RESUMO
Tuberculosis is a far-reaching, high-impact disease. It is among the top ten causes of death worldwide caused by a single infectious agent; 1.6 million tuberculosis-related deaths were reported in 2021 and it has been estimated that a third of the world's population are carriers of the tuberculosis bacillus but do not develop active disease. Several authors have attributed this to hosts' differential immune response in which cellular and humoral components are involved, along with cytokines and chemokines. Ascertaining the relationship between TB development's clinical manifestations and an immune response should increase understanding of tuberculosis pathophysiological and immunological mechanisms and correlating such material with protection against Mycobacterium tuberculosis. Tuberculosis continues to be a major public health problem globally. Mortality rates have not decreased significantly; rather, they are increasing. This review has thus been aimed at deepening knowledge regarding tuberculosis by examining published material related to an immune response against Mycobacterium tuberculosis, mycobacterial evasion mechanisms regarding such response and the relationship between pulmonary and extrapulmonary clinical manifestations induced by this bacterium which are related to inflammation associated with tuberculosis dissemination through different routes.
Assuntos
Mycobacterium tuberculosis , Tuberculose , Humanos , Citocinas , Inflamação , Saúde PúblicaRESUMO
Chagas disease is caused by the kinetoplastid parasite Trypanosoma cruzi, which is mainly transmitted by hematophagous insect bites. The parasite's lifecycle has an obligate intracellular phase (amastigotes), while metacyclic and bloodstream-trypomastigotes are its infective forms. Mammalian host cell recognition of the parasite involves the interaction of numerous parasite and host cell plasma membrane molecules and domains (known as lipid rafts), thereby ensuring internalization by activating endocytosis mechanisms triggered by various signaling cascades in both host cells and the parasite. This increases cytoplasmatic Ca2+ and cAMP levels; cytoskeleton remodeling and endosome and lysosome intracellular system association are triggered, leading to parasitophorous vacuole formation. Its membrane becomes modified by containing the parasite's infectious form within it. Once it has become internalized, the parasite seeks parasitophorous vacuole lysis for continuing its intracellular lifecycle, fragmenting such a vacuole's membrane. This review covers the cellular and molecular mechanisms involved in T. cruzi adhesion to, recognition of and internalization in host target cells.