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.
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.
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.