Changes in the capacity of macrophages and T cells to produce interleukins during marine malaria infection

Lelchuk, Rosalia; Rose, Gillian; Playfair, John

doi:10.1016/0008-8749(84)90097-2

Cited by 29 publications

(11 citation statements)

References 20 publications

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“…The greater sensitivity of NBNT cells to IL-3 in infected mice compared to normal mice might reflect an up-regulation of IL-3R expression in vivo. IL-3R expression has been shown to be induced by IL-1 [26] and by TNF- § [27], cytokines present at high concentrations during the first Th1-dominated week of P. chabaudi infection [28][29][30].…”

Section: Discussionmentioning

confidence: 99%

Expansion of IL-3-responsive IL-4-producing non-B non-T cells correlates with anemia and IL-3 production in mice infected with blood-stagePlasmodium chabaudi malaria

Helmby

Kullberg

1998

Eur. J. Immunol.

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A prominent switch of CD4 + T cells from Th1 to Th2 type response occurs in mice infected with the non-lethal malaria parasite Plasmodium chabaudi chabaudi AS around the time of peak parasitemia. This is reflected by a decrease in IFN-+ -and an increase in IL-4-producing cells.The peak occurs approximately 9-10 days after infection and is accompanied by anemia. The mechanism behind the switch in Th cell response is poorly understood. We here report on the production of IL-4 from a non-T cell source during P. chabaudi infection in BALB/c mice. Flow cytometric analysis of spleen and peripheral blood leukocytes (PBL) showed a dramatic increase in the percentage of non-B non-T (NBNT) cells 9-23 days after P. chabaudi infection with peak values by day 15 (˚30 % of splenocytes and˚55 % of PBL being NBNT cells). The expansion of NBNT cells correlated closely with the appearance of a cell type secreting IL-4 and IL-6 following stimulation with IL-3 and/or cross-linking of Fc + R. Compared to cells from uninfected animals, NBNT cells from P. chabaudi-infected mice were shown to be hyper-responsive to IL-3. The levels of the hematopoietic cytokine IL-3 were elevated in supernatants from unstimulated spleen cell cultures as well as in serum at the same time points at which NBNT cell-derived IL-4 and IL-6 were detected from spleen cultures and PBL. Thus, IL-3-responsive IL-4-producing NBNT cells may provide cytokines supporting the switch from Th1 to a Th2 response which is important for the final clearance of the parasite in P. chabaudi malaria.

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Section: Discussionmentioning

confidence: 99%

Expansion of IL-3-responsive IL-4-producing non-B non-T cells correlates with anemia and IL-3 production in mice infected with blood-stagePlasmodium chabaudi malaria

Helmby

Kullberg

1998

Eur. J. Immunol.

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“…Further, in recent years much evidence has accumulated that the functions of macrophages are changed during malarial infection in animals. These include an increase of phagocytosis in vitro (Loose 1984) and in uiuo (Lucia & Nussenzweig 1969, Roberts & Weidanz 1978, Dockrell, DeSouza & Playfair 1980, an enhanced ability to kill microorganisms (Loose 1984), an increased release of interleukin-1 (Lelchuk, Rose & Playfair 1984, Wood & Clark 1984, and a stimulation of plasminogen activator secretion (Lelchuk, Dockrell & Playfair 1983). In addition, attention has been drawn to the significant ability of macrophages and neutrophils to produce toxic oxygen radicals, which have been suggested to participate in parasite killing (Brinkmann et al 1984, Clark & Hunt 1983, Dockrell & Playfair 1983, Ockenhouse & Shear 1984 as well as in much of the clinical symptoms associated with malaria infection (Clark et al 1981).…”

Section: Introductionmentioning

confidence: 99%

Suppression of blood monocyte and neutrophil chemotaxis in acute human malaria

Nielsen

Kharazmi

Theander

1986

Parasite Immunology

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The host response to Plasmodia includes the production of enlarged populations of peripheral blood monocytes and tissue macrophages in the spleen and the liver. Since the hyperplasia of the mononuclear phagocyte system is believed to arise as a consequence of an enhanced blood monocyte influx, we tested monocyte chemotactic responsiveness in 19 patients with acute primary attack malaria. In addition, the neutrophil chemotaxis was measured in 12 patients. Before the initiation of antimalarial treatment a significant depression of monocyte chemotaxis was observed in approximately half of the patients when compared with healthy control subjects. The depression was found in Plasmodium falciparum malaria as well as in P. vivax or P. ovale malaria patients. The defective responsiveness was not receptor specific, since the responses towards casein and zymosan activated serum proved to be equally suppressed. The monocyte chemotaxis was followed in 14 of the patients, during treatment and after complete recovery. After 3 days of treatment the response had improved in most of the patients, and after 7 days all patients had a normal monocyte chemotaxis, which remained normal after one month. No significant differences between P. falciparum and P. vivax/ovale malaria was observed with respect to blood monocyte chemotactic responsiveness. Neutrophil chemotaxis in patients with P. falciparum infections was similarly suppressed before treatment (54% of controls), was still defective after 3 days of treatment, and nearly normalized after 7 days (87% of controls). Furthermore, monocyte phagocytic and candidacidal activities were assessed in the same patients on admission and during the follow-up. In contrast to chemotaxis, these functions were normal in all of the patients whenever measured. In conclusion, not all cell functions were altered in concert, and the previously unreported suppression of chemotactic migration might reflect a change in blood leucocyte subpopulations, deactivation in vivo or a direct suppressive effect of plasmodia induced products.

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“…The diminished T-cell responses and a defect in the production of IL-2 have been observed during the acute stage of infection with P. falciparum [6,16] and P. yoelii [9]. Moreover, Lucas et al [10] reported that the transcript for IL-2 was not detected in mice with acute P. yoelii malaria although mRNA for the cytokine was detectable late in the infection when mice cleared the parasites.…”

Section: Discussionmentioning

confidence: 99%

“…In an array of cytokines, the ability of spleen cells to produce IL-2 has been shown to be markedly reduced during P. yoelii-malaria infection [9,10]. To examine if the lack of IL-2 was involved in the defective antibody-forming capability of spleen cells from infected mice, recombinant IL-2 was added to the culture and the levels of specific antibody were determined.…”

Section: Effect Of Recombinant Il-2 On Antibody Responses To R32tet32mentioning

confidence: 99%

In vitro Antibody Response to the Tetrapeptide Repeats of Plasmodium falciparum Circumsporozoite Protein by Splenocytes from Mice Infected with P. yoelii yoelii.

Kobayashi

Tsuji

Weidanz

2001

The Journal of Veterinary Medical Science

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ABSTRACT. The antibody response to the recombinant protein, R32tet32, which contained the repetitive sequence (NANP) n of Plasmodium falciparum CSP was determined in C57BL/6 mice during the course of nonlethal infection with Plasmodium yoelii 17X. Marked suppression of the IgG antibody response to R32tet32 occurred when mice were immunized at peak parasitemia (on day 16). In vitro antibody responses of spleen cells from acutely infected mice to R32tet32 were similarly suppressed. Stimulation of normal spleen cells cultured for 5 days with 100 ng/ml of R32tet32 gave an optimal IgG antibody response, but spleen cells from infected mice obtained at peak parasitemia failed to respond to a broad range of antigen concentrations. Cocultivation studies employing enriched lymphocyte populations from infected and uninfected C57BL/6 mice indicated that both T and B cells from infected mice were defective in their response to R32tet32. The response to the repetitive region was restored by the addition of recombinant mouse interleukin-2 (IL-2) at a dose of 50 U/ml to cultures of spleen cells from infected mice.

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Changes in the capacity of macrophages and T cells to produce interleukins during marine malaria infection

Cited by 29 publications

References 20 publications

Expansion of IL-3-responsive IL-4-producing non-B non-T cells correlates with anemia and IL-3 production in mice infected with blood-stagePlasmodium chabaudi malaria

Expansion of IL-3-responsive IL-4-producing non-B non-T cells correlates with anemia and IL-3 production in mice infected with blood-stagePlasmodium chabaudi malaria

Suppression of blood monocyte and neutrophil chemotaxis in acute human malaria

In vitro Antibody Response to the Tetrapeptide Repeats of Plasmodium falciparum Circumsporozoite Protein by Splenocytes from Mice Infected with P. yoelii yoelii.

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