Open AccessHyperglycemia Impairs Neutrophil-Mediated Bacterial Clearance in Mice Infected with the Lyme Disease Pathogen
Author(s) -
Ashkan Javid,
Nataliya Zlotnikov,
Helena Pětrošová,
Taiwen Tang,
Yang Zhang,
Anil Kumar Bansal,
Rhodaba Ebady,
Maitry Parikh,
Mijhgan Ahmed,
Cong Sun,
Susan Newbigging,
Yae Ram Kim,
Marianna Santana Sosa,
Michael Glogauer,
Tara J. Moriarty
Publication year - 2016
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0158019
Subject(s) - borrelia burgdorferi , immunology , pathogen , immune system , innate immune system , inflammation , diabetes mellitus , medicine , lyme disease , biology , microbiology and biotechnology , endocrinology , antibody
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.