Changes in the superoxide anion generating capacity and respiratory burst enzymes of peripheral blood monocytes of monkeys during acute <i>Plasmodium knowlesi</i> infection

Jayshree, R. S.; Ganguly, Nirmal Kumar; Sethi, Amanpreet; Mahajan, R. C.

doi:10.1111/j.1365-3024.1989.tb00684.x

Cited by 9 publications

(2 citation statements)

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“…Phagocyte activity is maximal upon first infection and declines thereafter with repeated malarial episodes (9,10). Basically the same type of response has also been noted in animal malarial models (11)(12)(13). In vitro, PRBC are phagocytosed by human phagocytes.…”

Section: Nfection Of Nonimmune Patients With Plasmodiumfaki~rummentioning

confidence: 70%

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Impairment of macrophage functions after ingestion of Plasmodium falciparum-infected erythrocytes or isolated malarial pigment.

Schwarzer

Turrini

Ulliers

et al. 1992

The Journal of Experimental Medicine

279

249

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SummaryHuman monocyte-derived macrophages ingest diamide-treated red blood cells (RBC), anti-D immunoglobulin (Ig)G-opsonized RBC, or Plasmodium fakiparum ring-stage parasitized RBC (RPRBC), degrade ingested hemoglobin rapidly, and can repeat the phagocytic cycle. Monocytes fed with trophozoite-parasitized RBC (TPRBC), which contain malarial pigment, or fed with isolated pigment are virtually unable to degrade the ingested material and to repeat the phagocytic cycle. Monocytes fed with pigment display a long-lasting oxidative burst that does not occur when they phagocytose diamide-treated RBC or RPRBC. The phorbol myristate acetate-elicited oxidative burst is irreversibly suppressed in monocytes fed with TPRBC or pigment, but not in monocytes fed with diamide-treated or IgG-opsonized RBC. This pattern of inhibition of phagocytosis and oxidative burst suggests that malarial pigment is responsible for the toxic effects. Pigment iron released in the monocyte phagolysosome may be the responsible element. 3% of total pigment iron is labile and easily detached under conditions simulating the internal environment of the phagolysosome, i.e., pH 5.5 and 10/zM H202. Iron liberated from pigment could account for the lipid peroxidation and increased production of malondialdehyde observed in monocytes fed with pigment or in RBC ghosts and liposomes incubated at pH 6.5 in presence of pigment and low amounts of H202. Removal of the labile iron fraction from pigment by repeated treatments with 0.1 mM H202 at pH 5.5 reduces pigment toxicity. It is suggested that iron released from ingested pigment is responsible for the intoxication of monocytes. In acute and chronic falciparum infections, circulating and tissue-resident phagocytes are seen filled with TPRBC and pigment particles over long periods of time. Moreover, human monocytes previously fed with TPRBC are unable to neutralize pathogenic bacteria, fungi, and tumor cells, and macrophage responses decline during the course of human and animal malaria. The present results may offer a mechanistic explanation for depression of cellular immunity in malaria.

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Section: Nfection Of Nonimmune Patients With Plasmodiumfaki~rummentioning

confidence: 70%

“…Despite these favorable conditions, frequently, malaria cannot be controlled and death occurs, the final cause being acute anemia or cerebral malaria (1,35). The inability to control infection may be due to the incapacitation of the macrophages as evidenced in human (9,10), rodent (11,12), and simian (13) malarias.…”

Section: Discussionmentioning

confidence: 99%