Lipopolysaccharide (LPS) or endotoxin is a component of the cell wall of Gram-negative bacteria and triggers a strong immune response that is characterized, in part, by cytokine production.
Prior exposure to LPS can lead to lower LPS-induced cytokine responses, called endotoxin tolerance. However, the clinical significance of endotoxin tolerance in assessing immune function is debated.
Now in the Journal of Immunology, Julia Bohannon, Ph.D., Benjamin Fensterheim, Yin Guo and Edward Sherwood, M.D., Ph.D., report that the magnitude of the cytokine response induced by LPS does not correlate with resistance to infection.
They also provide evidence that various toll-like receptor (TLR) ligands can augment innate antimicrobial immunity but differentially modify LPS-induced cytokine responses.
Their work shows that the host response to endotoxin does not predict the host response to infection. Their works also advances the search for compounds that activate the immune response to improve resistance to infection.
The study was supported in part by a National Institutes of Health Shared Instrumentation Grant (OD018015).
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