The role of TLR2 in the host response to pneumococcal pneumonia in absence of the spleen

BMC Infectious Diseases

Tom van der Poll¹  Sandrine Florquin³  Onno J de Boer³  AlexanderPNA de Porto¹  Adriana J JLammers² 

[1] Center for Experimental and Molecular Medicine Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands;Room G2-105, CEMM, Academic Medical Center, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands;Department of Pathology Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands

关键词: Pneumonia;    Splenectomy;    Toll-like receptor 2;    Streptococcus pneumonia;   

Others  :  1175352
DOI  :  10.1186/1471-2334-12-139

 received in 2011-06-13, accepted in 2012-05-30,  发布年份 2012

【 摘 要 】

Background

Asplenic individuals are susceptible for overwhelming infection with Streptococcus pneumoniae, carrying a high mortality. Although Toll-like receptor (TLR)-2 is considered the major receptor for Gram-positive bacteria in innate immunity, it does not play a major role in host defense against pneumococcal pneumonia. We wanted to investigate if in absence of an intact spleen as a first line of defense, the role of TLR2 during pneumococcal pneumonia becomes more significant, thereby explaining its insignificant role during infections in immune competent hosts.

Methods

We intranasally infected splenectomized wildtype (WT), TLR2 knock-out (KO) and TLR2/4 double KO mice with either serotype 2 or 3 S. pneumoniae.

Results

There were no differences between asplenic WT and TLR2KO mice of bacterial loads in lung homogenates and blood, cytokine and chemokine levels in the lungs, and lung pathology scores. TLR2/4 double KO mice were not impaired in bacterial control as well, which indicates that besides the interaction between S. pneumoniae and TLR2, the interaction between pneumolysin and TLR4 does not stimulate antibacterial defense in the asplenic host either.

Conclusions

These results argue against a significant role of TLR2 in host defense during S. pneumoniae pneumonia in the asplenic state. Therefore, other components can provide sufficient backup mechanisms for TLR2 deficiency in the defense against intrapulmonary infections with S. pneumoniae of the otherwise immune competent host.

【 授权许可】

   
2012 Lammers et al.; licensee BioMed Central Ltd.

【 图 表 】

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