Article

Bacterial sensing, cell signaling, and modulation of the immune response during sepsis.

Division of Infectious Diseases, Department of Medicine, Hospital Sao Paulo, Escola Paulista de Medicina, Universidade Federal de Sao Paulo, São Paulo, Brazil.
Shock (Augusta, Ga.) (impact factor: 2.87). 07/2012; 38(3):227-42. DOI:10.1097/SHK.0b013e318262c4b0 pp.227-42
Source: PubMed

ABSTRACT Since the definition of systemic inflammatory response syndrome/sepsis was originally proposed, a large amount of new information has been generated showing a much more complex scenario of inflammatory and counterinflammatory responses during sepsis. Moreover, some fundamental mechanisms of sensing and destroying invading microorganisms have been uncovered, which include the discovery of TLR4 as the lipopolysaccharide (LPS) gene, implications of innate immune cells as drivers of the adaptive response to infection, and the modulation of multiple accessory molecules that stimulate or inhibit monocyte/macrophage and lymphocyte interactions. The complexity of the infection/injury-induced immune response could be better appreciated with the application of genomics and proteomics studies, and LPS was a useful tool in many of these studies. In this review, we discuss aspects of bacterial recognition and induced cellular activation during sepsis. Because of the relevance of endotoxin (LPS) research in the field, we focus on LPS and host interactions as a clue to understand microorganisms sensing and cell signaling, then we discuss how this response is modulated in septic patients.

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Keywords

aspects
 
bacterial recognition
 
complex scenario
 
counterinflammatory responses
 
endotoxin
 
host interactions
 
induced cellular activation
 
infection/injury-induced immune response
 
innate immune cells
 
large amount
 
lymphocyte interactions
 
modulation
 
monocyte/macrophage
 
multiple accessory molecules
 
proteomics studies
 
sepsis
 
septic patients
 
systemic inflammatory response syndrome/sepsis
 
TLR4
 
useful tool