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Published on: October 15, 2013
Protective cellular responses to Burkholderia mallei infection
Caroline A Rowland1, M Stephen Lever, Kate F Griffin
1Dstl, Biomedical Sciences, Porton Down, Salisbury SP40JQ, UK. carowland@dstl.gov.uk
Abstract:
Burkholderia mallei is a Gram-negative bacillus causing the disease glanders in humans. During intraperitoneal infection, BALB/c mice develop a chronic disease characterised by abscess formation where mice normally die up to 70 days post-infection. Although cytokine responses have been investigated, cellular immune responses to B. mallei infection have not previously been characterised. Therefore, the influx and activation status of splenic neutrophils, macrophages and T cells was examined during infection. Gr-1+ neutrophils and F4/80+ macrophages infiltrated the spleen 5 h post-infection and an increase in activated macrophages, neutrophils and T cells occurred by 24 h post-infection. Mice depleted of Gr-1+ cells were acutely susceptible to B. mallei infection, succumbing to the infection 5 days post-infection. Mice depleted of both CD4 and CD8 T cells did not succumb to the infection until 14 days post-infection. Infected μMT (B cell) and CD28 knockout mice did not differ from wildtype mice whereas iNOS-2 knockout mice began to succumb to the infection 30 days post-infection. The data presented suggests that Gr-1+ cells, activated early in B. mallei infection, are essential for controlling the early, innate response to B. mallei infection and T cells or nitric oxide are important during the later stages of infection.
Insights
Early immune responses involving Gr-1+ neutrophils are crucial for controlling Burkholderia mallei infection. Later stages of glanders disease rely on T cells and nitric oxide for survival.
Area of Science:
- Immunology
- Microbiology
- Infectious Diseases
Background:
- Burkholderia mallei causes glanders, a disease in humans and a chronic infection in BALB/c mice.
- Cellular immune responses to B. mallei infection remain poorly characterized.
- Understanding the immune response is critical for developing effective treatments.
Purpose of the Study:
- To characterize the cellular immune response to B. mallei infection in BALB/c mice.
- To investigate the roles of neutrophils, macrophages, and T cells in B. mallei pathogenesis.
- To identify key immune components essential for controlling glanders disease.
Main Methods:
- BALB/c mice were infected intraperitoneally with B. mallei.
- Splenic immune cell populations (neutrophils, macrophages, T cells) were analyzed for influx and activation.
- Depletion studies were performed using antibodies against Gr-1+ cells and CD4/CD8 T cells.
- Gene knockout mice (μMT, CD28, iNOS-2) were used to assess specific immune pathways.
Main Results:
- Gr-1+ neutrophils and F4/80+ macrophages infiltrated the spleen early post-infection.
- Activated macrophages, neutrophils, and T cells increased by 24 hours post-infection.
- Depletion of Gr-1+ cells led to acute susceptibility and rapid death.
- Depletion of CD4 and CD8 T cells delayed mortality.
- iNOS-2 knockout mice showed delayed mortality compared to wild-type controls.
Conclusions:
- Gr-1+ cells are essential for the early innate immune control of B. mallei infection.
- T cells and nitric oxide play critical roles in managing the later stages of glanders.
- This study elucidates key cellular players in B. mallei pathogenesis, informing future therapeutic strategies.
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