Endotoxaemia in patients with severe sepsis or septic shock

Venet, C.; Zéni, Fabrice; Viallon, Alain; Ross, Andrew Slavin; Pain, Pascal; Gery, Pierre; Page, Dominique; Vermesch, R.; Bertrand, Monique; Rançon, F; Bertrand, Jean Claude

doi:10.1007/s001340051201

Cited by 52 publications

(34 citation statements)

References 18 publications

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“…The mortality is related to both the severity of sepsis and the underlying disease that is nearly always present (42,43,413). In many cases of sepsis, the presence of microorganisms (bacteremia) or LPS in the blood (endotoxemia) cannot be established, which has prompted modification of the definitions of sepsis and septic shock (42,43,561). The definitions are as follows: bacteremia, positive blood cultures; sepsis, clinical evidence of infection, tachypnea (Ͼ20 breaths/min), tachycardia (Ͼ90 beats/min), hyperthermia, or hypothermia; sepsis syndrome, sepsis plus hypoxemia or elevated plasma lactate levels or oliguria; and septic shock, sepsis syndrome plus hypotension (despite adequate volume resuscitation).…”

Section: Sepsis and Septic Shockmentioning

confidence: 99%

Receptors, Mediators, and Mechanisms Involved in Bacterial Sepsis and Septic Shock

2003

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Bacterial sepsis and septic shock result from the overproduction of inflammatory mediators as a consequence of the interaction of the immune system with bacteria and bacterial wall constituents in the body. Bacterial cell wall constituents such as lipopolysaccharide, peptidoglycans, and lipoteichoic acid are particularly responsible for the deleterious effects of bacteria. These constituents interact in the body with a large number of proteins and receptors, and this interaction determines the eventual inflammatory effect of the compounds. Within the circulation bacterial constituents interact with proteins such as plasma lipoproteins and lipopolysaccharide binding protein. The interaction of the bacterial constituents with receptors on the surface of mononuclear cells is mainly responsible for the induction of proinflammatory mediators by the bacterial constituents. The role of individual receptors such as the toll-like receptors and CD14 in the induction of proinflammatory cytokines and adhesion molecules is discussed in detail. In addition, the roles of a number of other receptors that bind bacterial compounds such as scavenger receptors and their modulating role in inflammation are described. Finally, the therapies for the treatment of bacterial sepsis and septic shock are discussed in relation to the action of the aforementioned receptors and proteins

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Section: Sepsis and Septic Shockmentioning

confidence: 99%

Receptors, Mediators, and Mechanisms Involved in Bacterial Sepsis and Septic Shock

2003

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“…On the contrary, LPS can up-regulate T cell adherence to FN and downregulate T cell chemotaxis to SDF-1␣. These effects of LPS could be important clinically; increased amounts of LPS in the blood can occur during sepsis with Gram-negative bacteria (27), and chronic HIV infection and AIDS involve markedly increased blood levels of LPS originating from gut flora (3). Hence, some of the pathological effects of LPS might be due to the direct effects of LPS on T cells.…”

Section: Socs3 Mediates the Inhibitory Effect Of Lps On Human T Cell mentioning

confidence: 99%

Cutting Edge: T Cells Respond to Lipopolysaccharide Innately via TLR4 Signaling

Zanin-Zhorov

Tal-Lapidot

Cahalon

et al. 2007

The Journal of Immunology

102

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LPS, a molecule produced by Gram-negative bacteria, is known to activate both innate immune cells such as macrophages and adaptive immune B cells via TLR4 signaling. Although TLR4 is also expressed on T cells, LPS was observed not to affect T cell proliferation or cytokine secretion. We now report, however, that LPS can induce human T cells to adhere to fibronectin via TLR4 signaling. This response to LPS was confirmed in mouse T cells; functional TLR4 and MyD88 were required, but T cells from TLR2 knockout mice could respond to LPS. The human T cell response to LPS depended on protein kinase C signaling and involved the phosphorylation of the proline-rich tyrosine kinase (Pyk-2) and p38. LPS also up-regulated the T cell expression of suppressor of cytokine signaling 3, which led to inhibition of T cell chemotaxis toward the chemokine stromal cell-derived factor 1α (CXCL12). Thus, LPS, through TLR4 signaling, can affect T cell behavior in inflammation.

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“…Priming occurs in vivo and primed PMNs have been demonstrated in the circulation of patients after traumatic injury (8), during the course of the acute respiratory distress syndrome (9), and in the setting of sepsis (10). In addition, low concentrations of endotoxin are present in the plasma of patients with Gram-negative bacterial infections (11). Therefore, the study of endotoxin-mediated priming is highly relevant to disease pathogenesis.…”

mentioning

confidence: 99%

Endotoxin Priming of Neutrophils Requires NADPH Oxidase-generated Oxidants and Is Regulated by the Anion Transporter ClC-3

Moreland

Davis

Matsuda³

et al. 2007

Journal of Biological Chemistry

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Several soluble mediators, including endotoxin, prime neutrophils for an enhanced respiratory burst in response to subsequent stimulation. Priming of neutrophils occurs in vitro, and primed neutrophils are found in vivo. We previously localized the anion transporter ClC-3 to polymorphonuclear leukocytes (PMN) secretory vesicles and demonstrated that it is required for normal NADPH oxidase activation in response to both particulate and soluble stimuli. We now explore the contribution of the NADPH oxidase and ClC-3 to endotoxin-mediated priming. Lipooligosaccharide (LOS) from Neisseria meningitidis enhances the respiratory burst in response to formyl-Met-Leu-Phe, an effect that was impaired in PMNs lacking functional ClC-3 and under anaerobic conditions. Mobilization of receptors to the cell surface and phosphorylation of p38 MAPK by LOS were both impaired in PMN with the NADPH oxidase chemically inhibited or genetically absent and in cells lacking functional ClC-3. Furthermore, inhibition of the NADPH oxidase or ClC-3 in otherwise unstimulated cells elicited a phenotype similar to that seen after endotoxin priming, suggesting that basal oxidant production helps to maintain cellular quiescence. In summary, NADPH oxidase activation was required for LOS-mediated priming, but basal oxidants kept unstimulated cells from becoming primed. ClC-3 contributes to both of these processes.

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Endotoxaemia in patients with severe sepsis or septic shock

Cited by 52 publications

References 18 publications

Receptors, Mediators, and Mechanisms Involved in Bacterial Sepsis and Septic Shock

Receptors, Mediators, and Mechanisms Involved in Bacterial Sepsis and Septic Shock

Cutting Edge: T Cells Respond to Lipopolysaccharide Innately via TLR4 Signaling

Endotoxin Priming of Neutrophils Requires NADPH Oxidase-generated Oxidants and Is Regulated by the Anion Transporter ClC-3

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