregnancy, with median values around 128 pg/ml registered at delivery, which drop by more than two fold (∼58 pg/ml) immediately afterward [52]. Furthermore, serum IL-6 levels have been found to increase drastically during sepsis [53].…”

Section: Il6 Expression and Secretionmentioning

confidence: 99%

“…Many physiological factors such as diet, exercise and stress are known to regulate the secretion of IL-6 [47][48][49][50][51][52][53]. Exercise is an important stimulus for increased gene expression and production of IL-6 in skeletal muscle, and the majority of circulating IL-6 during exercise originates from contracting muscle, resulting in a 100-fold increase over the normal physiological level [50,54].…”

Section: Il6 Expression and Secretionmentioning

confidence: 99%

Role of interleukin-6 in cancer progression and therapeutic resistance

et al. 2016

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In the last several decades, the number of people dying from cancer-related deaths has not reduced significantly despite phenomenal advances in the technologies related to diagnosis and therapeutic modalities. The principal cause behind limitations in the curability of this disease is the reducing sensitivity of the cancer cells towards conventional anticancer therapeutic modalities, particularly in advance stages of the disease. Amongst several reasons, certain secretory factors released by the tumour cells into the microenvironment have been found to confer resistance towards chemo- and radiotherapy, besides promoting growth. Interleukin-6 (IL-6), one of the major cytokines in the tumour microenvironment, is an important factor which is found at high concentrations and known to be deregulated in cancer. Its overexpression has been reported in almost all types of tumours. The strong association between inflammation and cancer is reflected by the high IL-6 levels in the tumour microenvironment, where it promotes tumorigenesis by regulating all hallmarks of cancer and multiple signalling pathways, including apoptosis, survival, proliferation, angiogenesis, invasiveness and metastasis, and, most importantly, the metabolism. Moreover, IL-6 protects the cancer cells from therapy-induced DNA damage, oxidative stress and apoptosis by facilitating the repair and induction of countersignalling (antioxidant and anti-apoptotic/pro-survival) pathways. Therefore, blocking IL-6 or inhibiting its associated signalling independently or in combination with conventional anticancer therapies could be a potential therapeutic strategy for the treatment of cancers with IL-6-dominated signalling.

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Interleukin-6 at discharge predicts all-cause mortality in patients with sepsis

Cited by 23 publications

References 14 publications

TNF and CD28 Signaling Play Unique but Complementary Roles in the Systemic Recruitment of Innate Immune Cells after Staphylococcus aureus Enterotoxin A Inhalation

TNF and CD28 Signaling Play Unique but Complementary Roles in the Systemic Recruitment of Innate Immune Cells after Staphylococcus aureus Enterotoxin A Inhalation

Association of tumor necrosis factor α −308G/A and interleukin-6 −174G/C gene polymorphism with pneumonia-induced sepsis

Role of interleukin-6 in cancer progression and therapeutic resistance

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