Banca de DEFESA: GABRIELLA OLIVEIRA ALVES MOREIRA DE CARVALHO

Uma banca de DEFESA de DOUTORADO foi cadastrada pelo programa.
STUDENT : GABRIELLA OLIVEIRA ALVES MOREIRA DE CARVALHO
DATE: 24/04/2023
TIME: 08:30
LOCAL: Videoconferência
TITLE:

JUNCTIONAL COMMUNICATION IN MACROPHAGES IN THE INFLAMMATORY INFECTIOUS PROCESS WITH Toxoplasma gondii

KEY WORDS:

Gap junction; Macrophages; Toxoplasma gondii

PAGES: 187
BIG AREA: Ciências Biológicas
AREA: Fisiologia
SUBÁREA: Fisiologia Geral
SUMMARY:

Toxoplasma gondii (T. gondii) is the causative agent of toxoplasmosis. This protozoan has the characteristic of being obligate intracellular and having a high prevalence worldwide, where it is believed to have infected one third of the world's population, causing great morbidity and mortality. Given the complexity of this disease, several studies have been dedicated to the study of structures that are associated with parasitic diseases. Among these structures are the Communicating Junctions, which are responsible for the exchange of ions and small messengers that maintain tissue homeostasis. These transmembrane channels play an important role in intercellular communication in different tissues, as they allow communication in different cell types, including macrophages. With this, the morphological and functional characterization of gap junctions in macrophages, and in particular formed by connexin 43, has been the subject of study by several groups, but their regulatory mechanisms still deserve clarification, especially in the face of pathological changes, such as in infectiousinflammatory processes caused by T. gondii. In view of this, the main objective of this study was to evaluate the modulation of gap junctions in the macrophage lineage J774- G8, after infection with the parasite Toxoplasma gondii and subsequent activation with inflammatory pro-immune factors. As methodology, it was used: (1) Culture of J774-G8 cells; (3) Infection of the culture by the T. gondii strain RH; (4) Treatment with individual and conjugated pro-immunoinflammatory factors (IFN-γ, TNF-α, IFN-γ + TNF-α); (5) Immunoelectrophoretic assays (Western Blot); and (4) Immunofluorescence assays and analysis by confocal microscopy. The general results found were: (1) Improvement in the morphological profile of cultures of J774-G8 cells infected with T. gondii treated with proimmune-inflammatory factors; (2) Increased Cx43 protein expression in infected J774- G8 cells after treatment with pro-inflammatory immune factors for 24 and 48 hours; (3) Cell activation stimulated by treatment with conjugated factors; (4) The damage to the cellular cytoskeleton caused by the infection was irreversible, even after treatment with inflammatory pro-immune factors in infected cells; (5) Damage to the cytoskeleton prevented the transport and anchoring of Cx43 in the plasmatic membrane, however the factors provided an increase in the cytoplasmic levels of Cx43. With this, it was possible to conclude that: infection with T. gondii causes irreversible damage to macrophage cells, however treatment with pro-immune inflammatory factors stimulates the production of Cx43, which even though it fails to insert itself into the plasmatic membrane in infected cells due to damage to the cytoskeleton, may play important roles in the process of maintaining the infected cell structure.

COMMITTEE MEMBERS:
Interno - 1674073 - BRUNO GUIMARAES MARINHO
Presidente - ***.128.627-** - FABIO DA SILVA DE AZEVEDO FORTES - UEZO
Externa à Instituição - Regina Coeli dos Santos Goldenberg - UFRJ
Externo à Instituição - SERGIO HENRIQUE SEABRA
Interno - 386960 - WELLINGTON DA SILVA CORTES