Identification of defective early immune responses to Burkholderia pseudomallei infection in a diet-induced murine model of type 2 diabetes.

Affiliation

Morris JL(1), Govan BL(2), Rush CM(2), Ketheesan N(3).
Author information:
(1)College of Medicine and Dentistry, James Cook University, Queensland, 4811, Australia. Electronic address: [Email]
(2)College of Public Health, Medical and Veterinary Sciences, James Cook University, Queensland, 4811, Australia.
(3)Science & Technology, University of New England, New South Wales, 2351, Australia. Electronic address: [Email]

Abstract

Co-occurrence of bacterial infections with type 2 diabetes (T2D) is a global problem. Melioidosis caused by Burkholderia pseudomallei is 10 times more likely to occur in patients with T2D, than in normoglycemic individuals. Using an experimental model of T2D, we observed that greater susceptibility in T2D was due to differences in proportions of infiltrating leucocytes and reduced levels of MCP-1, IFN-γ and IL-12 at sites of infection within 24 h post-infection. However, by 72 h the levels of inflammatory cytokines and bacteria were markedly higher in visceral tissue and blood in T2D mice. In T2D, dysregulated early immune responses are responsible for the greater predisposition to B. pseudomallei infection.