ArticleThe journal of venomous animals and toxins including tropical diseases2015
Tissue apoptosis in mice infected with Leptospira interrogans serovar Icterohaemorrhagiae.
Article in The journal of venomous animals and toxins including tropical diseases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Necroptosis Contributes to Persistent Inflammation During Acute Leptospirosis.Frontiers in immunology · 2022Article
- Disassembly of the apical junctional complex during the transmigration of Leptospira interrogans across polarized renal proximal tubule epithelial cells.Cellular microbiology · 2021Article
- Leptospirosis Pathophysiology: Into the Storm of Cytokines.Frontiers in cellular and infection microbiology · 2018Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThis investigation aimed to evaluate the occurrence of some apoptotic features induced by Leptospira interrogans serovar Icterohaemorrhagiae infection in young BALB/c mice during 2, 4, 7, 10, 14 and 21 days post-infection (dpi).
methodsThe animals were euthanized and lung, liver and kidneys were harvested to histopathology analysis and immunohistochemistry to caspase-3 antigen detection was performed.
resultsChromatin condensation in kidney and liver tissues, but not in lung tissue, was observed. Caspase-3 reactive cells, mainly characterized as renal epithelial cells, were detected in the days 14 and 21 at high levels when compared to days 2, 4 and 7 (p = 0.025; p < 0.05). Lung sections revealed caspase-3 labeled alveolar cells in 10 and 14 days post-infection was higher than observed at 7 days (p = 0.0497; p < 0.05). Liver sections demonstrated reactive cells at a highest level at 14 and 21 days post-infection when comparison to 2, 4, 7 and 10 days (p = 0.0069; p < 0.05).
conclusionsOur results suggest that infection of L. interrogans induce in kidney, liver and lung an activation of apoptosis mediated by caspase-3 dependent pathway in later phases of infectious process.
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