Severe Sepsis is often caused by germs that release LPS or ß-glucans, that are toxic for blood monocytes. Monocyte fragments generate systemically circulating thrombin.
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Thomas,
Although LPS, beta-glucans and systemic thrombin play an important role in sepsis and since they trigger expression of different cytokines, reliable tests for LPS, beta-glucans and systemic thrombin are not that necessary. Their indirect monitoring and assessment can be done by monitoring the levels of various other cytokines.
For example levels of TNFalpha, IL-6, IL-10 , NO, MCP-1 could be measured. Other markers of coagulation activation can also be measured which might give an assessment of sepsis, rather than the exact levels of LPS or circulating thrombin in the blood. In my opinion reliable tests to measure LPS, beta-glucans and systemic thrombin may be quite cumbersome and may not help much rather than the indirect effects they cause.
Thomas,
Just like the response by Omer Iqbal, sepsis is a clinical syndrome and the severity of it depends a lot on the host response, more so I would say than the exact amount of pathogen.
LPS is a component of the cell wall of Gram negative organisms and it´s presence is believe to trigger a Toll-Like Receptor response activating the inflammatory cascade. Sepsis as a clinical problem depends more on the cytokine response to this insult that the amount of circulating LPS, or other cytotoxic agents.
I would lean more on having reliable test that can measure the host response and inflammatory cascade, over that of presence of bacterial components. There is growing evidence that humans interact with bacteria on different body sites, and more than the presence or not of bacterial is the fine balance of these bacterial communities.
For chronic sepsis maybe you might be right. Not so for acute sepsis. There cell necrosis and cell fragment- triggered intrinsic or extrinsic coagulation activation is the most important moment in pathogenesis of circulating micro-thrombi.
Thomas,
Pablo is making an important point that most often it is the gram negative bacteria responsible for the causation of acute sepsis, the LPS component of the cell wall of these bacteria trigger the Toll-Like receptor response activating the inflammatory cascade. In my opinion Pablo is right that this is the acute septic response rather than chronic sepsis. If Pablo can come up with some test to detect that acute response you may have the answer to your original question. Thanks to Pablo and Thomas for a good dialogue on this important subject.
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