Role of antibody and complement in the control of Encephalitozoon cuniculi infections by rabbit macrophages

Niederkorn, Jérry Y.; Shadduck, John A.

doi:10.1128/iai.27.3.995-1002.1980

Cited by 39 publications

(13 citation statements)

References 25 publications

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“…In vitro studies showed that some species of microsporidia, could replicate within parasitophorous vacuoles of the host cell due to an absence of fusion between the host cell lysosomes and the parasitophorous vacuole (Weidner 1975). Thioglycollate-ellicited lagomorph and murine peritoneal macrophages also support the growth and replication of E. cuniculi, but organisms opsonized with specific antibody are destroyed due to fusion of lysosomes with the parasitophorous vacuoles (Niederkorn & Shadduck 1980, Schmidt & Shadduck 1984. In addition, incubation of the murine elicited peritoneal murine (BALB/c) macrophages with sensitized T-enriched murine spleen-lymphocyte culture supernatants induced the macrophages to kill E. cuniculi (Schmidt & Shadduck 1984).…”

Section: Discussionmentioning

confidence: 99%

Reactive nitrogen intermediates implicated in the inhibition of Encephalitozoon cuniculi (phylum microspora) replication in murine peritoneal macrophages

Didier

1995

Parasite Immunology

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Encephalitozoon cuniculi (phylum microspora) is a protozoan parasite that can replicate within parasitophorous vacuoles in macrophages. Thioglycollate-elicited BALB/c peritoneal macrophages treated with murine recombinant interferon-gamma (rIFN-gamma; 100 7/ml) in combination with lipopolysaccharide (LPS; 10 ng/ml) for 24 h killed E. cuniculi as determined by significant reductions in the number of parasites and percent of infected macrophages 48 h later compared with cultures treated with medium only. Treatment of the elicited macrophages with murine rIFN-gamma (10 u/ml or 100 u/ml) only, resulted in microbistatic activity. Significantly higher levels of nitrite (NO2) were detected in supernatants from macrophage cultures treated with rIFN-gamma (10 u/ml or 100 u/ml) which induced microbistatic macrophage activity as well as from macrophage cultures treated with LPS + rIFN- when compared with levels of nitrite detected in supernatants of infected macrophages treated with medium only. Addition of the L-arginine analogue, N3 monomethyl-L-arginine (NMMA) at concentrations of 50, 100 or 250 uM significantly inhibited nitrite synthesis and prevented microsporidia killing. Addition of exogenous L-arginine at concentrations of 5 mM or 10 mM reversed the NMMA-induced inhibition of parasite killing. These results indicate that reactive nitrogen intermediates contribute to the killing of E. cuniculi by LPS + rIFN-gamma-activated murine peritoneal macrophages in vitro.

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Section: Discussionmentioning

confidence: 99%

Reactive nitrogen intermediates implicated in the inhibition of Encephalitozoon cuniculi (phylum microspora) replication in murine peritoneal macrophages

Didier

1995

Parasite Immunology

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“…Coating live L. pneumophila with antibody, with or without complement, promotes fusion with lysosomes of a proportion of the bacterial phagosomes. Antibody has also been reported to promote fusion with lysosomes ofphagosomes containing M. tuberculosis (27), T. gondii (28), C. psittaci (6), and E. cuniculi (8).…”

Section: Discussionmentioning

confidence: 99%

The Legionnaires' disease bacterium (Legionella pneumophila) inhibits phagosome-lysosome fusion in human monocytes.

Horwitz¹

1983

The Journal of Experimental Medicine

652

555

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The interactions between the L. pneumophila phagosome and monocyte lysosomes were investigated by prelabeling the lysosomes with thorium dioxide, an electron-opaque colloidal marker, and by acid phosphatase cytochemistry. Phagosomes containing live L. pneumophila did not fuse with secondary lysosomes at 1 h after entry into monocytes or at 4 or 8 h after entry by which time the ribosome-lined L. pneumophila replicative vacuole had formed. In contrast, the majority of phagosomes containing formalin-killed L. pneumophila, live Streptococcus pneumoniae, and live Escherichia coli had fused with secondary lysosomes by 1 h after entry into monocytes. Erythromycin, a potent inhibitor of bacterial protein synthesis, at a concentration that completely inhibits L. pneumophila intracellular multiplication, had no influence on fusion of L. pneumophila phagosomes with secondary lysosomes. However, coating live L. pneumophila with antibody or with antibody and complement partially overcame the inhibition of fusion. Also activating the monocytes promoted fusion of a small proportion of phagosomes containing live L. pneumophila with secondary lysosomes. Acid phosphatase cytochemistry revealed that phagosomes containing live L. pneumophila did not fuse with either primary or secondary lysosomes. In contrast to phagosomes containing live bacteria, the majority of phagosomes containing formalin-killed L. pneumophila were fused with lysosomes by acid phosphatase cytochemistry. The capacity of L. pneumophila to inhibit phagosome-lysosome fusion may be a critical mechanism by which the bacterium resists monocyte microbicidal effects.

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“…While the link between Ab‐mediated protection, FcR engagement, and lysosomal localization of the pathogen has only been made for a few infectious agents, reports about other pathogens point toward this being a more general mechanism active against intracellular pathogens. For instance, Ab‐mediated targeting into lysosomes has been reported for the intracellular bacterium Rickettsia conorii and the protozoan parasite Encephalitozoon cuniculi ; both pathogens evade phagolysosomal fusion in the absence of specific Abs 83, 84. Furthermore, macrophage killing of Chlamydia was shown to be strongly enhanced in the presence of Abs 38.…”

Section: Opposing Signals: Fcr Triggering Versus Evasion Of Lysosomalmentioning

confidence: 96%

Antibody – Fc receptor interactions in protection against intracellular pathogens

2011

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Intracellular pathogen-specific antibodies (Abs) can contribute to host protection by a number of different mechanisms. Ab opsonization of pathogens residing outside a host cell can prevent infection of target cells either via neutralization of the critical surface epitopes required for host cell entry, complement-mediated degradation, or via subsequent intracellular degradation. In the case of intracellular localization, Abs can bind to infected cells and thus mark them for destruction by Fc receptor (FcR)-bearing effector cells. This review focuses on the protective role of Abs against intracellular bacteria and parasites involving FcR interactions that modulate the intracellular trafficking of the pathogen, the ability of FcRs to interfere with the establishment of an intracellular replicative niche and the involvement of FcRs to modulate pathogen-specific T-cell responses.

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Role of antibody and complement in the control of Encephalitozoon cuniculi infections by rabbit macrophages

Cited by 39 publications

References 25 publications

Reactive nitrogen intermediates implicated in the inhibition of Encephalitozoon cuniculi (phylum microspora) replication in murine peritoneal macrophages

Reactive nitrogen intermediates implicated in the inhibition of Encephalitozoon cuniculi (phylum microspora) replication in murine peritoneal macrophages

The Legionnaires' disease bacterium (Legionella pneumophila) inhibits phagosome-lysosome fusion in human monocytes.

Antibody – Fc receptor interactions in protection against intracellular pathogens

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