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Titlebook: Immune Response in the Critically Ill; John C. Marshall (Professor of Surgery),Jonathan C Book 2002 Springer-Verlag Berlin Heidelberg 2002

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The Pro-Inflammatory Cytokine Cascade, severe inflammation may contribute to deleterious consequences. The capacity of interleukin (IL)-l and tumor necrosis factor-alpha (TNF-a) to induce inflammatory mediators contributes to their pro-inflammatory properties. Phospholipase, cyclooxygenase and lipoxygenase are activated by IL-1 and TNF-
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Inhibitory Cytokines,ch as the lipopolysaccharide (LPS, endotoxin) of Gram-negative bacteria and the exotoxins or cell-wall fragments of Gram-positive bacteria, have been shown to be potent activators of a wide range of cells, including monocytes/macrophages, neutrophils and endothelial cells. On stimulation, these cell
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,Interleukin-1β and Interleukin-18: Two Cytokine Precursors for Interleukin-1 β Converting Enzyme (C Daltons but lacking a signal peptide. The interpretation of this leaderless precursor of IL-1β was rather difficult since it was not clear how the mature form was cleaved naturally. We had expressed an intermediate form of recombinant IL-1β with a molecular weight of 21000 Daltons. This species of
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Bacterial Toxins Induce Selective Cytokine Patterns , and ,,ety [.]. Currently, 28-day mortality in sepsis is estimated to be 20–40% depending on the etiological agent and presence of complicating medical disorders [.–.]. An even higher mortality has been associated with septic shock, affecting approximately half of the patients with sepsis. Investigations p
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Regulation of Cellular Responses to Bacterial Endotoxin,e immunity has also been pointed out [.–.]. In particular, there are remarkable parallels when the innate immune responses to microbial pathogens by lower organisms and mammals are compared [.–.]. The innate immune system functions to provide signals to the host that microbial pathogens are present.
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