Banca de DEFESA: BEATRIZ MARIA DA CONCEIÇÃO MURILO

Uma banca de DEFESA de MESTRADO foi cadastrada pelo programa.
STUDENT : BEATRIZ MARIA DA CONCEIÇÃO MURILO
DATE: 30/04/2026
TIME: 09:00
LOCAL: meet.google.com/fbp-jqib-yoi
TITLE:

STANDARDIZATION OF AN EXPERIMENTAL MODEL OF ACUTE LUNG INJURY INDUCED BY Plasmodium berghei STRAIN NK65-GFP.

KEY WORDS:

Experimental malaria; Pulmonary immunopathogenesis; Severe malaria; Murine model.

PAGES: 70
BIG AREA: Ciências Biológicas
AREA: Parasitologia
SUMMARY:

Malaria is an infectious parasitic disease caused by protozoa of the genus Plasmodium and, in its severe forms, may Malaria is an infectious-parasitic disease caused by protozoa of the genus Plasmodium that, in its severe forms, can lead to pulmonary complications such as acute lung injury (ALI) and acute respiratory distress syndrome associated with malaria (ARDS-MA). These conditions are characterized by intense pulmonary inflammation, increased permeability of the alveolar-capillary barrier, edema, and impaired respiratory function. Despite the established use of murine models, gaps remain in understanding the immunopathological mechanisms involved in the induction of  ALI, particularly regarding the differences between mouse strains. In this context, this study mechanistically investigated ALI in BALB/c and C57BL/6 mice infected with Plasmodium berghei NK65-GFP, emphasizing the relationship between parasite load and pulmonary pathophysiology. The animals were infected with different inocula and monitored for clinical evolution and survival. Parasitemia was assessed using blood smears and flow cytometry, enabling a more sensitive analysis of the infection. The pulmonary response was investigated by quantifying leukocyte migration in bronchoalveolar lavage and by histopathological evaluation of lung tissue. The results demonstrated that, although the parasitemia was similar among the strains, the pulmonary responses differed significantly. BALB/c mice presented more intense inflammation, greater cell recruitment, and more extensive histopathological lesions, indicating greater susceptibility to APL. In contrast, C57BL/6 mice exhibited a more moderate inflammatory response and later progression. These findings suggest that the severity of APL does not depend exclusively on the systemic parasite load, but on intrinsic differences in the immune response. Thus, the model with P. berghei NK65-GFP is expected to contribute to studies aimed at elucidating the mechanisms of the physiopathogenesis of APL in malaria.

COMMITTEE MEMBERS:
Interna - 1346635 - JANEUSA TRINDADE DE SOUTO
Externo à Instituição - JOSUE DA COSTA LIMA JUNIOR - Fiocruz - RJ
Externa ao Programa - ***.788.694-** - JULIANE SANTOS DE FRANÇA DA SILVA - UFPB
Interno - 2213126 - VALTER FERREIRA DE ANDRADE NETO