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In Vivo Infection with Leishmania amazonensis to Evaluate Parasite Virulence in Mice
Published on: February 20, 2020
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Innate Resistance to Leishmania amazonensis Infection in Rat Is Dependent on NOS2
Yun-Fu Chen1, Si-Fei Yu2, Chang-You Wu2
1Guangdong Provincial Key Laboratory of Aquatic Economic Animals, Key Laboratory of Gene Engineering of the Ministry of Education, State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-Sen University, Guangzhou, China.
Frontiers in Microbiology
|November 15, 2021
Summary
Rats resist Leishmania amazonensis infection due to a specific nitric oxide synthase pathway (NOS2). Macrophages lacking NOS2 become susceptible, highlighting NOS2
Area of Science:
- Immunology
- Infectious Diseases
- Parasitology
Background:
- Leishmania infection presents diverse clinical outcomes influenced by host and parasite factors.
- Mice show variable resistance to Leishmania major but high susceptibility to Leishmania amazonensis.
- Rats exhibit strong resistance to Leishmania amazonensis, with underlying mechanisms previously unknown.
Purpose of the Study:
- To investigate the role of inducible nitric oxide synthase (NOS2) in rat resistance to Leishmania amazonensis infection.
- To elucidate the mechanisms behind rat innate immunity against Leishmania.
Main Methods:
- Utilized a NOS2 gene knockout rat model (Nos2-/- rat).
- Assessed susceptibility to Leishmania amazonensis infection in wild-type and Nos2-/- rats.
- Performed adoptive transfer of NOS2-competent macrophages into Nos2-/- rats.
Main Results:
- Diversion toward the NOS2 pathway is critical for rat resistance against Leishmania amazonensis.
- Nos2-/- rats are susceptible to Leishmania amazonensis infection despite a robust immune response.
- Adoptive transfer of NOS2-competent macrophages significantly reduced disease progression and parasite burden in Nos2-/- rats.
Conclusions:
- Distinct L-arginine metabolism in rat macrophages, leading to NOS2 activation, forms the basis of strong innate resistance to Leishmania.
- Macrophages possess unique properties across different hosts, influencing innate immune responses and disease outcomes in Leishmania infections.
