Serial changes in cellular immunity of septic patients with multiple organ-system failure

Nishijima, Masako K.; Takezawa, Jun; Hosotsubo, Kikumi; Takahashi, Hideo; Yasuhiro, Shimada; Yoshiya, Ikuto

doi:10.1097/00003246-198602000-00002

Cited by 38 publications

(11 citation statements)

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“…Therefore, a role for T lymphocytes in severe systemic bacterial infections has been described in several studies, and the findings of other investigations have supported the notion that T lymphocytes are involved in the pathogenesis of septic shock (Holub et al 2000;Holub et al 2003;Kabisch et al 1990;Lin et al 1993;Nishijima et al 1986). The NK compartment is characterized as CD3 -CD56 + cells that can be cytotoxic (CD16 + Bright) or produce high amount of cytokines such as IFNγ (CD16 + Dim) (Romagnani et al 2007).…”

Section: Role Of Peripheral Blood Lymphocytes In Septic Shock Outcomementioning

confidence: 70%

“…A drop in circulating CD3 + CD4 + and CD3 + CD8 + T cells has been described in patients with severe sepsis or septic shock at admission to the ICU (Holub et al 2000;Holub et al 2003;Kabisch et al 1990;Lin et al 1993;Nishijima et al 1986). In our kinetic study, we also observed that this T lymphopenia persists during the first week of follow up and is independent of the outcome.…”

Section: Interpretation Of Blood Lymphocyte Count Alterations In Patimentioning

confidence: 98%

“…The role of the lymphocytes in the septic shock it's not clear and it has been studied extensively in the last decades (Holub et al 2000;Holub et al 2003;Lin et al 1993;Menges et al 1999;Nishijima et al 1986). However, there are not many authors that have proposed to use lymphocytes as biomarkers for the outcome of these patients (Keane et al 1983;Monserrat et al 2009a).…”

Section: Role Of Peripheral Blood Lymphocytes In Septic Shock Outcomementioning

confidence: 99%

See 2 more Smart Citations

Cellular and Molecular Markers of Outcome in Septic Shock

Monserrat¹,

Pablo²,

Díaz³

et al. 2012

Severe Sepsis and Septic Shock - Understanding a Serious Killer

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Section: Role Of Peripheral Blood Lymphocytes In Septic Shock Outcomementioning

confidence: 70%

Section: Interpretation Of Blood Lymphocyte Count Alterations In Patimentioning

confidence: 98%

Section: Role Of Peripheral Blood Lymphocytes In Septic Shock Outcomementioning

confidence: 99%

See 1 more Smart Citation

Cellular and Molecular Markers of Outcome in Septic Shock

Monserrat¹,

Pablo²,

Díaz³

et al. 2012

Severe Sepsis and Septic Shock - Understanding a Serious Killer

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“…Recent availability of flow cytometric immunofluorescence methods with the use of monoclonal antibodies has revealed the pattern of immune suppression in patients with multiple organ failure (Nishijima et al 1986). Abnormalities in the immune system have included decreased T-cell response to mitogens, decreased antibody concentrations, alteration of T-cell subsets, decreased levels of IL-1 and IL-2, high suppressor:helper T-cell ratios, and the presence of an immunosuppression peptide (Abraham & Change, 1986;Radosevich et al 1988).…”

Section: Immunotherapymentioning

confidence: 99%

Nutrition, Immune Function, and Inflammation: an overview

1989

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The account of acute inflammation is one of the classical clinical descriptions in medicine. However, those early physicians describing Rubor et tumor cum calor et dolore (Celsus in 50 BC) could hardly have imagined the complexity of the events that they were observing.In a healthy individual, the response to tissue injury and infection is rapid and efficient, with resolution occurring before involvement of the specific immune system. However, when the inflammatory stimulus is overwhelming, or if the patient is already malnourished or chronically ill, a series of inter-related events are set in motion. Among these are the interaction of immune cells, phagocytes and release of powerful cytokines that affect the utilization of nutritional substrates in the body. Moreover, antigen processed by macrophages is presented to lymphocytes, thus eliciting a specific immune response.The present paper summarizes our present understanding of the pathophysiology of inflammation and explores the objectives for nutritional support in the presence of immunodysfunction. The rationale for adjunctive nutritional support is explained, and modified regimens, tailored both to provide metabolic substrates and to enhance immunity to disease, are given. Pathophysiology of the inflammatory responseThe immune system is phylogenetically separated into innate or non-specific immunity and the adaptive or specific immune system. While understanding that both processes are often working together, events in each system will be considered individually at a cellular and molecular level.Non-specific immunity. Tissue injury leads to release of Hageman factor (XIIa-XII) and to the degranulation of tissue mast cells. Factor XI1 initiates the process, causing complement activation and bradykinin production locally. Micro-organisms and endotoxin may also trigger this pathway, directly activate complement, or cause mast cell degranulation ( Fig. 1) (Schlesinger, 1975). This mechanism ensures the presence of inflammatory mediators such as the complement factors C3a and C5a, bradykinin, and histamine. Damaged cell membranes release products of arachidonic acid (AA) metabolism, such as prostaglandins (PG) and leukotrienes (LT) (Goetzl, 1981), both of which are eicosanoids having important mediating functions in acute inflammation. The net effect is to increase vascular pernieability, which causes the accumulation of acute-phase at https://www.cambridge.org/core/terms. https://doi

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“…Studies in adult rats have shown that injuries, such as sepsis, trauma and burn, induce a suppressed immune response characterized by decreased T-lymphocyte prolif-eration and interleukin 2 production [4][5][6][7][8]. Such suppression can alter the host defense against sepsis [9,10].…”

Section: Introductionmentioning

confidence: 99%

Sepsis-Induced Alteration in T-Cell Ca<sup>2+</sup> Signaling in Neonatal Rats

et al. 2001

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Sepsis-induced suppression in T-cell proliferation follows deranged Ca²⁺ signaling in adult rats. In preliminary studies, we observed suppression in T-cell proliferation in septic neonatal rats as well. In this study, we assessed splenic T-cell cytosolic Ca²⁺ concentration, [Ca²⁺]_i, as its elevation plays an important role in T-cell proliferation. Also, we investigated the role of PGE₂ in sepsis-related changes in T-cell [Ca²⁺]_i in animals pretreated with cyclooxygenase-1 (COX-1) inhibitor (resveratrol) and cyclooxygenase-2 (COX-2) inhibitor (NS-398). Sepsis was induced in 15-day-old rat pups by intraperitoneal implantation of fecal pellets containing Escherichia coli and Bacteroides fragilis. The sham group consisted of pups implanted with sterile fecal pellets. Septic and sham pups were sacrificed 24 h after implantation and their spleens were removed. The spleens from sham and septic pups, along with spleens from unoperated control pups, were processed for single cell suspensions, and T cells were isolated using nylon wool columns. Fura-2 fluorophotometry was employed for the measurement of [Ca²⁺]_i (in nM units) in T cells stimulated with concanavalin A (ConA). Our results show that ConA-mediated T-cell [Ca²⁺]_i response is significantly suppressed in septic neonatal rats. Pretreatment of pups with COX-2, but not COX-1 inhibitor, prevented the decrease in the [Ca²⁺]_i response. These findings suggest that PGE₂ might induce the attenuation in T-cell Ca²⁺ signaling during sepsis in neonatal rats.

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Serial changes in cellular immunity of septic patients with multiple organ-system failure

Cited by 38 publications

References 0 publications

Cellular and Molecular Markers of Outcome in Septic Shock

Cellular and Molecular Markers of Outcome in Septic Shock

Nutrition, Immune Function, and Inflammation: an overview

Sepsis-Induced Alteration in T-Cell Ca<sup>2+</sup> Signaling in Neonatal Rats

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