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Passive immunization with heterologous antivirus antiserum beginning at birth successfully suppressed infectious murine leukemia virus expression in Lake Casitas wild mice (Musmusculus) at 5-7 weeks of age.
Passive administration of specific immunoglobulin led to a transient rise in antiphospholipase IgG. An observed rise of 2 microgram/ml (twofold in three cases) was associated with a very diminished response to bee venom. This did not prevent the patient's own IgG response to challenge, which was at least as good as that of non-infused patients. The infusion of IgG cannot be proposed at present as a routine mode of therapy in insect allergy. However, we present the results of our study as the best evidence to date that blocking antibody is protective.
Passive immunity in neonatal calves is influenced by environment. Placing newly born Holstein calves (108 head) in three different housing environments (shade, cooled shade, hutch) during hot weather produced differences in body temperature, serum cortocosteroids, immunoglobulin IgG1 concentrations, and mortality. Experimental design permitted examination of effects due to treatments, time, differences in colostrum, and climatic environment in an analysis of variance. Calves exposed to the hotter, less desirable environment responded by having a higher mortality, higher serum corticosteroid concentration, and lower serum immunoglobulin IgG1 at 2 and 10 days after birth. All of these were correlated. Calves that died had serum immunoglobulin IgG1 falling below the mean for all experimental calves.
Mature Suffolk ewes were either actively or passively immunized against the synthetic fragment of porcine inhibin alpha, pI alpha(1-30), to determine the effects on gonadotrophin secretion and ovulation rate. Thirteen control ewes were immunized against human serum albumin, 12 ewes were actively immunized against pI alpha(1-30) and 36 ewes were passively immunized with pI alpha(1-30) antiserum. Blood samples were collected at 4-h intervals for 72 h from oestrus-synchronized ewes following the withdrawal of the progestagen pessaries. Mean gonadotrophin concentrations measured during the oestrous cycle of control ewes, ewes actively immunized against pI alpha(1-30) and ewes passively immunized against pI alpha(1-30) were similar, but their secretory profiles differed. Serum concentrations of follicle-stimulating hormone (FSH) were highest in ewes which had received antiserum at the time of pessary withdrawal; FSH concentrations did not decrease during the follicular phase of the oestrous cycle in ewes given antiserum 24 h after pessary withdrawal. Subtle but significant increments in serum FSH concentrations were observed in all passively immunized ewes in which sampling commenced at the time of treatment. The amplitude of the preovulatory luteinizing hormone (LH) peak, but not of the FSH peak, and the postovulatory secondary rise in FSH were lower (P less than 0.05) in actively immunized ewes than in control ewes. The mean (+/- s.e.) ovulation rate for actively immunized ewes (6.6 +/- 1.0) was 3 times higher (P less than 0.05) than that for control ewes (2.0 +/- 0.2), but was unaffected by passive immunization (range, 1.8-2.3).(ABSTRACT TRUNCATED AT 250 WORDS)
Rabbits were actively immunized using a barbiturate--BGG conjugate as the immunogen. The antiserum obtained from actively immunized rabbits was administered intravenously to mice to accomplish passive immunization. The antibody binding capacity for 3H-phenobarbital was shown to be sustained in passively immunized mice for periods of up to three weeks. Serum levels of 3H-phenobarbital in passively immunized mice and control mice were compared following drug administration and found to be altered in the antibody-containing mice. There was a 4-fold higher amount of 3H-phenobarbital present in the serum of passively immunized mice compared to control animals. The higher barbiturate levels were due to binding of 3H-phenobarbital to globulin fraction of serum in passively immunized mice. Additionally, decreased pentobarbital-induced ataxia was demonstrated in passively immunized mice. The decreased responsiveness was selective for barbiturates in passively immunized mice and did not modify the ataxia produced in these animals by another depressant agent, ethanol.
Neonatal lambs and adult wethers were passively immunized with ovine antibody directed against ovalbumin or Brucella abortus. Estimates for the biological half-lives of the antibodies ranged from 18 to 24 days in neonatal lambs and 12 to 17 days in adult wethers. The evidence suggested that both normal and immunosuppressed wethers which were passively immunized with serum antibody catabolized this antibody at a faster rate than did neonatal lambs. The data provided no support for the hypothesis that the growth factors and immunomodulatory factors, which are known to be present in colostrum, can influence the biological half-life of homologous antibody following passive immunization.
The influence of passive immunity on the immune response to swine fever virus (S.F.V.) was investigated in pigs injected with variable amounts of S.F.V. antibodies instead of piglets from immune sows. The passive immunity suppresses the primary serum antibody response normally observed after vaccination with the Thiverval strain of S.F.V. This inhibition is either partial or complete depending on the amount of injected antibodies. Whatsoever the passive immunity intensity, a priming occurred (even in absence of any detectable primary response). This priming was evidenced by the clinical signs and the type of immune response following a virulent challenge. Two vaccination routes were tested: intramuscular and intranasal: 48 pigs were checked and no significant differences established, concerning protective efficiency. Intranasal vaccination induced local antibody production in pharyngeal secretions. Even in the absence of any detectable immunoglobulin transudation from serum to these secretions, local antibody synthesis was completely inhibited in passively immunized animals.
Evidence of a role for human factor(s) in immunity to experimental syphilis has been provided by the demonstration that passive immunization of rabbits by daily i.v. injections of immune serum significantly delays the appearance and markedly diminishes the severity and duration of lesions which develop after challenge with Treponema pallidum. Five rabbits were injected daily over 37 days with 3 ml/kg body weight of pooled immune rabbit serum injection with 1.1 X 10(3) T. pallidum, Nichols strain, at each of four sites. The animals developed atypical lesions of short duration after an average delay in onset of 28 days short duration after an average delay in onset of 28 days beyond the development of typical lesions in control animals similarly injected with nonimmune serum or saline. The failure of passive immunization to provide complete protection was evident not only in the development of the atypical lesions, but also in the demonstration of disseminated infection in the tissues of three of the four surviving animals 7 months after challenge. The possibility that incomplete protection may have been due to 1) insufficient immune serum levels, 2) intracellular location of T. pallidum, and/or 3) cell-mediated mechanisms is discussed.
Rats were passively immunized by an intraperitoneal injection of homologous anti-BSA serum and their salivary glands were challenged 20 min or 24 hours later with BSA by the intraductal route. Immune complex sialoadenitis developed only when challenge was early. It is concluded that immunoglobulins are transferred from the circulation into the salivary glands and are relatively rapidly cleared by a mechanism yet unknown, possibly by salivary flow.
Passive immunity, naturally acquired from immune mothers or artificially induced by the administration of homologous hyperimmune serum, conferred on suckling mice a high degree of resistance against infection with Junín virus. Maternal antibodies in the circulating blood of the young were not detectable in the first days after birth, but rised rapidly from the 8th to the 20th day of lactation. By cross-foster nursing experiments it was shown that the greater part of the transmission of passive immunity occurred after birth, although there was transmission of a significant, though small part, before birth. The virus passage from mothers to offspring was excluded, since Junín virus was not recovered from brains, livers, spleens and kidneys of uninfected young, born from infected mothers.
The effect of various doses of specific serum administered in passive immunization on the formation of primary and secondary adaptive immunity in mice of the CBA strain was studied. Primary and secondary response was more sensitive to passive immunization on a model of adaptive immunity than in vivo. Most sensitive to the immunodepressive action of specific antibodies IgM and IgG were plaque-forming cells, and most resistant -- rosette-forming cells and cells. This led to a supposition that antibodies administered in passive immunization depressed the development of the immunological response acting at the level of T- and B cells.
Passive immunization of adult male hamsters for 12 weeks against peptide (As-PIP), a sperm coating antigen, resulted in selective elevation of the blood levels of FSH, impairment of spermatogenesis, and complete infertility when males were mated with normal cycling females. Passive immunization of male marmosets with As-PIP for 8 weeks was also effective and was reversible, without causing any obvious change in mating behaviour. These preliminary studies in hamsters and marmosets indicate that antibodies to a prostatic 'inhibin' peptide represent a promising new approach to male contraception.
The active and passive immunization of laboratory animals against Ixodes antigens has been experimentally shown to lead to the development of their resistance to homologous Arthropoda species and a change in the intensity of the circulation of tick-borne encephalitis virus between carriers and their hosts. The immunization of vertebrates with Ixodes antigens may supposedly lead to a decrease in the number of bloodsucking arthropods-carriers of the causative agents of infectious diseases-and protect animals from infections whose causative agents are transmitted by Ixodes ticks.
Mice were treated with serum containing antibodies to herpes simplex virus type 1 (HSV-1) or normal serum, 1 day before inoculation on the cornea with HSV-1 strain McKrae. As expected, without passive immunization, mice developed high levels of serum neutralizing antibody. By contrast, in passively immunized animals, such antibody became undetectable by 29 days after inoculation of serum, in spite of the virus infection. There was no difference between passively immunized mice and those given normal serum in the duration of shedding of virus in tears and the duration and severity of corneal epithelial disease. However, non-immunized mice had a high incidence of mortality and developed disease of the iris, corneal stroma and lids, and their corneas became opaque and vascularized. In non-immunized animals, the timing of isolation of virus from nervous tissues and the sequence of appearance of virus antigens in ocular tissues indicate that the disease of deeper eye tissue was caused by virus spreading from the nervous system back to the eye. Restriction of such spread in passively immunized animals seems the likely explanation for their protection from death and severe ocular damage. Despite this restricted spread, passively immunized animals had a high incidence of latent infection in the ophthalmic part of the trigeminal ganglion. However, in comparison with mice given normal serum, there was a far lower incidence of such infection in the other two parts of this ganglion and in the superior cervical ganglion. Since passively immunized animals have a high incidence of latent infection in the ophthalmic part of the trigeminal ganglion and their eyes are normal, they will prove useful in studies involving induction of recurrent disease.
Specific passive immunity against Pseudomonas aeruginosa sepsis was assessed in granulocytopenic dogs. Dogs were infused with either normal or antipseudomonas immune plasma 24 h before pseudomonas challenge. They were challenged intravenously with 10(7) serotype 6 P. aeruginosa during granulocytopenia. Treatment was evaluated by observation of survival periods, febrile responses, type 6 pseudomonas antibody titers, and quantitative cultures of blood and tissues. The results demonstrated that passively immunized dogs did not survive infection. Both normal-plasma and immune-plasma recipients had bacteremia at death, with median values of 980 and 470 pseudomonas per ml of blood, respectively. All dogs had marked febrile responses 24 h after pseudomonas challenge and had high concentrations of pseudomonas in their lung tissue at death, with median values of 10(8) pseudomonas per g of wet tissue weight. After plasma infusion, immune-plasma recipients had high concentrations of anti-pseudomonas antibody, with total antibody titers ranging from 256 to 1,024 and a median value of 1,024. These titers were comparable to titers attained in a previous study from our laboratory using active immunization with pseudomonas lipopolysaccharide vaccine, where the median total anti-pseudomonas antibody titer was 2,048. Actively immunized animals, however, were significantly protected against pseudomonas sepsis and had prolonged survival periods and prevention of bacteremia. The present study demonstrates that circulating type-specific antibody is not solely responsible for the protection afforded to granulocytopenic dogs actively immunized against pseudomonas.
The effect of passive immunization with immunoglobulin Y (IgY) antibody against Marek's disease virus (MDV) was examined in MDV-susceptible chickens. The production of IgY, immunoglobulin M, and probably also immunoglobulin A was depressed in passively immunized chickens when compared with that in MDV-exposed chickens which had not been given IgY anti-MDV antibody. In passively immunized chickens, the synthesis of immunoglobulin M and IgY anti-MDV antibodies in response to MDV infection also was delayed as determined by agar gel precipitin and indirect fluorescence antibody tests.
Antibodies to neuropeptides or hormones are frequently used in passive immunization studies to unravel their physiological role in signal transfer. In such in vivo experiments antibodies are considered to bind and thereby to biologically inactivate the endogenous substance during its journey from its site of secretion to its site of action (signalling time). However, little is known about the mechanism of action and characteristics of antibodies that determine such biological activity. Since the signalling time in neuronal and hormonal communication is short, the kinetics of antibody binding is an important feature. Here, we present a theoretical framework to describe antibody binding kinetics which can contribute to the design of passive immunization protocols. The specific effects of variation in antibody concentration, dissociation constant, and on-rate constant on these binding kinetics are demonstrated. Simple methods are described to determine these parameters, which may guide the selection of antibodies for passive immunization studies. When time is limited, the on-rate constant and the local antibody concentration are the most important determinants. Several points are illustrated for CRF signal transfer in the rat. CRF signalling time in the hypothalamo-pituitary complex, as established from dye transport experiments, was 3-7 sec. Based on parameters measured for a rat monoclonal antibody to CRF (PFU 83), we computed that half-maximal and full blockades of ether-induced ACTH secretion were associated with approximately 85% and more than 99% binding of CRF, respectively. From the theoretical framework presented in this study we conclude that, in general, the kinetics of antigen binding are sufficiently fast for antibodies to interfere with hormonal and probably nonsynaptic neuronal signal transfer. However, interference with fast signalling processes (less than 10 msec), which may occur in the brain, is unlikely.
Adult male rats were passively immunized against GnRH and given iv infusions of saline or 60 or 300 ng NIDDK ovine LH-24/100 g BW.24 h in continuous regimens of 2.5 or 12.5 ng/100 g BW.h and pulsatile regimens of 1-min pulses of 5 or 25 ng/100 g BW every 2 h. Control animals were treated with nonimmune serum and saline. After 10 days of in vivo treatment, Leydig cells were purified and incubated in vitro with 1) increasing concentrations of hCG (0-50 mIU/ml) in the presence or absence of methylisobutylxanthine, 2) a maximally stimulatory concentration of 8-bromo-cAMP (8-Br-cAMP; 1 mM), and 3) a saturating concentration of 25-hydroxycholesterol (10 microM). LH receptor concentrations were quantified by [125I]hCG binding assay. Maximum testosterone production in the presence of hCG, 8-Br-cAMP, or 25-hydroxycholesterol was reduced by more than 90% in Leydig cells from anti-GnRH serum-treated rats (compared to that in cells from control rats), and this reduction in steroidogenic capacity was prevented in a dose-dependent manner by concurrent infusion of LH in either the continuous or pulsatile regimens. These results confirm that the trophic actions of LH on Leydig cells in vivo 1) do not depend on pulsatile secretion of the hormone, and 2) include induction/maintenance of one or more of the enzymes catalyzing the conversion of cholesterol to testosterone. Trophic actions on constituents or processes before cholesterol side-chain cleavage were not apparent; in vivo treatments had no obvious differential effects on hCG-stimulated, 8-Br-cAMP-stimulated, or 25-hydroxycholesterol-supported testosterone production. Sensitivity to hCG was increased (EC50 for stimulation of testosterone production was decreased) by passive immunization against GnRH, and this effect was prevented in a dose-dependent manner by concurrent infusion of LH in either the continuous or pulsatile regimens. Thus, intermittent exposure to low concentrations of LH in vivo desensitizes Leydig cells as effectively as continuous exposure. Neither specific binding of [125I]hCG nor the effect of methylisobutylxanthine on sensitivity to hCG in vitro differed among treatment groups. Therefore, both the trophic and desensitizing actions of LH appear to occur by mechanisms that are independent of changes in available LH receptor concentration and phosphodiesterase activity.