|
|
||||||||
The Journal of Immunology, Vol 127, Issue 4 1438-1443, Copyright © 1981 by American Association of Immunologists
ARTICLES |
RD Pearson and RT Steigbigel
The role of polymorphonuclear leukocytes (PMN) in host defense against Leishmania donovani, the protozoan that causes visceral leishmaniasis, is unknown. To assess the ability of PMN to ingest and kill the infecting promastigote stage of the organism, cytocentrifuge preparations were made from tumbled suspensions of 5 X 10(6) PMN, an equal number of promastigotes, and fresh human serum deficient in the 6th component of complement. 53 +/- 9% PMN were found to have 1 or more associated promastigotes, and 81 +/- 14 promastigotes were found per 100 PMN after 15 min at 37 degrees C. There was a corresponding decrease in extracellular promastigotes from 5 x 10(6) ml to 2.7 X 10(4)/ml. Superoxide anion was generated during phagocytosis. Ingetion was saturable with respect to promastigote concentration, required heat labile factors, and was minimal when suspensions were incubated in ice water. Intracellular killing of promastigotes was indicated by a decline in cell-associated organisms without a concomitant increase in extracellular promastigotes. Light and electron microscopy showed disintegration of intracellular promastigotes. Oxidative killing mechanisms appear to be required for PMN killing of this protozoan organism, since there was no decline in intracellular organisms in PMN from a donor with chronic granulomatous disease. Promastigotes studied in a phagocyte-free system were susceptible to H2O2 generated from glucose by glucose oxidase or added directly at greater than or equal to 10(-5) M. Killing was enhanced by the addition of lactoperoxidase (50 mU/ml) with KI (0.05 mM) and inhibited by fresh, but not boiled catalase in the glucose-glucose oxidase system. These studies demonstrate that human PMN can ingest and kill L. donovani by the H2O2- peroxidase-halide system and may be capable of providing host defense against the invading, promastigote stage of this pathogen.
This article has been cited by other articles:
![]() |
E. McFarlane, C. Perez, M. Charmoy, C. Allenbach, K. C. Carter, J. Alexander, and F. Tacchini-Cottier Neutrophils Contribute to Development of a Protective Immune Response during Onset of Infection with Leishmania donovani Infect. Immun., February 1, 2008; 76(2): 532 - 541. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Ahmed, M. Colmenares, L. Soong, K. Goldsmith-Pestana, L. Munstermann, R. Molina, and D. McMahon-Pratt Intradermal Infection Model for Pathogenesis and Vaccine Studies of Murine Visceral Leishmaniasis Infect. Immun., January 1, 2003; 71(1): 401 - 410. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. Aga, D. M. Katschinski, G. van Zandbergen, H. Laufs, B. Hansen, K. Muller, W. Solbach, and T. Laskay Inhibition of the Spontaneous Apoptosis of Neutrophil Granulocytes by the Intracellular Parasite Leishmania major J. Immunol., July 15, 2002; 169(2): 898 - 905. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. Laufs, K. Muller, J. Fleischer, N. Reiling, N. Jahnke, J. C. Jensenius, W. Solbach, and T. Laskay Intracellular Survival of Leishmania major in Neutrophil Granulocytes after Uptake in the Absence of Heat-Labile Serum Factors Infect. Immun., February 1, 2002; 70(2): 826 - 835. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. Bogdan, N. Donhauser, R. Doring, M. Rollinghoff, A. Diefenbach, and M. G. Rittig Fibroblasts as Host Cells in Latent Leishmaniosis J. Exp. Med., June 19, 2000; 191(12): 2121 - 2130. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Dominguez and A. Torano Immune Adherence-mediated Opsonophagocytosis: The Mechanism of Leishmania Infection J. Exp. Med., January 4, 1999; 189(1): 25 - 35. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |