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Brugia malayi: rat cell interactions with infective larvae mediated by complement
Abstract:
Albino rat macrophages and neutrophils, in the presence of fresh normal rat serum as a source of complement, adhered to and promoted killing of Brugia malayi infective larvae in vitro. Eosinophils, by themselves, were marginally cytotoxic at a high cell-target ratio but promoted cytotoxicity when mixed with macrophages. Eosinophil culture supernatants enhanced the macrophage mediated killing of infective larvae. The complement of fresh normal rat serum was found to act by the alternate pathway. Fresh normal rat serum depleted of alternate pathway complement activity by treatment with zymosan A, or of Factor B by heating at 50 C for 20 min, or of Factor D by passing through Sephadex G75 column, failed to promote cell adherence to the parasite. C3 molecules were detected on the surface of infective larvae by immunofluorescence. There was a significant consumption of complement when Brugia malayi infective larvae were incubated in fresh normal rat serum. Albino rat cells were more potent in inducing cytotoxicity to infective larvae in vitro than those from jird or Mastomys natalensis, which may reflect the greater resistance offered by the rat to B. malayi infection. There was much less cellular infiltration on introduction of Brugia malayi infective larvae into the peritoneal cavity of jirds compared to rats and Mastomys natalensis indicating the greater susceptibility of jirds to intraperitoneally induced infections.
Insights
Rat immune cells, including macrophages and neutrophils, effectively kill Brugia malayi infective larvae in vitro, utilizing the complement system. This study highlights rat cells
Area of Science:
- Immunology
- Parasitology
- Cell Biology
Background:
- Brugia malayi is a filarial nematode responsible for lymphatic filariasis.
- The host immune response, particularly the role of complement and cellular components, is crucial in controlling parasitic infections.
- Understanding the mechanisms of parasite killing is vital for developing effective therapeutic strategies.
Purpose of the Study:
- To investigate the in vitro cytotoxic activity of albino rat immune cells against Brugia malayi infective larvae.
- To elucidate the role of complement and its pathways in mediating cellular adherence and parasite killing.
- To compare the efficacy of rat immune cells with those from other rodent species.
Main Methods:
- Incubation of Brugia malayi infective larvae with albino rat macrophages, neutrophils, and eosinophils in the presence of normal rat serum.
- Assessment of cell adherence and parasite killing using in vitro assays.
- Complement pathway analysis by depleting specific complement components (zymosan A, Factor B, Factor D) and evaluating cytotoxicity.
- Immunofluorescence detection of C3 molecules on larvae and measurement of complement consumption.
Main Results:
- Albino rat macrophages and neutrophils, supported by complement, adhered to and killed Brugia malayi infective larvae.
- Eosinophils showed marginal cytotoxicity alone but enhanced macrophage-mediated killing.
- The complement system acted via the alternate pathway, as evidenced by the failure of depleted serum to support cell adherence.
- C3 molecules were detected on larvae, and significant complement consumption occurred.
- Rat immune cells were more potent killers than those from jirds or Mastomys natalensis.
Conclusions:
- Albino rat macrophages and neutrophils, activated by the alternate complement pathway, are effective in killing Brugia malayi infective larvae in vitro.
- Eosinophils contribute to parasite killing, particularly in conjunction with macrophages.
- The potent cytotoxic activity of rat immune cells correlates with the natural resistance of rats to B. malayi infection.