Defects in early cell recruitment contribute to the increased susceptibility to respiratory Klebsiella pneumoniae infection in diabetic mice
- Microbes Infect. 2016 Oct;18(10):649-655. doi: 10.1016/j.micinf.2016.05.007.
- 1. Division of Pulmonary, Allergy and Critical Care, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01655, USA.
- 2. Division of Pulmonary, Allergy and Critical Care, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01655, USA; Australian Institute of Tropical Health and Medicine, James Cook University, Queensland 4811, Australia.
- 3. Program in Innate Immunity, Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01655, USA; CEMIR, Department of Cancer Research and Molecular Medicine, NTNU, Trondheim, Norway.
- 4. Division of Pulmonary, Allergy and Critical Care, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01655, USA. Electronic address: [email protected].
Diabetes is associated with increased susceptibility to Klebsiella pneumoniae and poor prognosis with Infection. We demonstrate accelerated mortality in mice with streptozotocin-induced diabetes following tracheal instillation of K. pneumoniae. Diabetic mice recruited fewer granulocytes to the alveolar airspace and had reduced early production of CXCL1, CXCL2, IL-1β and TNF-α following tracheal instillation of K. pneumoniae-lipopolysaccharide. Additionally, TLR2 and TIRAP expression following K. pneumoniae-lipopolysaccharide exposure was decreased in hyperglycemic mice. These findings indicate that impaired innate sensing and failure to rapidly recruit granulocytes to the site of Infection is a mechanism for diabetic susceptibility to respiratory K. pneumoniae Infection.
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Cat. No.Product NameDescriptionTargetResearch Area
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target: Toll-like Receptor (TLR)Research Areas: Inflammation/Immunology