scholarly journals Lactoferrin inhibits or promotes Legionella pneumophila intracellular multiplication in nonactivated and interferon gamma-activated human monocytes depending upon its degree of iron saturation. Iron-lactoferrin and nonphysiologic iron chelates reverse monocyte activation against Legionella pneumophila.

1991 ◽  
Vol 88 (4) ◽  
pp. 1103-1112 ◽  
Author(s):  
T F Byrd ◽  
M A Horwitz
Keyword(s):  
Interferon Gamma ◽  
Legionella Pneumophila ◽  
Human Monocytes ◽  
Iron Chelates ◽  
Monocyte Activation ◽  
Iron Saturation ◽  
Intracellular Multiplication

scholarly journals Legionella pneumophila inhibits acidification of its phagosome in human monocytes.

1984 ◽  
Vol 99 (6) ◽  
pp. 1936-1943 ◽  
Author(s):  
M A Horwitz ◽  
F R Maxfield
Keyword(s):  
Legionella Pneumophila ◽  
Sheep Erythrocyte ◽  
Bacterial Pathogen ◽  
Human Monocytes ◽  
E Coli ◽  
The Mean ◽  
Intracellular Multiplication ◽  
Fluorescence Images ◽  
Activated Monocytes ◽  
Quantitative Fluorescence

We used quantitative fluorescence microscopy to measure the pH of phagosomes in human monocytes that contain virulent Legionella pneumophila, a bacterial pathogen that multiplies intracellularly in these phagocytes. The mean pH of phagosomes that contain live L. pneumophila was 6.1 in 14 experiments. In the same experiments, the mean pH of phagosomes containing dead L. pneumophila averaged 0.8 pH units lower than the mean pH of phagosomes containing live L. pneumophila, a difference that was highly significant (P less than 0.01 in all 14 experiments). In contrast, the mean pH of phagosomes initially containing live E. coli, which were then killed by monocytes, was the same as for phagosomes initially containing dead E. coli. The mean pH of L. pneumophila phagosomes in activated monocytes, which inhibit L. pneumophila intracellular multiplication, was the same as in nonactivated monocytes. To simultaneously measure the pH of different phagosomes within the same monocyte, we digitized and analyzed fluorescence images of monocytes that contained both live L. pneumophila and sheep erythrocytes. Within the same monocyte, live L. pneumophila phagosomes had a pH of approximately 6.1 and sheep erythrocyte phagosomes had a pH of approximately 5.0 or below. This study demonstrates that L. pneumophila is capable of modifying the pH of its phagocytic vacuole. This capability may be critical to the intracellular survival and multiplication of this and other intracellular pathogens.

scholarly journals Formation of a novel phagosome by the Legionnaires' disease bacterium (Legionella pneumophila) in human monocytes.

1983 ◽  
Vol 158 (4) ◽  
pp. 1319-1331 ◽  
Author(s):  
M A Horwitz
Keyword(s):  
Legionella Pneumophila ◽  
Vacuolar Membrane ◽  
Common Mechanism ◽  
Cytoplasmic Vacuole ◽  
Human Monocytes ◽  
Vacuole Formation ◽  
Cytoplasmic Organelles ◽  
Membrane Bound ◽  
Legionnaires Disease ◽  
Intracellular Multiplication

Previous studies have shown that L. pneumophila multiplies intracellularly in human monocytes and alveolar macrophages within a membrane-bound cytoplasmic vacuole studded with ribosomes. In this paper, the formation of this novel vacuole is examined. After entry into monocytes, L. pneumophila resides in a membrane-bound vacuole. During the first hour after entry, vacuoles containing L. pneumophila are found surrounded by smooth vesicles fusing with or budding off from the vacuolar membrane and by mitochondria closely apposed to the vacuolar membrane. By 4 h, vacuoles are found less frequently surrounded by these cytoplasmic organelles, but now ribosomes and rough vesicles are found gathered about the vacuole. By 8 h, the ribosome-lined vacuole has formed. Erythromycin, at concentrations that completely inhibit the intracellular multiplication of L. pneumophila, has no effect on vacuole formation. Formalin-killed L. pneumophila also reside in a membrane-bound vacuole after entry into monocytes. In contrast to the situation with live L. pneumophila, cytoplasmic organelles are not found surrounding vacuoles containing formalin-killed L. pneumophila at any time after entry. Formalin-killed bacteria are rapidly digested, and by 4 h, few remain intact. The L. pneumophila-containing vacuole has certain features in common with other intracellular organisms that inhibit phagosome-lysosome fusion; these organisms may share a common mechanism for vacuole formation and inhibition of phagosome-lysosome fusion.

Sign in / Sign up

Export Citation Format

Share Document