The role of granulocyte macrophage-colony stimulating factor in gastrointestinal immunity to salmonellosis
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Updated: Jun 21, 2026
Chronic Salmonella Infection Induced Intestinal Fibrosis
Published on: September 22, 2019
1Discipline of Pathology, Bosch Institute, University of Sydney, New South Wales, Australia.
Abstract:
Human Salmonella infection, in particular, typhoid fever is a highly infectious disease that remains a major public health problem causing significant morbidity and mortality. The outcome of these infections depends on the host's immune response, particularly the actions of granulocytes and macrophages. Using a mouse model of human typhoid fever, with Salmonella typhimurium infection of wild type and granulocyte macrophage-colony stimulating factor (GM-CSF) knock out mice we show a delay in the onset of immune-mediated tissue damage in the spleens and livers of GM-CSF(-/-) mice. Furthermore, GM-CSF(-/-) mice have a prolonged sequestration of S. typhimurium in affected tissues despite an increased production of F4/80+ effector cells. Moreover in the absence of GM-CSF, a decrease in pro-inflammatory cytokine expression of tumor necrosis factor-alpha, interleukin-12 (IL-12) and IL-18 was found, which may alter the host's immune response to infection. GM-CSF appears to play an important role in the pathogenesis of Salmonellosis, and may contribute significantly to the development of protective gastrointestinal mucosal immune responses against oral pathogens.
Insights
Granulocyte-macrophage colony-stimulating factor (GM-CSF) influences Salmonella infection outcomes. GM-CSF knockout mice show delayed tissue damage but prolonged bacterial presence, indicating its complex role in host defense.
Area of Science:
- Immunology
- Microbiology
- Pathogenesis
Background:
- Salmonella infection, including typhoid fever, is a significant global health concern.
- Host immune responses, particularly involving granulocytes and macrophages, are critical in determining infection outcomes.
- Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a key cytokine involved in immune cell development and function.
Purpose of the Study:
- To investigate the role of GM-CSF in the pathogenesis of Salmonella infection using a mouse model.
- To elucidate how GM-CSF deficiency affects immune-mediated tissue damage, bacterial load, and inflammatory responses.
Main Methods:
- Infection of wild-type and GM-CSF knockout (GM-CSF(-/-)) mice with Salmonella typhimurium.
- Assessment of immune-mediated tissue damage in spleen and liver.
- Quantification of S. typhimurium sequestration in tissues.
- Analysis of F4/80+ effector cell populations.
- Measurement of pro-inflammatory cytokine expression (TNF-alpha, IL-12, IL-18).
Main Results:
- GM-CSF(-/-) mice exhibited delayed onset of immune-mediated tissue damage in spleen and liver.
- A prolonged sequestration of S. typhimurium was observed in affected tissues of GM-CSF(-/-) mice.
- Despite increased F4/80+ effector cells, GM-CSF deficiency led to decreased expression of pro-inflammatory cytokines (TNF-alpha, IL-12, IL-18).
Conclusions:
- GM-CSF plays a crucial role in the pathogenesis of Salmonellosis.
- The absence of GM-CSF alters the host immune response, impacting tissue damage and bacterial clearance.
- GM-CSF may be important for developing protective gastrointestinal mucosal immunity against oral pathogens.
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