Successful passive transfer of resistance to Fasciola hepatica infection in rats by immune serum and transfer factor

Mitchell, Gillian; Armour, J.; Rossf, J.G.; Halliday, W.G.

doi:10.1016/s0034-5288(18)32591-8

Cited by 11 publications

(4 citation statements)

References 7 publications

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“…The protection of naive rats by intraperitoneal injection of sera from F. hepatica ‐infected sheep, cattle or rats suggests a killing mechanism at that site dependent on the presence of parasite‐specific antibody (20–25). The protective response in these studies required challenge infection on the day of transfer with killing of NEJ liver fluke occurring within 48 h, prior to entry into the liver (20–23) and therefore is likely to involve resident PLCs.…”

Section: Discussionmentioning

confidence: 96%

“…Monocytes/macrophages have not been specifically studied in the killing of NEJ liver fluke but are one of the major effector cells involved in the killing of parasites by the production of free radicals (16–19). Resident peritoneal lavage cells (PLCs) of naive rats are a source rich in monocytes/macrophages and passive transfer of sera from F. hepatica ‐infected sheep, cattle or rats protect naive rats from F. hepatica infection when injected intraperitoneally (20–25). Most juvenile parasites are killed within the gut and peritoneum before reaching the liver, suggesting that resident PLCs such as monocytes/macrophages could be involved in the killing of NEJ liver fluke by a mechanism dependent on parasite‐specific antibody (2,20–23).…”

Section: Introductionmentioning

confidence: 99%

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Antibody‐dependent cell‐mediated cytotoxicity to newly excysted juvenile Fasciola hepatica in vitro is mediated by reactive nitrogen intermediates

Piedrafita

Parsons²,

Sandeman

et al. 2001

Parasite Immunology

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Passive intraperitoneal transfer of sera from Fasciola hepatica-infected sheep, cattle or rats can protect naive rats from F. hepatica infection, suggesting a parasite killing mechanism within the peritoneal cavity that is dependent on the presence of parasite-specific antibody. We investigated antibody-dependent cell-mediated cytotoxicity by resident peritoneal lavage cell populations, containing large numbers of monocytes/macrophages, as a potential host resistance mechanism by which juvenile flukes could be killed within the peritoneal cavity of naive rats. Comparative studies were conducted using cell populations containing large numbers of monocytes/macrophages from sheep. The results demonstrate that monocyte/macrophage-rich lavage cell populations from rat and sheep differ substantially in their ability to generate nitric oxide. Only resident rat peritoneal lavage cells were able to mediate antibody-dependent cell-mediated cytotoxicity against newly excysted juvenile liver fluke. The mechanism of cytotoxicity was dependent on, and directly proportional to, the production of nitric oxide and required attachment of effector cells to the newly excysted juvenile liver fluke tegument, which occurred following the addition of sera from F. hepatica-infected animals. This is the first report demonstrating a mechanism of cell-mediated cytotoxicity to newly excysted juvenile liver fluke.

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Section: Discussionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 99%

Antibody‐dependent cell‐mediated cytotoxicity to newly excysted juvenile Fasciola hepatica in vitro is mediated by reactive nitrogen intermediates

Piedrafita

Parsons²,

Sandeman

et al. 2001

Parasite Immunology

View full text Add to dashboard Cite

show abstract

“…Peritoneal exudate cells were found to transfer resistance in mice (Lang et al 1967); spleen and lymph node cells from infected animals were shown to confer resistance in rats and cattle (Corba et al 1971) as well a s in sheep (Armour & Dargie 1974). Mitchell et al (1981) also demonstrated that transfer factor could transfer resistance between infected and uninfected rats, but not between cattle. However, all of these transfer studies are critically dependent o n the time when the cells used for transfer are taken after infection.…”

Section: Introductionmentioning

confidence: 95%

Cell mediated immunity to liver fluke antigens during experimental Fasciola hepatica infection of cattle

Oldham

Williams

1985

Parasite Immunology

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Cell mediated immunity (CMI) to Fasciola hepatica antigens was detected by lymphocyte proliferation and interleukin-2 (IL-2) production tests in cattle during the first 4 weeks following liver fluke infection. From the fifth week of infection onwards peripheral blood lymphocytes were unresponsive to fluke antigens by these in vitro tests. Investigations into the cause of this unresponsiveness found no evidence to suggest a selective loss of the IL-2 producing lymphocyte sub-population or that macrophages were responsible for the suppression or that antigen responsive cells were being sequestered in the spleen and mesenteric lymph nodes. Tests carried out on culture supernatants demonstrated the production during this unresponsive period of factors capable of suppressing in vitro responses to PHA. Although further tests failed to show antigen specific suppressor factors the presence of MHC restricted suppressor factors could not be ruled out. The early and transient appearance of CMI during F. hepatica infection of cattle indicates that delayed type hypersensitivity is unlikely to be important in protective immunity in cattle.

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“…In an investigation of the competence of lymphocytes obtained from immune and non-immune donors to cause expulsion of Nippostrongvhts braziliensis in the rat, DINEEN et al (1973) record the failure of lymphocytes from non-immune donors given intravenously to cause expulsion while KELLER & KEIST (1972) report expulsion with similar non-immune donor lymphocytes given intraperitoneally. Evidence of reduced infections were also obtained by MITCHELL et al (1981) following intraperitoneal administration of normal sera in rats to infection with Fasciola hepatica and it is therefore possible that the intraperitoneal route of administration favours a non-specific immune sequel although there are many examples in the literature of material given intraperitoneally producing no resistance to various types of challenge infection (KLESIUS & FUDENM-RG, 1977;KLESIUS et al, 1978;LARSH et al, 1970).…”

Section: Discussionmentioning

confidence: 99%

Investigations of transfer factor activity in resistance toTrichostrongylus colubriformisinfections in guinea-pigs

Ross¹,

Halliday²

1982

J. Helminthol.

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Resistance to challenge infection with Trichostrongylus colubriformis was studied in an outbred strain of guinea-pigs. Resistance was conferred by previous infections of 50 or 100 infective larvae and by intraperitoneal, intramuscular and subcutaneous administration of dialysed transfer factor prepared from guinea-pigs infected with T. colubriformis, by intraperitoneal administration of transfer factor prepared from the blood of sheep infected with T. colubriformis and on one of three occasions using transfer factor prepared from guinea-pigs which had not been infected with T. colubriformis. No significant resistance was transferred by administration of antigen prepared from adult T. colubriformis, or by non-dialysed transfer factor, or by dialysed transfer factor prepared from T. colubriformis-infected guinea-pig tissue which had been stored for several months at −20°C.

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Successful passive transfer of resistance to Fasciola hepatica infection in rats by immune serum and transfer factor

Cited by 11 publications

References 7 publications

Antibody‐dependent cell‐mediated cytotoxicity to newly excysted juvenile Fasciola hepatica in vitro is mediated by reactive nitrogen intermediates

Antibody‐dependent cell‐mediated cytotoxicity to newly excysted juvenile Fasciola hepatica in vitro is mediated by reactive nitrogen intermediates

Cell mediated immunity to liver fluke antigens during experimental Fasciola hepatica infection of cattle

Investigations of transfer factor activity in resistance toTrichostrongylus colubriformisinfections in guinea-pigs

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