Differences in human macrophage receptor usage, lysosomal fusion kinetics and survival between logarithmic and metacyclic Leishmania infantum chagasi promastigotes.
Differences in human macrophage receptor usage, lysosomal fusion kinetics and survival between logarithmic and metacyclic Leishmania infantum chagasi promastigotes.
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DOI:
10.1111/j.1462-5822.2009.01374.x
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发表时间:
2009-12
影响因子:
3.4
通讯作者:
Wilson ME
中科院分区:
文献类型:
--
作者:
Ueno N;Bratt CL;Rodriguez NE;Wilson ME
The obligate intracellular protozoan, Leishmania infantum chagasi (Lic) undergoes receptor-mediated phagocytosis by macrophages, followed by a transient delay in phagolysosome maturation. We found differences in the pathway through which virulent Lic metacyclic promastigotes or avirulent logarithmic promastigotes are phagocytosed by human monocyte-derived macrophages (MDMs). Both logarithmic and metacyclic promastigotes entered MDMs through a compartment lined by the third complement receptor (CR3). In contrast, many logarithmic promastigotes entered through vacuoles lined by mannose receptors (MR) whereas most metacyclic promastigotes did not (p < 0.005). CR3 positive vacuoles containing metacyclic promastigotes stained for caveolin-1 protein, suggesting CR3 localizes in caveolae during phagocytosis. Following entry, the kinetics of phagolysosomal maturation and intracellular survival also differed. Vacuoles containing metacyclic parasites did not accumulate lysosome-associated membrane protein-1 (LAMP-1) at early times after phagocytosis, whereas vacuoles with logarithmic promastigotes did. MDMs phagocytosed greater numbers of logarithmic than metacyclic promastigotes, yet metacyclics ultimately replicated intracellularly with greater efficiency. These data suggest that virulent metacyclic Leishmania promastigotes fail to ligate macrophage MR, and enter through a path that ultimately enhances intracellular survival. The relatively quiescent entry of virulent Leishmania spp. into macrophages may be accounted for by the ability of metacyclic promastigotes to selectively bypass deleterious entry pathways.
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DOI:
10.1016/s0923-2494(99)80040-6
发表时间:
1998-09-01
期刊:
RESEARCH IN IMMUNOLOGY
影响因子:
--
作者:
Desjardins, M;Descoteaux, A
通讯作者:
Descoteaux, A
影响因子:
3.4
作者:
Dermine, JF;Scianimanico, S;Desjardins, M
通讯作者:
Desjardins, M
DOI:
10.1084/jem.20051239
发表时间:
2005-10-03
期刊:
The Journal of experimental medicine
影响因子:
--
作者:
Kang PB;Azad AK;Torrelles JB;Kaufman TM;Beharka A;Tibesar E;DesJardin LE;Schlesinger LS
通讯作者:
Schlesinger LS
DOI:
10.1084/jem.162.1.324
发表时间:
1985-07-01
期刊:
The Journal of experimental medicine
影响因子:
--
作者:
Blackwell JM;Ezekowitz RA;Roberts MB;Channon JY;Sim RB;Gordon S
通讯作者:
Gordon S
影响因子:
2.1
作者:
HOWARD, MK;SAYERS, G;MILES, MA
通讯作者:
MILES, MA