Inflammation and innate immune function in critical illness. Issue 3 (June 2016)
- Record Type:
- Journal Article
- Title:
- Inflammation and innate immune function in critical illness. Issue 3 (June 2016)
- Main Title:
- Inflammation and innate immune function in critical illness
- Authors:
- Muszynski, Jennifer A.
Thakkar, Rajan
Hall, Mark W. - Abstract:
- Abstract : Purpose of review: The purpose of review is to highlight the inflammatory response in critical illness and the importance of immune monitoring and modulation in the diagnosis and treatment of critical illness-induced innate immune suppression. Recent findings: The pro and anti-inflammatory responses are known to be concurrently activated in many patients requiring intensive care, with innate immune suppression emerging as an important, and potentially reversible, complication of critical illness. Summary: The initial inflammatory response to critical illness is typically driven by innate immune cells, including neutrophils, monocytes, and macrophages. The proinflammatory mediators made by these cells are responsible for many of the pathophysiologic features of critical illness. Concurrent with this, however, is a compensatory anti-inflammatory response, including the elaboration of anti-inflammatory mediators and impairment of innate immune cell function. This includes reduction of monocyte human leukocyte antigen-DR expression and impairment of the ability of innate immune cells to produce tumor necrosis factor alpha when stimulated ex vivo . In its most severe form this is referred to as immunoparalysis, and is associated with markedly increased risks for secondary infection and death in the ICU. Prospective testing can detect this phenomenon, and immunostimulatory strategies, including the use of granulocyte macrophage-colony stimulating factor, have theAbstract : Purpose of review: The purpose of review is to highlight the inflammatory response in critical illness and the importance of immune monitoring and modulation in the diagnosis and treatment of critical illness-induced innate immune suppression. Recent findings: The pro and anti-inflammatory responses are known to be concurrently activated in many patients requiring intensive care, with innate immune suppression emerging as an important, and potentially reversible, complication of critical illness. Summary: The initial inflammatory response to critical illness is typically driven by innate immune cells, including neutrophils, monocytes, and macrophages. The proinflammatory mediators made by these cells are responsible for many of the pathophysiologic features of critical illness. Concurrent with this, however, is a compensatory anti-inflammatory response, including the elaboration of anti-inflammatory mediators and impairment of innate immune cell function. This includes reduction of monocyte human leukocyte antigen-DR expression and impairment of the ability of innate immune cells to produce tumor necrosis factor alpha when stimulated ex vivo . In its most severe form this is referred to as immunoparalysis, and is associated with markedly increased risks for secondary infection and death in the ICU. Prospective testing can detect this phenomenon, and immunostimulatory strategies, including the use of granulocyte macrophage-colony stimulating factor, have the potential to restore innate immune function in this setting. … (more)
- Is Part Of:
- Current opinion in pediatrics. Volume 28:Issue 3(2016:Jun.)
- Journal:
- Current opinion in pediatrics
- Issue:
- Volume 28:Issue 3(2016:Jun.)
- Issue Display:
- Volume 28, Issue 3 (2016)
- Year:
- 2016
- Volume:
- 28
- Issue:
- 3
- Issue Sort Value:
- 2016-0028-0003-0000
- Page Start:
- 267
- Page End:
- 273
- Publication Date:
- 2016-06
- Subjects:
- critical illness -- immune suppression -- immunoparalysis -- inflammation -- monocyte
Pediatrics -- Periodicals
Pediatrics -- Periodicals -- Bibliography -- Periodicals
618.92 - Journal URLs:
- http://journals.lww.com/co-pediatrics/pages/default.aspx ↗
http://journals.lww.com/pages/default.aspx ↗ - DOI:
- 10.1097/MOP.0000000000000352 ↗
- Languages:
- English
- ISSNs:
- 1040-8703
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 3500.776800
British Library DSC - BLDSS-3PM
British Library STI - ELD Digital store - Ingest File:
- 1139.xml