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Immunostimulating properties of intragastrically administered Acetobacter-derived soluble branched
Wei Li1, Toshiki Yajima, Kimika Saito
1Division of Host Defense, Research Center for Prevention of Infectious Diseases, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-8582, Japan.
Infection and Immunity
|November 24, 2004
Summary
Oral administration of AC-1, a (1,4)-beta-D-glucan, enhances protective immunity against Listeria monocytogenes by boosting interleukin-12 (IL-12) production and T-helper 1 (Th1) responses via Toll-like receptor 4 (TLR-4) signaling.
Area of Science:
- Immunology
- Microbiology
- Biochemistry
Background:
- AC-1, an extracellular polysaccharide from Acetobacter xylinum, is a (1,4)-beta-D-glucan.
- AC-1 induces interleukin-12 (IL-12) and tumor necrosis factor alpha (TNF-α) via Toll-like receptor 4 (TLR-4) signaling in macrophages.
- The role of AC-1 in vivo protective immunity against bacterial infections is not well understood.
Purpose of the Study:
- To investigate the effect of oral AC-1 administration on protective immunity against Listeria monocytogenes.
- To elucidate the underlying mechanisms of AC-1-mediated protection, particularly the involvement of TLR-4 and Th1 responses.
Main Methods:
- Mice were orally administered AC-1 or phosphate-buffered saline (PBS) before and after Listeria monocytogenes infection.
- Survival rates and bacterial loads were assessed.
- Serum IL-12 p40 levels and CD4+ Th1/CD8+ Tc1 responses were measured.
- Experiments were repeated in C3H/HeJ mice with mutated TLR-4.
Main Results:
- AC-1 treatment significantly improved survival rates and reduced bacterial growth in mice infected with L. monocytogenes.
- AC-1 administration led to significantly higher serum IL-12 p40 levels and enhanced CD4+ Th1 and CD8+ Tc1 responses.
- The protective effect of AC-1 was diminished in C3H/HeJ mice with mutated TLR-4, indicating TLR-4 dependency.
Conclusions:
- AC-1 enhances protective immunity against L. monocytogenes infection through TLR-4-mediated induction of IL-12 and augmentation of Th1 responses.
- Oral administration of AC-1, a (1,4)-beta-D-glucan, shows potential for preventing infectious diseases caused by intracellular microorganisms.
- AC-1 represents a promising immunomodulatory agent for enhancing host defense mechanisms.