A.G. Cuenca et al. 2015. Innate Immunity 21:386-91. 

Delayed emergency myelopoiesis following polymicrobial sepsis in neonates.

   The term “emergency myelopoesis” has been used to describe the reconstitution of bone marrow and splenic innate immune cells that occurs after myeloid cells, particularly neutrophils, have emigrated into the blood in response to inflammatory stimuli.  These authors used a septic mouse model to show that emergency myelopoiesis is delayed in neonates and that, contrary to expectation, neither MyD88 nor TRIF was necessary for emergency myelopoiesis to occur in either neonates or adults.   Uncovering the players that control such rapid production of myeloid cells should be very interesting.  

U. Gopinathan, et al. 2015.  Innate Immunity 21:429-449. 

IL-10 immunodepletion from meningococcal sepsis plasma induces extensive changes in gene expression and cytokine release in stimulated human monocytes. 

   In an influential article published in 1996, this Norwegian research team found that LPS-laden plasma from children with meningococcemia was minimally stimulatory to naïve human monocytes.  Immunoadsorption to remove IL-4 and IL-10 rendered the plasma more stimulatory.   These anti-inflammatory cytokines thus seemed to be preventing monocyte responses to very large amounts of LPS in plasma – a finding that seemed even more significant when high IL-10 plasma levels were found to predict mortality in patients with severe sepsis.  Now the team has provided a detailed analysis of the impact of IL-10 in meningococcal sepsis plasma, showing that the cytokine regulates a “variety of genes and signaling pathways likely leading to an overall inhibitory effect on the inflammatory response…”   It seems likely that, by increasing plasma IL-10, the body is attempting to prevent inflammation in the blood and tissues.  Very high levels indicate failure.