Replication or death: distinct fates of pathogenic Leptospira strain Lai within macrophages of human or mouse origin
Authors: Liwei Li
Sumei Liao
Haiyan Dong
Feng Xue
Jie Yan
Shijun Li
David M Ojcius
Journal: Innate Immunity (2010)
Discipline: IMMUNOLOGY
Keywords: Leptospires; infection diversity; macrophages; human; mouse
Affiliations: Division of Basic Medical Microbiology, State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, First Affiliated Hospital of Zhejiang University, Hangzhou, P.R. China, Department of Medical Microbiology and Parasitology, College of Medicine, Zhejiang University, Hangzhou, P.R. China, School of Natural Sciences, University of California, Merced, California, USA, School of Life Sciences, Zhejiang University, Hangzhou, P.R. China, Division of Basic Medical Microbiology, State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, First Affiliated Hospital of Zhejiang University, Hangzhou, P.R. China, Department of Medical Microbiology and Parasitology, College of Medicine, Zhejiang University, Hangzhou, P.R. China,

Abstract:  Pathogenic leptospires evoke severe diseases in humans but only cause mild chronic or asymptomatic infection in many host animals. The reasons for this diversity of infection remain unclear. Here, we demonstrated that Leptospira interrogans serovar Lai strain Lai had a similar ability to adhere to and enter primary and immortal (THP-1 and J774A.1) macrophages from human and mouse, but its intracellular fate in human macrophages differed markedly from that in mouse. The leptospires resided within membrane-bound vacuoles in the murine macrophages, but occurred free in the cytosol of human macrophages, with no surrounding vesicular membrane. Most leptospires in murine macrophages co-localized with the late-endosomal/lysosomal marker LAMP-1 and then were killed by lysosomal hydrolases, while most leptospires in human macrophages did not co-localize with this marker and survived. Enumeration of colony-forming units plus quantitative fluorimetry showed that in human, but not in murine, macrophages, the amounts of leptospires increased with incubation time. The infected human macrophages differed from mouse macrophages by displaying gradually enhanced apoptosis, in parallel with the increase in number of leptospires. These data strongly suggest that the outcome for intracellular leptospires depends on differences among host macrophages, which may account for some of the differences in the severity of leptospirosis in humans and animals. 

Retracted: No

PubPeer comments:
 This paper has a hard-to-find Corrigendum (I could not see it linked to on the abstract page of the paper), here: https: journals.sagepub.com doi pdf 10.1177 1753425910370399 , which corrects the legend of Figure 5C. However, could the authors please check Figure 10A? There appear to be two sets of panels that look quite similar. I have marked them here in red and blue boxes, respectively. The dots in the graphs are similar, but the gated percentage are different, which is puzzling. ![file] , 
 Dear Elisabeth, Thank you very much for your comments. We will check the Fig you marked and respond to you as sooner as possible. Best regards, Shijun Li , 
 Dear Dr. Li, Thank you for your reply, and for looking into the lab archives. Much appreciated. , 
 Thank you for your analysis. We are repeating the experiment in Figure 10A, and will contact the journal for advice. Jie Yan , 
 Duplication in figure 4. ![file] From [Komi Kounkoura] ![file] , 
 Dear Edentulina Martensi, Thank you for bringing this issue to our attention about this publication. I am Shijun Li, the first author of this publication (Replication or death: distinct fates of pathogenic Leptospira strain Lai within macrophages of human or mouse origin). This article was published in 2010 and I am sure that the Figure 4 in this article is correct and is come from the experiment performed by myself. Further, the two papers contain duplication were published in 2012 (Komi, et al.) and 2014 ( Lei Z, et al.) , respectivelyt, which is later than this article. I will contact the corresponding author (Jie Yan) and I think he will explain what happened. Best, Shijun ,