The Open Pathology Journal




(Discontinued)

ISSN: 1874-3757 ― Volume 8, 2014

Type 2 Diabetes: Local Inflammation and Direct Effect of Bacterial Toxic Components


The Open Pathology Journal , 2008, 2: 86-95

Judith Miklossy, Ralph Martins, Nune Darbinian, Kamel Khalili , Patrick L. McGeer

University of British Columbia, Kinsmen Laboratory of Neurological Research, 2255 Wesbrook Mall, Room 3N6, Vancouver BC, V6T 1Z3, Canada.

Electronic publication date 12/9/2008
[DOI: 10.2174/1874375700802010086]

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Abstract:

Objectives:

It has been known for almost a century that amyloidosis is frequently associated with chronic bacterial infection. Islet amyloid deposit is characteristic of type 2 diabetes. Periodontal disease, which is predominantly caused by several Gram negative bacteria, is a risk factor for type 2 diabetes. The goal of the study was to explore whether bacteria or their toxic components may play a role in type 2 diabetes.

Material & Methods:

The pancreas in 22 autopsy cases was analyzed for the presence of lipopolysaccharide (LPS), bacterial peptidoglycan (BPG) and local inflammatory processes. Ten of the cases had clinically diagnosed type 2 diabetes, and 12 were age matched controls.

Results:

The results of an immunohistochemical analysis showed the presence of LPS and BPG in association with islet amyloid deposits in all the 10 diabetic cases as well as in 3 controls with clinically silent amyloid deposits. Chlamydia pneumoniae and Helicobacter pylori specific antigens were detected in the affected islets in a subset of diabetic patients. Clumps of HLA-DR positive activated macrophages, abundant immunoreactivity to the activated complement components C3d, C4d and C5b-9, the terminal attack complex, and a mild numbers of T4 and particularly of T8 lymphocytes were present in the pancreas of all diabetic cases.

Conclusions:

These results suggest that bacteria or their slowly degradable remnants may initiate and sustain chronic inflammation in the pancreas and therefore play a role in the pathogenesis of type 2 diabetes. They also indicate that local immune responses, including activation of the classical complement pathway are important in the pathogenesis of type 2 diabetes. There may also be some involvement of the adaptive immune system. Further investigations are essential since a parallel use of antibacterial and anti-inflammatory drugs may prevent or slow down the disease progression.


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