Open AccessCharacteristic features of intracellular pathogenic Leptospira in infected murine macrophages
Author(s) -
Toma Claudia,
Okura Nobuhiko,
Takayama Chitoshi,
Suzuki Toshihiko
Publication year - 2011
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/j.1462-5822.2011.01660.x
Subject(s) - leptospira interrogans , biology , phagosome , microbiology and biotechnology , intracellular , vacuole , macrophage , intracellular parasite , pathogen , leptospira , immune system , innate immune system , leptospirosis , extracellular , virology , phagocytosis , immunology , cytoplasm , biochemistry , in vitro
Summary Leptospira interrogans is a spirochaete responsible for a zoonotic disease known as leptospirosis. Leptospires are able to penetrate the abraded skin and mucous membranes and rapidly disseminate to target organs such as the liver, lungs and kidneys. How this pathogen escape from innate immune cells and spread to target organs remains poorly understood. In this paper, the intracellular trafficking undertaken by non‐pathogenic Leptospira biflexa and pathogenic L. interrogans in mouse bone marrow‐derived macrophages was compared. The delayed in the clearance of L. interrogans was observed. Furthermore, the acquisition of lysosomal markers by L. interrogans ‐containing phagosomes lagged behind that of L. biflexa ‐containing phagosomes, and although bone marrow‐derived macrophages could degrade L. biflexa as well as L. interrogans, a population of L. interrogans was able to survive and replicate. Intact leptospires were found within vacuoles at 24 h post infection, suggesting that bacterial replication occurs within a membrane‐bound compartment. In contrast, L. biflexa were completely degraded at 24 h post infection. Furthermore, L. interrogans but not L. biflexa , were released to the extracellular milieu. These results suggest that pathogenic leptospires are able to survive, replicate and exit from mouse macrophages, enabling their eventual spread to target organs.