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High Blood Sugar Impairs Neutrophil Function in Lyme Disease

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By A. Javid, et al. • www.ProHealth.com • October 3, 2017


High Blood Sugar Impairs Neutrophil Function in Lyme Disease. Neutrophils that help to eliminate Borrelia may be reduced in those with hyperglycemia.
Neutrophils that help to eliminate Borrelia may be reduced in those with hyperglycemia.
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Hyperglycemia Impairs Neutrophil-Mediated Bacterial Clearance in Mice Infected with the Lyme Disease Pathogen
 
Abstract
 
Insulin-insufficient type 1 diabetes is associated with attenuated bactericidal function of neutrophils, which are key mediators of innate immune responses to microbes as well as pathological inflammatory processes. Neutrophils are central to immune responses to the Lyme pathogen Borrelia burgdorferi. The effect of hyperglycemia on host susceptibility to and outcomes of B. burgdorferi infection has not been examined.
 
The present study investigated the impact of sustained obesity-independent hyperglycemia in mice on bacterial clearance, inflammatory pathology and neutrophil responses to B. burgdorferi. Hyperglycemia was associated with reduced arthritis incidence but more widespread tissue colonization and reduced clearance of bacterial DNA in multiple tissues including brain, heart, liver, lung and knee joint.
 
B. burgdorferi uptake and killing were impaired in neutrophils isolated from hyperglycemic mice. Thus, attenuated neutrophil function in insulin-insufficient hyperglycemia was associated with reduced B. burgdorferi clearance in target organs.
 
These data suggest that investigating the effects of comorbid conditions such as diabetes on outcomes of B. burgdorferi infections in humans may be warranted.
 
Source: By Javid A1, Zlotnikov N1, P?trošová H1, Tang TT1, Zhang Y1, Bansal AK1, Ebady R1, Parikh M1, Ahmed M1, Sun C1, Newbigging S2, Kim YR1, Santana Sosa M1, Glogauer M1, Moriarty TJ1. Hyperglycemia Impairs Neutrophil-Mediated Bacterial Clearance in Mice Infected with the Lyme Disease Pathogen. PLoS One. 2016 Jun 24;11(6):e0158019. doi: 10.1371/journal.pone.0158019. eCollection 2016.
 




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