YopH inhibits early pro-inflammatory cytokine responses during plague pneumonia

BMC Immunology

Research Article

Peter H Dube¹  Angelene M Cantwell¹  Sarah S Bubeck² 

[1] Department of Microbiology and Immunology, The University of Texas Health Science Center at San Antonio, 7703, Floyd Curl Dr, 78229, San Antonio, TX, USA;Department of Microbiology and Immunology, The University of Texas Health Science Center at San Antonio, 7703, Floyd Curl Dr, 78229, San Antonio, TX, USA;Department of Biology, University of Texas at San Antonio, One UTSA circle, 78249, San Antonio, TX, USA;

关键词: Plague;    Bronchial Epithelium;    Yersinia Pestis;    Bacterial Burden;    Intranasal Infection;   

DOI  :  10.1186/1471-2172-11-29

 received in 2009-11-18, accepted in 2010-06-16,  发布年份 2010

来源: Springer

【 摘 要 】

BackgroundYersinia pestis is the causative agent of pneumonic plague; recently, we and others reported that during the first 24-36 hours after pulmonary infection with Y. pestis pro-inflammatory cytokine expression is undetectable in lung tissues.ResultsHere, we report that, intranasal infection of mice with CO92 delta yopH mutant results in an early pro-inflammatory response in the lungs characterized by an increase in the pro-inflammatory cytokines Tumor Necrosis Factor-alpha and Interleukin one-beta 24 hours post-infection. CO92 delta yopH colonizes the lung but does not disseminate to the liver or spleen and is cleared from the host within 72 hours post-infection. This is different from what is observed in a wild-type CO92 infection, where pro-inflammatory cytokine expression and immune cell infiltration into the lungs is not detectable until 36-48 h post-infection. CO92 rapidly disseminates to the liver and spleen resulting in high bacterial burdens in these tissues ultimately cumulating in death 72-94 h post-infection. Mice deficient in TNF-alpha are more susceptible to CO92 delta yopH infection with 40% of the mice succumbing to infection.ConclusionsAltogether, our results suggest that YopH can inhibit an early pro-inflammatory response in the lungs of mice and that this is an important step in the pathogenesis of infection.

【 授权许可】

Unknown   
© Cantwell et al; licensee BioMed Central Ltd. 2010. 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.