Figure 1.
Ultrastructure of nascent phagosomes and phagolysosomes within phagocytic cells in a murine model of tuberculosis.
(A) Nascent phagosomes containing phagocytosed mycobacteria (arrows) are seen in the cytoplasm of a neutrophil. In (B), macrophage pseudopods encircle an apoptotic cell (arrowheads). (C) Typical phagolysosomes (Ph) within a macrophage show heterogenous content and varying sizes and electron-density. A degenerating bacterium is observed (arrow). Mice were infected with Mycobacterium bovis bacillus Calmette-Guerin (BCG) and cells from the pleural cavity processed for transmission electron microscopy as before [3]. Scale bars, 1 µm (A, B), 500 nm (C).
Figure 2.
Lipid body (LB) structure and composition.
(Ai–Aiii) A LB within a human blood eosinophil is observed by transmission electron microscopy (TEM) at different magnifications (boxed area in Ai is shown in Aii and Aiii). LBs are delimited by a monolayer of phospholipids differing from the structural organization (phospholipid bilayer membrane) of all other organelles, vesicles, and plasma membrane (arrowheads in Aii and box in Aiii). Structural proteins from the perilipin family are associated with the LB surface while the LB core contains mainly sterol esters (SE), triacylglycerols (TAG), diacilglycerols (DAG), and cholesterol. Numerous proteins are frequently found in LBs such as Rab GTPases, lipid metabolism enzymes, kinases, caveolins, and chaperones. Nu, nucleus; Gr, secretory granule. Scale bar, 600 nm.
Figure 3.
Lipid bodies (LBs) increase in number and interact with phagosomes within heart inflammatory macrophages during parasite infection.
LBs with different sizes are seen as electron-dense or electron-lucent organelles surrounding and in contact (arrow) with a large phagolysosome containing an intact amastigote (*), the intracellular form of the parasite Trypanosoma cruzi. Rats were infected with the Y strain of T. cruzi and samples of the heart, a target organ of the parasite, processed for transmission electron microscopy at day 12 of infection [6], [68], [69]. Nu, nucleus. Scale bar, 800 nm.
Table 1.
Pathogen-induced lipid body (LB) formation and LB-phagosome interaction in mammalian cells.
Figure 4.
Human lipid bodies (LBs) observed with an ultrastructural method for autoradiography after a pulse of tritiated arachidonic acid and exposure to zymosan.
(A) 3H-arachidonate incorporated by a human macrophage is localized predominantly in LBs in association with zymosan-filled phagosomes. In (B), a LB labeled with numerous silver grains is seen in higher magnification. Note that the labeled lipid content is projecting into the zymosan-containing phagosome lumen. Scale bars, 1 µm (A), 600 nm (B).
Figure 5.
Lipid bodies (LBs) translocate to phagolysosomes in infected macrophages.
(Ai) LBs with different electron-densities are observed around a large phagolysosome (outlined in red in Aii) in the macrophage cytoplasm. Note that several LBs (highlighted in yellow in Aii) are seen within the phagolysosome. Rats were infected with the Y strain of T. cruzi and heart samples processed for transmission electron microscopy at day 12 of infection [6], [68], [69]. Nu, nucleus. Scale bar, 600 nm.
Figure 6.
Schematic representation of pathogen-mediated LB formation, LB translocation to phagosomes, and possible consequences of the LB-phagosome interaction.
Different pathogens induce LB formation within infected cells, such as macrophages. LB biogenesis occurs after both cell exposition to pathogens and/or receptor-mediated pathogen uptake. Cytoplasmic newly formed LBs relocate in the cytoplasm, dock at the surface of pathogen-containing phagosomes, and translocate into their lumen. This interaction may enable acquisition of nutrients for pathogen survival and multiplication or may be linked to host cell defense mechanisms favoring phagosome maturation and pathogen killing. Within macrophages and other inflammatory cells, LBs actively produce eicosanoids, such as prostaglandin E2 (PGE2), which may also contribute to pathogen outcome by inhibiting Th1 responses.