Host susceptibility factors contributing to increased risk of bacterial infections in type 2 diabetes will undoubtedly be multifactorial, depending on tissue tropism, the type of protective immune response required and the unique life cycles of various pathogens. We are only beginning to understand the molecular mechanisms underlying susceptibility, and future research will reveal how the diabetic state, involving hyperglycemia and chronic oxidative stress, modifies tissues and organs such as the bladder, airway, liver, skin, and blood cells in different ways that encourage bacterial pathogenesis.
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