What is Sepsis?  Inflammation

A Description of the Inflammatory Cascades

The presence of pathogens in the bloodstream elicits an inflammatory response. There is an intricate linkage between the inflammation and coagulation. Here is, briefly, a description of the inflammatory cascade (6;7) .

Tissue injury or pathogens (bacterial, viruses, fungi or parasites) causes stimulation of monocytes, the kingpins of the immune system within tissues, to produce interleukin-1 (IL-1), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNFα). These cytokines subsequently modulate the release and activation of a medley of different agents – interleukin-8, complement, histamine, kinins, histamine, serotonin, selectins, ecosanoids and, of course neutrophils. The result of the activation of these compounds is local vasodilatation (further amplified by inducible nitric-oxide, about which later), release of various cytotoxic chemicals and, hopefully, destruction of the invading pathogen. Unfortunately, in a particular subgroup of patients (i.e. those who end up being admitted to intensive care), there is an extra-ordinary amount of “friendly fire” and damage to the patient’s own tissues, not only locally, but throughout the body. This is akin to killing a cockroach with a grenade. As this process invariably occurs within the vasculature, so most of the damage is to the capillary lining, the endothelium. Unfortunately, the endothelium is not a passive surface, it is a potent endocrine organ that is widely involved in maintenance of circulating volume and in coagulation and fibrinolysis (see figures 1 thru 6).

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References

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THIS TUTORIAL BY PATRICK NELIGAN MD, UNIVERSITY OF PENNSYLVANIA

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