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- W2287743904 abstract "Mycobacterium tuberculosis executes numerous defense strategies for the successful establishment of infection under a diverse array of challenges inside the host. One such strategy that has been delineated in this study is the abrogation of lytic activity of lysozyme by a novel glycosylated and surface-localized lipoprotein, LprI, which is exclusively present in M. tuberculosis complex. The lprI gene co-transcribes with the glbN gene (encoding hemoglobin (HbN)) and both are synchronously up-regulated in M. tuberculosis during macrophage infection. Recombinant LprI, expressed in Escherichia coli, exhibited strong binding (Kd ≤ 2 nm) with lysozyme and abrogated its lytic activity completely, thereby conferring protection to fluorescein-labeled Micrococcus lysodeikticus from lysozyme-mediated hydrolysis. Expression of the lprI gene in Mycobacterium smegmatis (8–10-fold) protected its growth from lysozyme inhibition in vitro and enhanced its phagocytosis and survival during intracellular infection of peritoneal and monocyte-derived macrophages, known to secrete lysozyme, and in the presence of exogenously added lysozyme in secondary cell lines where lysozyme levels are low. In contrast, the presence of HbN enhanced phagocytosis and intracellular survival of M. smegmatis only in the absence of lysozyme but not under lysozyme stress. Interestingly, co-expression of the glbN-lprI gene pair elevated the invasion and survival of M. smegmatis 2–3-fold in secondary cell lines in the presence of lysozyme in comparison with isogenic cells expressing these genes individually. Thus, specific advantage against macrophage-generated lysozyme, conferred by the combination of LprI-HbN during invasion of M. tuberculosis, may have vital implications on the pathogenesis of tuberculosis. Mycobacterium tuberculosis executes numerous defense strategies for the successful establishment of infection under a diverse array of challenges inside the host. One such strategy that has been delineated in this study is the abrogation of lytic activity of lysozyme by a novel glycosylated and surface-localized lipoprotein, LprI, which is exclusively present in M. tuberculosis complex. The lprI gene co-transcribes with the glbN gene (encoding hemoglobin (HbN)) and both are synchronously up-regulated in M. tuberculosis during macrophage infection. Recombinant LprI, expressed in Escherichia coli, exhibited strong binding (Kd ≤ 2 nm) with lysozyme and abrogated its lytic activity completely, thereby conferring protection to fluorescein-labeled Micrococcus lysodeikticus from lysozyme-mediated hydrolysis. Expression of the lprI gene in Mycobacterium smegmatis (8–10-fold) protected its growth from lysozyme inhibition in vitro and enhanced its phagocytosis and survival during intracellular infection of peritoneal and monocyte-derived macrophages, known to secrete lysozyme, and in the presence of exogenously added lysozyme in secondary cell lines where lysozyme levels are low. In contrast, the presence of HbN enhanced phagocytosis and intracellular survival of M. smegmatis only in the absence of lysozyme but not under lysozyme stress. Interestingly, co-expression of the glbN-lprI gene pair elevated the invasion and survival of M. smegmatis 2–3-fold in secondary cell lines in the presence of lysozyme in comparison with isogenic cells expressing these genes individually. Thus, specific advantage against macrophage-generated lysozyme, conferred by the combination of LprI-HbN during invasion of M. tuberculosis, may have vital implications on the pathogenesis of tuberculosis." @default.
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- W2287743904 date "2016-02-01" @default.
- W2287743904 modified "2023-10-15" @default.
- W2287743904 title "Lipoprotein LprI of Mycobacterium tuberculosis Acts as a Lysozyme Inhibitor" @default.
- W2287743904 cites W1484551801 @default.
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- W2287743904 cites W1847996750 @default.
- W2287743904 cites W1907819046 @default.
- W2287743904 cites W1915631326 @default.
- W2287743904 cites W1942505014 @default.
- W2287743904 cites W1949772429 @default.
- W2287743904 cites W1983443091 @default.
- W2287743904 cites W1986191025 @default.
- W2287743904 cites W1990240868 @default.
- W2287743904 cites W1996247940 @default.
- W2287743904 cites W2004224847 @default.
- W2287743904 cites W2005195131 @default.
- W2287743904 cites W2025960504 @default.
- W2287743904 cites W2027070879 @default.
- W2287743904 cites W2034181544 @default.
- W2287743904 cites W2038444095 @default.
- W2287743904 cites W2038942210 @default.
- W2287743904 cites W2042430880 @default.
- W2287743904 cites W2059763497 @default.
- W2287743904 cites W2061177902 @default.
- W2287743904 cites W2072167551 @default.
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- W2287743904 cites W2113230494 @default.
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- W2287743904 cites W2136349095 @default.
- W2287743904 cites W2137108435 @default.
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- W2287743904 cites W2141195253 @default.
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- W2287743904 doi "https://doi.org/10.1074/jbc.m115.662593" @default.
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