Mechanisms of killing of Toxoplasma gondii by rat peritoneal macrophages

McCabe, Robert E.; Remington, J S

doi:10.1128/iai.52.1.151-155.1986

Cited by 21 publications

(3 citation statements)

References 23 publications

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“…In contrast, serum‐opsonized C. albicans is normally ingested and killed by macrophages derived from cord blood, although these cells have a reduced capacity to respond to interferon‐γ (IFN‐γ) 38 . Furthermore, antimicrobial activity was similar in peritoneal macrophages from neonatal and adult mice, 39 and rats 40 , 41 . Apparently, the mechanisms of phagocytosis and killing in macrophages in the lungs are less mature when compared to macrophages from other sites in the first weeks after birth.…”

Section: Discussionmentioning

confidence: 90%

Functional immaturity of rat alveolar macrophages during postnatal development

et al. 1998

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SUMMARYAlveolar macrophages (AM ) are important in the regulation of immune responses in the lung, through their role as scavenger cells and through the production of many bioactive factors. Because in early infancy pulmonary infections are a recurrent problem, we studied the postnatal functional maturation of AM in a rat model. AM were isolated from rat lungs by bronchoalveolar lavage at several time intervals after birth and tested for their ability to ingest Escherichia coli in the presence of surfactant protein A (SP-A). Furthermore, their capacity to produce nitric oxide (NO) and interleukin-1b (IL-1b) after in vitro lipopolysaccharide (LPS ) stimulation was analysed, as well as their capacity to downregulate proliferation of T cells from both mature and neonatal rats. SP-A-mediated phagocytosis of E. coli by AM was reduced in 14-day-old neonatal rats, as compared with mature rats (P≤0·05). Also the IL-1b production by rat AM after LPS stimulation was impaired at 14 days of age, as compared with IL-1b production by AM from mature rats (P≤0·05). In contrast, the LPS-induced NO production by rat AM as well as the capacity to inhibit T-cell proliferation were well developed at all ages tested. In conclusion, during postnatal development the rat AM is functionally immature, with respect to phagocytosis and secretion of inflammatory mediators. These differences may underly the enhanced susceptibility to pulmonary infections as found in human neonates.

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Section: Discussionmentioning

confidence: 90%

Functional immaturity of rat alveolar macrophages during postnatal development

et al. 1998

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“…In vitro experiments have demonstrated that mouse peritoneal macrophages permit proliferation of Toxoplasma tachyzoites, but rat peritoneal macrophages, human alveolar and peritoneal macrophages, and human monocytes do not (Jones & Hirsch, 1972;Wilson & Remington, 1979;McLeod et al 1983;Chincilla, Portilla & Guerrero, 1986;McCabe & Remington, 1986;Catterall et al 1987). However, little information is available about the interaction between Toxoplasma and neutrophils which are the first inflammatory cells to infiltrate any site of infection.…”

Section: Introductionmentioning

confidence: 99%

Neutrophil chemotactic factors secreted fromToxoplasma gondii

Nakao

Konishi

1991

Parasitology

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Neutrophil chemotactic activity was detected in the fluid of Toxoplasma gondii cultures by the agarose plate and the Boyden chamber methods. Toxoplasma culture fluid was obtained by incubating the tachyzoites at 37 degrees C in a 5% CO2 atmosphere for 6 h in Dulbecco's modified Eagle's minimum essential medium containing 10% heat-inactivated foetal calf serum. Soluble extracts from tachyzoites had negligible activity, indicating that the chemotactic factors were metabolites secreted from tachyzoites. The chemotactic activity in Toxoplasma culture fluid depended on the number of tachyzoites and the period of incubation. The substances responsible for neutrophil chemotaxis were two heat-labile peptides with estimated Mr 4.5 and 14 kDa with N-terminal groups free.

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“…These species are highly susceptible to T. gondii, and their resident macrophages are unable to kill the organism. In contrast, resident alveolar and peritoneal macrophages from rats are capable of killing large numbers of T. gondii (4,20), and we recently postulated that this might account for the remarkable resistance of rats to Toxoplasma infection (4,15,33). The results of the present study are consistent with that view, since human subjects are also relatively resistant to T. gondii and their macrophages also kill this parasite.…”

Section: Discussionmentioning

confidence: 99%

Nonoxidative microbicidal activity in normal human alveolar and peritoneal macrophages

Catterall¹,

Black²,

Leventhal³

et al. 1987

Infect Immun

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Although Toxoplasma gondii multiplies within normal murine alveolar and peritoneal macrophages, it is killed by normal rat alveolar and peritoneal macrophages. The killing by rat macrophages is by a nonoxidative mechanism. Studies on normal human alveolar macrophages have reported disparate results in regard to their ability to inhibit or kill T. gondii. We considered it of interest to explore further the effect of normal human alveolar and peritoneal macrophages on T. gondii. Unstimulated alveolar macrophages from each of seven individuals demonstrated a marked ability to kill or inhibit multiplication of T. gondii in vitro (e.g., the number of parasites per 100 alveolar macrophages was 31 at time zero and 2 at 18 h, whereas this value increased from 37 at time zero to 183 at 18 h in murine macrophages assayed in parallel). In quantitative assays of superoxide, alveolar macrophages released a substantial amount of superoxide when exposed to phorbol myristate acetate or to candidae. In contrast, alveolar macrophages incubated with T. gondii released no more superoxide than when in medium alone. Scavengers of superoxide anions, hydrogen peroxide, singlet oxygen, and hydroxyl radicals failed to inhibit killing of T. gondii by alveolar macrophages. Peritoneal macrophages from each of six normal women undergoing laparoscopy killed T. gondii in vitro; results of quantitative superoxide assays and scavenger experiments demonstrated that no oxidative burst was triggered in these macrophages by exposure to T. gondii. These data indicate that normal human alveolar and peritoneal macrophages can kill an intracellular parasite by nonoxidative mechanisms and suggest that these mechanisms are important in inhibition or killing of other opportunistic intracellular pathogens.

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Mechanisms of killing of Toxoplasma gondii by rat peritoneal macrophages

Cited by 21 publications

References 23 publications

Functional immaturity of rat alveolar macrophages during postnatal development

Functional immaturity of rat alveolar macrophages during postnatal development

Neutrophil chemotactic factors secreted fromToxoplasma gondii

Nonoxidative microbicidal activity in normal human alveolar and peritoneal macrophages

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