Actually sepsis is well understood. For a bacteria to invade the bloodstream there must be a complete collapse of both the innate and adaptive immune responses. In healthy people granulocytes usually remove invading bacteria in most cases prior to the involvement of the adaptive response. However, in some cases a coordinated effort between both the innate and adaptive response is required, this is why individuals with "functional" immunosuppression are at high risk of sepsis. This includes the obvious cases of immunosuppression due to things like HIV infection but also includes large classes of the population like the elderly (>65 yo) who have a diminished immune response. In fact the whole list of comorbidities that increase the risk of sepsis also initiate immune system defects which help create the right conditions for the higher risk of sepsis.

Data on high mortality in the development of sepsis indicate the relevance of studies aimed at clarifying the causes of sepsis and ways to stop sepsis. I posted in the attachment a copy of two articles on this issue.

Many bacteria and some fungus, virus and parasite may intiate sepsis. It is found more among the people having immunosuppression due to any reason.

But sepsis itself immunosuppressive?

May be, as many toxins secreted by many bacteria have immunosuppressive effects.

Attached is a nice review from Lancet infectious diseases. A bit old, but I suspect still very relevant. See in particular the Panel: “Clinical or laboratory evidence for sepsis being an immunosuppressive disorder” (page 263) for a brief summary of evidence supporting a role for immunerepressive phenotype in sepsis.

This is exactly what I was looking for....thanks Gustav van Niekerk

Nice question.

Today, PICS is the best term and explication for prolonged inmmunosupresion in sepsis. Prolonged inmunusuoresion catabolism syndrome.

Immunosuppression in sepsis is a real problem and very individual. Epigentic and metabolic reporgramming as well as the chronic release of DAMPS during the course of sepsis influence immunosuppression. The high prevalence of secondary viral infection (e.g. EBV, CMV) is one result of these processes. You might also find this articel informative. Article Immunotherapy in sepsis - brake or accelerate?

Immunosuppression induced by sepsis is multifocal, there is lack of complement factors due to inadequate activation of complement by pathogen - associated molecular patterns (and this lead to coagulation dysfunction on the other way). Hyperstimulation of NF-kB synthesis and production of proinflammatory cytokines (IL-1 group) afterwards leads to neutrophil dysfunction in some way associated with interleukin 18 acting. There are many aspects of sepsis - induced immunosuppression and it's always pathogen - type (viral/bacterial/fungal sepsis) dependent.