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Updated: Jul 20, 2026

In Vivo Infection with Leishmania amazonensis to Evaluate Parasite Virulence in Mice
Published on: February 20, 2020
Platelet activating factor receptor-deficient mice present delayed interferon-gamma upregulation and high
Helton C Santiago1, Maíra Faria Braga Pires, Daniele G Souza
1Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, CP 486, Av. Antonio Carlos 6627, Pampulha, CEP 30161-970 Belo Horizonte, MG, Brazil.
Abstract:
We investigated the role of the platelet activation factor (PAF) receptor (PAFR) in the outcome of infection with Leishmania amazonensis. PAFR deficient (PAFR(-/-)) mice were infected with L. amazonensis and the course of infection was followed. We found that PAFR(-/-) mice in the C57BL/6 background were more susceptible to infection with L. amazonensis than the wild-type controls, as seen both by lesion size and parasite number at the site of infection. Interferon (IFN)-gamma production was delayed in PAFR(-/-) mice, and lower levels of Ccl5 were found in lesions. Expression of nitric oxide synthase-2 mRNA was found impaired in PAFR(-/-) associated with higher levels of arginase-1 mRNA. Moreover, higher levels of antibodies were produced in response to L. amazonensis by PAFR(-/-) mice. We conclude that signaling through the PAFR is essential for the ability of the murine host to control L. amazonensis infection by driving an adequate immune response.
Insights
Platelet-activating factor receptor (PAFR) signaling is crucial for controlling Leishmania amazonensis infections. PAFR-deficient mice show increased susceptibility and impaired immune responses to this parasitic infection.
Area of Science:
- Immunology
- Parasitology
- Molecular Biology
Background:
- Leishmania amazonensis is a protozoan parasite causing cutaneous and visceral leishmaniasis.
- The platelet-activating factor receptor (PAFR) plays a role in inflammatory and immune responses.
- Understanding host-pathogen interactions is key to developing effective treatments for leishmaniasis.
Purpose of the Study:
- To investigate the role of PAFR in the host's immune response to L. amazonensis infection.
- To determine the impact of PAFR deficiency on disease progression and immune cell function.
Main Methods:
- Infection of PAFR-deficient (PAFR(-/-)) and wild-type C57BL/6 mice with L. amazonensis.
- Monitoring of lesion development and parasite burden.
- Quantification of cytokine (IFN-gamma, Ccl5) and enzyme (nitric oxide synthase-2, arginase-1) mRNA expression.
- Analysis of antibody production.
Main Results:
- PAFR(-/-) mice exhibited increased susceptibility to L. amazonensis, characterized by larger lesions and higher parasite loads.
- Delayed interferon-gamma production and reduced Ccl5 levels were observed in PAFR(-/-) mice.
- Impaired nitric oxide synthase-2 mRNA expression and elevated arginase-1 mRNA levels were found in deficient mice.
- PAFR(-/-) mice produced higher levels of antibodies against L. amazonensis.
Conclusions:
- PAFR signaling is essential for mounting an effective immune response against L. amazonensis.
- PAFR deficiency leads to a less controlled infection due to altered immune cell function and cytokine profiles.
- Targeting PAFR may represent a therapeutic strategy for leishmaniasis.
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