- Poster presentation
- Open Access
In vivo natural killer and natural killer T-cell depletion affects mortality in a murine pneumococcal pneumonia sepsis model
© Christaki et al.; licensee BioMed Central Ltd. 2012
- Published: 20 March 2012
- Natural Killer
- Natural Killer Cell
- Streptococcus Pneumoniae
- Pneumococcal Pneumonia
- Bacterial Inoculation
Apart from macrophages and neutrophils, natural killer (NK) and natural killer T (NKT) cells have been found to play a role in the early stages of bacterial infection. In this study, we investigated the role of NK and NKT cells in host defense against Streptococcus pneumoniae, using a murine pneumococcal pneumonia sepsis model. Our hypothesis was that NK and NKT cells play an immune-regulatory role during sepsis and thus in vivo depletion of those cell populations may affect mortality.
We used four groups of C57BL/6 mice (A, B, C and D, n = 10 mice/group). Animals were infected intratracheally with 50 μl of S. pneumoniae suspension (106 cfu). Twenty-four hours prior to bacterial inoculation, Group A received 50 μl of anti-asialoGM1 rabbit polyclonal antibody (Wako Chemicals GmbH, Neuss, Germany) intravenously (i.v.) to achieve in vivo NK cell inactivation; in Group B, NKT cell depletion was performed by targeting the CD1d receptor using 2 mg/kg of the monoclonal antibody anti-CD1d, clone 1B1 (BD Pharmingen, San Diego, CA, USA) i.v.; Group C (control) received an equivalent amount of isotype antibody control (nonspecific Ig). Group D received sham intratracheal installation of normal saline. Animals were observed daily for 7 days and deaths were recorded. The survival analysis was plotted using the Kaplan-Meier method and differences in survival between groups were compared with the log-rank test.
Our study has shown that NK cells appear to contribute to mortality in pneumococcal pneumonia. More research is needed to explore their role in host response to bacterial infection and sepsis.
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.