Phenotypical Characterization of Spleen Remodeling in Murine Experimental Visceral Leishmaniasis.

Clicks: 292
ID: 106906
2020
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Emerging

Ranked #34 of 111 articles by views in Frontiers in immunology

Most read Least read

Bar heights use a square-root scale.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Abstract
Visceral leishmaniasis (VL) is caused by or infection. One of the main problems related to this disease is the emergence of severe clinical forms with a lethality of 5-20%, even while under specific treatment. In humans and other species susceptible to fatal VL, such as dogs and hamsters, the disruption of splenic white pulp (WP) is accompanied by disease progression. Control of VL progression is seen in BALB/c mice, as evidenced by a mild clinical presentation and controlled parasite replication in the liver and spleen. In this study, we investigated the features involved in the morphological remodeling of splenic compartments associated with the control of VL progression to death. We evaluated cohorts of BALB/c mice after 30, 60, and 90 days of infection by . Spleen morphology, cell population subsets and cytokine production were studied in the spleen using flow- and histo-cytometry. Intraperitoneal infection with 10 promastigotes of led to progressive increases in spleen size at 60 and 90 days after infection. Splenomegaly was the only clinical sign of disease observed. At 30 days after infection, hyperplasia in the WP and decreased numbers of plasmacytoid dendritic cells were observed. The WP hyperplasia subsided at 60 days post-infection. However, the splenomegaly remained in association with increased numbers of macrophages, B and T lymphocytes and plasma cells. An increased number of lymphoid tissue inducer (LTi) cells was observed; these were distributed around the periarteriolar lymphoid sheath in control mice and scattered throughout the red pulp in the -infected mice. After 90 days of infection, increased IL-6 and IFN-γ production was seen in the spleen, as well as higher frequencies of follicular and plasmacytoid dendritic cells. The data presented herein emphasizes the potential role of spleen remodeling in the control of severe forms of VL and highlights features potentially involved in this process.
Reference Key
de-melo2020phenotypicalfrontiers Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors de Melo, Caroline Vilas Boas;Hermida, Micely D'El-Rei;Mesquita, Bianca R;Fontes, Jonathan L M;Koning, Jasper J;Solcà, Manuela da Silva;Benevides, Bruno B;Mota, Girlândia B S;Freitas, Luiz A R;Mebius, Reina E;Dos-Santos, Washington L C;
Journal Frontiers in immunology
Year 2020
DOI
10.3389/fimmu.2020.00653
URL
Keywords
visceral leishmaniasis lymphoid tissue inducer cells spleen disorganization spleen pathology white pulp remodeling

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

Comments

No comments yet. Be the first to comment on this article.