Filariasis mediated immunomodulation against metabolic diseases is a recently identified novel phenomenon. There seems to be an inverse relationship between filarial infections and type-2 diabetes. Rapid elimination of filarial diseases, due to mass drug administration has somehow fueled the sudden and rampant increase in type-2 diabetes, at least in certain tropical countries, like India and Indonesia. Filarial infections are in a way unique, since they bring about immunomodulation, in contrast to inflammation which is triggered by viral and bacterial infections. This dampens immunity and confers better survival for the pathogen. However, this also attenuates chronic inflammation and insulin resistance and thereby confers protection against type-2 diabetes. This chapter elucidates the various immune mechanisms involved in immunomodulation against insulin resistance and type-2 diabetes induced by helminth infection.
Part of the book: Inflammation in the 21st Century
The epidemic increase in diabetes mellitus (DM) is taking place in the world were one third of the population is latently infected with tuberculosis (TB). DM, as a chronic metabolic disease, weakens the immune system and increases the risk of Mycobacterium tuberculosis (M.tb) infection. In those who are already latently infected, it increases the risk of reactivation. This is called DM-TB synergy. While the role of immune cells and cytokines has been well studied in DM-TB synergy, the role played by chemokines is largely unrecognized. Chemokines are low molecular weight proteins that are rapidly secreted by both immune and non-immune cells and guide the directorial migration of these cells. Impairment in chemokine secretion or signaling can lead to delayed immune response and can mediate DM-TB synergy. This chapter describes the role played by various chemokines and their receptors in DM-TB synergy.
Part of the book: Chemokines Updates