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Passive immunization of macaques against SIV infection.

Passive immunization with plasma from an inactivated-whole SIVmac vaccine protected monkey conferred complete or partial protection to rhesus macaques challenged intravenously 4 or 18 hours later with 10 AID50 of homologous cell-free virus. In contrast, passive immunization with inactivated plasma or purified immunoglobulin (Ig) from SIVmac infected asymptomatic monkeys failed to protect any recipients similarly challenged and may have enhanced infection and accelerated disease. Administered 24 hours post challenge, anti-SIV Ig may also have enhanced the infection.

Acquired Immunodeficiency Syndrome↗

Passive immunity against rotavirus in infants.

Passive immunity against a variety of gastrointestinal infections, using orally administered human antibodies, has been tried in a number of clinical trials. Recently, antibodies from other species such as cows and chickens, which have shown efficacy in experimental animal systems, have also been tried in humans. This review summarizes published data on the use of immunoglobulin-containing preparations for prophylaxis and therapy against rotavirus infections in infants and children, and directions for their future use are suggested.

Administration, Oral↗

Cytotrophoblast cells: a barrier to maternofetal transmission of passive immunity.

The human fetus receives passive immunity via the chorioallantoic placenta in the form of maternal immunoglobulin G (IgG) class antibodies. This provides protection against pathogens at a time when the fetus is immunologically naive. We localized endogenous human IgG using confocal laser scanning fluorescence microscopy and immunoelectron microscopy of frozen sections of chorionic villi from early and late gestation. With confocal microscopy we also investigated the distribution of a receptor for IgG (Fc gamma RIII; CD16) that is typically expressed on the surface of human leukocytes. Endogenous IgG was present in the syncytiotrophoblast that surrounds chorionic villi but underlying cytotrophoblast cells were devoid of endogenous antibody. Fc gamma RIII immunoreactivity was confined to the syncytiotrophoblast and was also absent from cytotrophoblast cells. We propose that cytotrophoblast cells present a barrier to the transmission of maternally derived IgG across the human placenta. This accounts for the paradox that there are low levels of transport in the first trimester when the syncytiotrophoblast is known to express receptors for IgG. Cytotrophoblast cells form an almost complete epithelial layer underlying the syncytiotrophoblast at this stage of gestation, but this becomes discontinuous as the placenta matures, thus removing the cellular impediment to IgG transmission.

Cesarean Section↗

Swine fever: influence of passive immunity on pig immune response following vaccination with a live virus vaccine (Thiverval strain).

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.

Administration, Intranasal↗

Kidding rates of angora goats passively immunized against estrogens.

The objective of this study was to determine the effect of passive immunization against estrone (E1), estradiol (E2) or estrogens (nonspecific; Ens) on ovulation rate and kidding rate in Angora does. On d 0 of the study, Angora does were divided into four treatment groups: 1) passively immunized against E1 (n = 14); 2) passively immunized against E2 (n = 24); 3) passively immunized against Ens (n = 9); and 4) injected with normal goat serum (control; n = 23). Fertile bucks were allowed to mate with the does from d 2 to 44. Immunization treatments did not influence (P greater than .1) percentage of does exhibiting estrus, percentage of does kidding or kid death rate. Ovulation rate was greater (P less than .06) in E2 and Ens immunized does than in control does. Both E2 and Ens treatments resulted in a greater (P less than .05) percentage of does giving birth to twins rather than singles compared with E1 or control treatments (70, 83, 27 and 31% twin births for E2, Ens, E1 and control, respectively). This increase in twin births resulted in kid crops per doe exposed of 142 and 122% for E2 and Ens compared with 100 and 91% for E1 and control treatments (P less than .05 for E2 vs control). These results demonstrate that the incidence of twin births can be increased by passively immunizing does against E2.

Animals↗

Effect of immunization on reproducvive performance, embryo quality and progesterone in Rasa Aragonesa ewes actively immunized against androstenedione or passively immunized against testosterone.

A total of 217 Rasa Aragonesa ewes were used to test two immunization treatments: 1.Active immunization against androstenedione: ewes immunized in previous matings (androstenedione, reimmunized; AR groups, n=58) or not (first immunization; AF groups n=64) were boosted either 2 or 4 wk before mating. 2.Passive immunization against testosterone: antisera were injected either at sponge withdrawal (zero time; T0 group, n=21) or 1 wk previously (Tl group, n=22). We used 52 ewes as controls (C group). Half of each group was used either to record reproductive performance or to embryo viability assessment. Prolificacy was significantly increased in ewes which reached a moderate antibody level, independently of the treatment. Fertility was lower in AR ewes that attained a high antibody titre (P<0.01). The percentage of viable embryos recovered was lower in AF ewes (P<0.01), and in ewes whose testosterone antibody titre was high (P<0.05), compared to C group. It was proven that similar or lower antibody levels were more harmful for ewes from AF and Tl than for ewes from AR or T0 groups. The proportion of nonfertilized recovered ova was not significant. Progesterone levels were notably increased in AR ewes (P<0.001) independently of ovulation rate and were positively correlated to antibody titre at mating (P<0.01) but these events were not observed in T ewes. These findings indicate that after androgen immunoneutralization, only those ewes having antibody titres within a limited range at mating had improved reproductive performance. Further research is needed in order to understand the role that progesterone plays in immunized ewes.

Journal Article↗

[Immune complex formation during the passive immunization of mice infected with the tick-borne encephalitis virus].

The results of investigations, indicating that the development of the infectious process in experimental encephalitis is accompanied by the formation of immune complexes circulating in the blood and localized in the brain tissue, are presented. The intravenous injections of a homologous serum preparation into intact animals induces the appearance of a rather low level of circulating immune complexes, which precedes the elimination of antibodies. The intravenous injection of a specific serum preparation two days after the infection of the animals with tick-borne encephalitis virus is accompanied by the formation of immune complexes; the course of infection is not aggravated.

Animals↗

Specificity of monoclonal antibodies in local passive immunization against Streptococcus mutans.

Local oral passive immunization in human subjects with a monoclonal antibody (MoAb) raised against the 185-kD antigen I/II from S. mutans significantly reduced or prevented oral colonization of an exogenous strain of the organism. In subjects sham-immunized with either saline or an unrelated MoAb, however, significantly greater proportions of S. mutans persisted for a longer duration than in those immunized with the specific anti-streptococcal MoAb. Recolonization of indigenous S. mutans after this organism was reduced to undetectable levels by an antimicrobial agent has also been completely prevented with specific MoAb. Indeed, S. mutans was not detected for a period of over 1 year, as compared with recolonization within 10-82 days in the control subjects. The specificity of MoAb in preventing colonization of the streptococci was studied with four MoAb. This revealed that: (1) the sub-class of antibody is not an essential factor, as both MoAb Guy's 1 and 13 prevented colonization, although Guy's 1 is an IgG2a and Guy's 13 is an IgG1 class of antibody; (2) serotype specificity is important, as MoAb Guy's 9, which only recognizes S. sobrinus (serotypes d and g), does not prevent colonisation by S. mutans (serotype c); (3) neither protein nor carbohydrate nature of the putative adhesin was a determining factor, because MoAb Guy's 1 recognizes a carbohydrate and Guy's 13 a protein determinant and both MoAb prevented adherence of S. mutans; and (4) epitope specificity appears to be the most important factor in preventing adherence of S. mutans, as MoAb Guy's 11 and 13 share the same serotype specificity and both recognize a protein determinant, yet only Guy's 13 prevents colonisation. The long duration of protection from re-colonization by indigenous S. mutans, lasting about 1 year after application of the specific MoAb was stopped, cannot be accounted for by functional MoAb remaining on the teeth. We suggest that initially the MoAb prevents colonization by S. mutans and that the ecological niche vacated by this streptococcus is filled by other organisms from the oral flora, thereby discouraging re-colonization by S. mutans.

Adult↗

Humoral immunity in experimental syphilis. I. The demonstration of resistance conferred by passive immunization.

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.

Animals↗

Experimental allergic sialoadenitis. VII. Reactivity of the parotid gland to antigenic challenge in passively immunized rats.

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.

Animals↗

Progesterone production and clearance in cyclic ewes passively immunized against progesterone.

The effects of passive immunization of ewes against progesterone on plasma progesterone concentrations and on the metabolic clearance rate (MCR) and production rate (PR) of progesterone were investigated. Three treatment groups were studied: 1) nonimmunized controls, 2) ewes passively immunized with antiprogesterone serum, and 3) immunized progestagen-treated ewes, treated concomitantly with anti-serum and with a synthetic progestagen that is not bound by the antiserum. Progesterone levels in the immunized ewes reached a maximum of 27.7+/-4.8 nmol/l and were significantly higher (P<0.05) than in the nonimmunized controls (9.2+/-1.1 mol/l) or the immunized progestagen-treated ewes (15.6+/-1.6 nmol/l). Mean progesterone MCR in the immunized ewes was 1.6+/-0.5 and 2.1+/-0.3 liter/min on Days 7 and 13 of the estrous cycle, respectively, compared with 0.8+/-0.2 and 1.4+/-0.3 liter/min, respectively, in nonimmunized controls. The progesterone production rate in the immunized ewes was significantly higher than in nonimmunized controls, and reached 12.0+/-2.2 and 19.7+/-1.6 nmol/min on Days 7 and 13 of the estrous cycle, respectively, compared with 4.6+/-0.6 and 10.0+/-2.5 nmol/min in nonimmunized controls (P<0.03 for both comparisons). Treatment with progestagen had no significant effect on progesterone MCR or PR of immunized ewes. The LH pulse frequency on Days 10 to 11 of the cycle was 0.7+/-0.3, 1.8+/-0.3 and 0.0+/-0.0 pulses/6 h in the control, immunized and immunized progestagen-treated groups, respectively (P<0.05). It is concluded that the increased plasma progesterone levels in the immunized ewes are the result of an increased progesterone production rate, which may have been induced by an increase in gonadotrophin secretion or by a direct effect of the anti-progesterone serum on the ovary.

Journal Article↗

Passive immunity against Junín virus in mice.

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.

Animals↗

[Study of the immunodepressive effect of passive immunization on a model of adaptive immunity].

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.

Animals↗

A passive immunization technique against the teleost hypocalcemic hormone stanniocalcin provides evidence for the cholinergic control of stanniocalcin release and the conserved nature of the molecule.

An in vivo bioassay based on 45Ca uptake from the ambient medium was used to test the efficacy of serum from rabbits immunized against trout stanniocalcin to passively immunize trout, tilapia, American eel, and guppy against endogenous stanniocalcin. The passive immunization was effective in all species. The fact that this procedure worked under both homologous and heterologous conditions, and in fish from different taxonomic infradivisions, is consistent with the view that the stanniocalcins in the four species examined share common antigenic determinants. The trout stanniocalcin antiserum had no effect on whole body calcium uptake (inCa2+) in stanniectomized eels, indicating that the effect of the antiserum was dependent on the presence of functional Stannius corpuscles. The technique was then used to show that the inhibitory effects that calcium loading and the injection of the cholinoreceptor agonist carbachol have on inCa2+ probably involve a catecholamine-induced release of endogenous stanniocalcin from the Stannius corpuscles.

Anguilla↗

Passive immunization against prostatic 'inhibin' peptide as a male contraceptive.

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.

Animals↗