Protective cellular responses to Burkholderia mallei infection

• Published in: Microbes and infection Vol. 12; no. 11; pp. 846 - 853
• Main Authors: Rowland, Caroline A., Lever, M. Stephen, Griffin, Kate F., Bancroft, Gregory J., Lukaszewski, Roman A.
• Format: Journal Article
• Language: English
• Published: Kidlington Elsevier SAS 01-10-2010; Elsevier
• Subjects: Animals; Bacillus; Bacteriology; Biological and medical sciences; Burkholderia mallei; Burkholderia mallei - immunology; Disease Models, Animal; Female; Fundamental and applied biological sciences. Psychology; Glanders - immunology; Injections, Intraperitoneal; Leukocyte Reduction Procedures; Macrophages; Macrophages - immunology; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Microbiology; Miscellaneous; Neutrophils; Neutrophils - immunology; Nitric Oxide - immunology; Spleen - immunology; Survival Analysis; T cells; T-Lymphocytes - immunology; Burkholderia mallei; T cells; Macrophages; Neutrophils; T-Lymphocyte; Bacteria; Neutrophil; Macrophage
• ISSN: 1286-4579; 1769-714X
• DOI: 10.1016/j.micinf.2010.05.012

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.