Splenic Transcriptional Responses in Severe Visceral Leishmaniasis: Impaired Leukocyte Chemotaxis and Cell Cycle Arrest

Structural changes in the spleen have been reported in several infectious diseases. In visceral leishmaniasis (VL), a severe parasitic disease caused by spp., the loss of white pulp accompanies a severe clinical presentation. Hamster model reproduces aspects of human VL progression. In the early sta...

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Bibliographic Details
Published in:Frontiers in immunology 2021-11, Vol.12, p.716314-716314
Main Authors: de Melo, Caroline Vilas Boas, Guimarães Torres, Felipe, Hermida, Micely D'El-Rei, Fontes, Jonathan L M, Mesquita, Bianca Ramos, Brito, Reginaldo, Ramos, Pablo Ivan P, Fernandes, Gabriel R, Freitas, Luiz Antônio Rodrigues, Khouri, Ricardo, Costa, Carlos Henrique Nery, Dos-Santos, Washington L C
Format: Article
Language:English
Subjects:
Animals
Calcium-Binding Proteins - genetics
Calcium-Binding Proteins - metabolism
Cell Cycle Checkpoints - genetics
Chemotaxis, Leukocyte - genetics
Cricetinae
Cyclin-Dependent Kinase Inhibitor p16 - genetics
Cyclin-Dependent Kinase Inhibitor p16 - metabolism
Female
Gene Expression Profiling
hamster
Humans
Hyperplasia - pathology
Immunology
Leishmaniasis, Visceral - immunology
Leishmaniasis, Visceral - pathology
Leukocytes - parasitology
Leukocytes - pathology
Male
Membrane Proteins - genetics
Membrane Proteins - metabolism
Middle Aged
Spleen - immunology
Spleen - parasitology
Spleen - pathology
spleen disorganization
Transcriptome
transcriptomic (RNA-Seq)
visceral leishmanaisis
white pulp remodeling
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Summary:Structural changes in the spleen have been reported in several infectious diseases. In visceral leishmaniasis (VL), a severe parasitic disease caused by spp., the loss of white pulp accompanies a severe clinical presentation. Hamster model reproduces aspects of human VL progression. In the early stages, a transcriptomic signature of leukocyte recruitment was associated with white pulp hyperplasia. Subsequently, impaired leukocyte chemotaxis with loss of T lymphocytes in the periarteriolar lymphoid sheath occurred. This differential gene expression was subsequently corroborated by transcriptomic profiling of spleens in severe human VL. At the latest stage, spleen disorganization was associated with increasing clinical signs of VL. White pulp disruption was accompanied by decreased expression. The expression of and decreased, likely regulated by overexpression. Our findings enlighten a pathway implying cell cycle arrest and decreased gene expression involved in spleen organization.
ISSN:1664-3224
1664-3224
DOI:10.3389/fimmu.2021.716314