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Lack of galectin-3 alters the balance of innate immune cytokines and confers resistance to Rhodococcus equi infection.
Abstract: Galectin-3 is a beta-galactoside-binding lectin implicated in the fine-tuning of innate immunity. Rhodococcus equi, a facultative intracellular bacterium of macrophages, causes severe granulomatous bronchopneumonia in young horses and immunocompromised humans. The aim of this study is to investigate the role of galectin-3 in the innate resistance mechanism against R. equi infection. The bacterial challenge of galectin-3-deficient mice (gal3-/-) and their wild-type counterpart (gal3+/+) revealed that the LD50 for the gal3(-/-) mice was about seven times higher than that for the gal3+/+ mice. When challenged with a sublethal dose, gal3(-/-) mice showed lower bacteria counts and higher production of IL-12 and IFN-gamma production, besides exhibiting a delayed although increased inflammatory reaction. Gal3(-/-) macrophages exhibited a decreased frequency of bacterial replication and survival, and higher transcript levels of IL-1beta, IL-6, IL-10, TLR2 and MyD88. R. equi-infected gal3+/+ macrophages showed decreased expression of TLR2, whereas R. equi-infected gal3(-/-) macrophages showed enhanced expression of this receptor. Furthermore, galectin-3 deficiency in macrophages may be responsible for the higher IL-1beta serum levels detected in infected gal3(-/-) mice. Therefore galectin-3 may exert a regulatory role in innate immunity by diminishing IL-1beta production and thus affecting resistance to R. equi infection.
Publication Date: 2008-10-01 PubMed ID: 18825751DOI: 10.1002/eji.200737986Google Scholar: Lookup The Equine Research Bank provides access to a large database of publicly available scientific literature. Inclusion in the Research Bank does not imply endorsement of study methods or findings by Mad Barn.
- Journal Article
- Research Support
- Non-U.S. Gov't
Summary
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The research aims to understand the role of a protein called galectin-3 in the body’s innate immunity response to Rhodococcus equi, a bacterium causing severe lung infection in young horses and immunocompromised humans. The findings suggest that absence of galectin-3 makes mice more resistant to this bacterial infection.
Definition of Key Elements
- Galectin-3: A type of protein in the body that binds to specific sugars and plays a role in many biological activities, including immunity regulation.
- Rhodococcus equi: A bacterium that infects the cells of the immune system—known as macrophages—and causes serious lung infections in certain species and conditions.
- Macrophages: Immune system cells that ingest harmful foreign particles and bacteria, contributing to the body’s defense mechanism.
- LD50: A measure used in toxicology studies, indicating the lethal dose of a substance that kills 50% of the test population—used here to measure the response to bacterial infection.
Research Methodology
- The researchers compared the response to R. equi infection in two groups of mice: galectin-3-deficient mice (gal3-/-) and normal or wild-type mice (gal3+/+).
- They studied the levels of bacterial growth, presence of immune system signaling proteins (cytokines like IL-12 and IFN-gamma), inflammatory reaction, and the expression of additional immune-system related genes (IL-1beta, IL-6, IL-10, TLR2 and MyD88).
Key Findings
- Galectin-3-deficient mice demonstrated a stronger resistance to R. equi, represented by a seven times higher LD50.
- When challenged with a sublethal dose of the bacteria, these mice had lower bacteria counts and a higher production of specific immunity-related proteins (IL-12 and IFN-gamma).
- Furthermore, the absence of galectin-3 in macrophages affected many aspects of the immune response, including a decreased frequency of bacterial replication, increased gene expression levels related to immune response, and enhanced expression of TLR2 receptor—a key molecular player in recognizing foreign substances and triggering immune response.
- The absence of galectin-3 also appears to cause higher serum levels of another immune response-related protein (IL-1beta) present in infected mice.
- All these results together suggest galectin-3 could have a regulatory function in the innate immune response.
Final Interpretation
- The research suggests galectin-3 may play a key role in regulating how our immune system responds to pathogens like R. equi. In its absence, the body seems to mount a stronger immune response.
- The implication of these findings could be significant for understanding and potentially improving treatment strategies for diseases caused by such bacteria, especially in vulnerable populations like young horses and immunocompromised humans.
Cite This Article
APA
Ferraz LC, Bernardes ES, Oliveira AF, Ruas LP, Fermino ML, Soares SG, Loyola AM, Oliver C, Jamur MC, Hsu DK, Liu FT, Chammas R, Roque-Barreira MC.
(2008).
Lack of galectin-3 alters the balance of innate immune cytokines and confers resistance to Rhodococcus equi infection.
Eur J Immunol, 38(10), 2762-2775.
https://doi.org/10.1002/eji.200737986 Publication
Researcher Affiliations
- Departamento de Biologia Celular e Molecular e Bioagentes Patogênicos, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto-SP, Brazil.
MeSH Terms
- Actinomycetales Infections / immunology
- Actinomycetales Infections / microbiology
- Animals
- Cytokines / biosynthesis
- Cytokines / genetics
- Cytokines / immunology
- Galectin 3 / deficiency
- Galectin 3 / immunology
- Galectin 3 / metabolism
- Gene Knockdown Techniques
- Immunity, Innate
- Interleukin-12 / biosynthesis
- Interleukin-1beta / biosynthesis
- Interleukin-1beta / immunology
- Liver / cytology
- Liver / immunology
- Liver / microbiology
- Macrophages / immunology
- Macrophages / microbiology
- Mice
- Mice, Inbred C57BL
- Myeloid Differentiation Factor 88 / genetics
- Myeloid Differentiation Factor 88 / metabolism
- RNA, Messenger / genetics
- RNA, Messenger / metabolism
- Rhodococcus equi / immunology
- Spleen / cytology
- Spleen / immunology
- Spleen / microbiology
- Toll-Like Receptor 2 / genetics
- Toll-Like Receptor 2 / immunology
- Toll-Like Receptor 2 / metabolism
Citations
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