The effects of nitric oxide on the immune system during Trypanosoma cruzi infection

Trypanosoma cruzi infection triggers substantial production of nitric oxide (NO), which has been shown to have protective and toxic effects on the host's immune system. Sensing of trypomastigotes by phagocytes activates the inducible NO-synthase (NOS2) pathway, which produces NO and is largely responsible for macrophage-mediated killing of T. cruzi. NO is also responsible for modulating virtually all steps of innate and adaptive immunity. However, NO can also cause oxidative stress, which is especially damaging to the host due to increased tissue damage. The cytokines IFN-³ and TNF-±, as well as chemokines, are strong inducers of NOS2 and are produced in large amounts during T. cruzi acute infection. Conversely, TGF-² and IL-10 negatively regulate NO production. Here we discuss the recent evidence describing the mechanisms by which NO is able to exert its antimicrobial and immune regulatory effects, the mechanisms involved in the oxidative stress response during infection and the implications of NO for the development of therapeutic strategies against T. cruzi.

The eosinophils in parasitic infections

Local and peripheal eosinophilia is a common feature of many helminth infections that present large, non-phagocytable surfaces to the inmune system. The effect of the eosinophils on these organisms has been studied in the last 18 years using schistosoma mansoni, trichinella spiralis, and other helminths as models. The early infection causes a nonspecific inflammation rich in macrophages, lymphocytes and neutrophils that sets the stage for a subsequent inmune response. The predominant effector elements of the inmune response are anaphylactic antibodies, mast cells, and eosinophils. Mast cell products attract eosinophils and concentrate antibodies and complement-covered parasites by their Fc and/or C3c receptors and release oxygen radicals and/or preformed proteins on the helmith surface. The radicals alter molecules of the parasite and the proteins disrupt its tegument or cuticle. Occasionally, they may harm host cells. Eosinophils also phagocytize and harm extracellular trypanosoma cruzi and may play a role in the damage to the host heart tissue. The eosinophil response is regulated by eosinophilopoietic factors (interleukines [IL] 3 and 5, and granulocyte macrophage colony-stimulating factor) eosinophilotactic factors (C5a from complement, eosinophil chemotactic factor of anaphylaxis [ECF-A], histamine, platelet stimulating factor, and other ECFs from mast cells and basophils, and ECF from parasites), and eosinophiloactivating factors (IL-5 from Th2 lymphocytes, tumor necrosis factor from macrophages, antibodies, and complement components). Other phagocytic cells (macrophages and neutrophils) also exhibit important anti-helminthic activities

Parasitosis, nutrición e inmunidad / parasitosis, nutrition and immunity

La interacción entre nutrición, función inmune e infección, funciona en ambos sentidos. La desnutrición deteriora la función inmune y la infección parasitaria es más grave en el paciente desnutrido e inmunodeficiente que en una persona bien nutrida e inmunocompetente, aunque en algunos casos la desnutrición parece proteger al huésped de algunas infecciones. A su vez, la infección parasitaria deteriora el estado nutricional y la función del sistema inmune del huésped. Finalmente, la inmunodeficiencia favorece la infección por determinados parásitos con la subsiguiente pérdida de nutrimentos y mayor afectación del estado general del paciente