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At least 307 records · Page 17Linked to original sources
PubMed1998

Spaceflight and development of immune responses.

The NIH.R1 Space Shuttle experiment was designed to study the effects of spaceflight on rodent development. Pregnant rats were flown on the Space Shuttle for 11 days, and pregnant control rats were maintained in animal enclosure modules in a ground-based chamber under conditions approximating those in flight. Additional controls were in standard housing. The effects of the flight on immunological parameters of dams, fetuses, and pups were determined. Blastogenesis of spleen cells in response to mitogen was inhibited in flown dams but was not inhibited in cells from their pups. Interferon-gamma production by spleen cells showed a trend toward inhibition in flown dams but not in their pups. The response of bone marrow cells to colony-stimulating factor showed a trend toward inhibition after spaceflight in dams, but the response of fetus and pup liver cells was not inhibited. Total serum IgG was not affected by spaceflight. None of the examined immune parameters that were altered in rat dams after spaceflight was found to be altered in their offspring.

Animals↗
PubMed2005

Peak shift and epidemiology in a seasonal host-nematode system.

Insight into the dynamics of parasite-host relationships of higher vertebrates requires an understanding of two important features: the nature of transmission and the development of acquired immunity in the host. A dominant hypothesis proposes that acquired immunity develops with the cumulative exposure to infection, and consequently predicts a negative relationship between peak intensity of infection and host age at this peak. Although previous studies have found evidence to support this hypothesis through between-population comparisons, these results are confounded by spatial effects. In this study, we examined the dynamics of infection of the nematode Trichostrongylus retortaeformis within a natural population of rabbits sampled monthly for 26 years. The rabbit age structure was reconstructed using body mass as a proxy for age, and the host age-parasite intensity relationship was examined for each rabbit cohort born from February to August. The age-intensity curves exhibited a typical concave shape, and a significant negative relationship was found between peak intensity of infection and host age at this peak. Adult females showed a distinct periparturient rise in T. retortaeformis infection, with higher intensities in breeding adult females than adult males and non-breeding females. These findings are consistent with the hypothesis of an acquired immune response of the host to a parasite infection, supporting the principle that acquired immunity can be modelled using the cumulative exposure to infection. These findings also show that seasonality can be an important driver of host-parasite interactions.

Age Factors↗
PubMedDate not supplied

Unstable malaria in Sudan: the influence of the dry season. Clone multiplicity of Plasmodium falciparum infections in individuals exposed to variable levels of disease transmission.

Studies of infection and immunity to malaria often take little account of the fact that the amount of infectious challenge individuals receive is very variable. Classic studies in areas of holoendemic transmission showed that clinical immunity develops quite rapidly during childhood, although the processes through which increasing levels of resistance to infection are acquired are still not understood. However, holoendemic transmission is one end of the spectrum of malaria epidemiology and the development of clinical immunity is also affected by factors such as the infection rate and the local parasite species composition. An exceptionally simple type of malaria transmission occurs during the short, autumnal malaria outbreaks of the Sudanese sahel-savannah belt, where a sparse 200-500 mm of rain falls in 2-3 summer months, Plasmodium falciparum causes > 95% of malaria cases in most areas, and the entomological inoculation rate (EIR) is very low by African standards; thus the population dynamics of malaria parasites are less affected by super-infection. A comparison of certain features of parasite genetic diversity, particularly the average number of parasite clones present in infections in the Sudanese sahel and in malaria study sites with different levels of transmission, is presented. It is proposed that increasing EIRs are associated with progressively smaller increases in the average number of malaria parasite clones per host and the implications of this relationship for studies on malaria infection and immunity are discussed.

Animals↗
PubMed2000

Progesterone inhibits glucocorticoid-induced murine thymocyte apoptosis.

Sex and sex hormones modulate immune development and responses. A primary target of their effects is the structure and cellularity of the thymus; therefore, we examined the effects of sex and sex steroids on thymocyte apoptosis. We demonstrate initially that male DBA mice have a significantly higher percentage of glucocorticoid-induced apoptotic thymocytes (46.1+/-3.8%) than their female counterparts (31.6+/-3.1%; P=0.012). We postulated that this gender difference was due to differential modulation of glucocorticoid-induced apoptosis by sex hormones such as estrogen, testosterone or progesterone. Both estrogen and testosterone increased in vitro thymocyte apoptosis. In contrast, progesterone not only inhibited spontaneous in vitro thymocyte apoptosis, but also prevented in vitro glucocorticoid-induced apoptosis. Progesterone administration also suppressed glucocorticoid-induced in vivo thymocyte apoptosis. These results suggest that anti-apoptotic effects of progesterone may influence T cell development and subsequent immune responses.

Animals↗
PubMed2001

Immune diversity and genomic stability: opposite goals but similar paths.

DNA damage response mechanisms serve to protect cells from exogenous and endogenous DNA damaging agents with the aim of maintaining genomic stability. In contrast, the generation of an efficient immune response requires the creation of a repertoire of distinct immunoglobulin and T cell receptor genes able to recognise the huge array of antigens that may be encountered in a lifetime. Surprisingly, cells have exploited the same mechanisms used to maintain genomic integrity to create genetic diversity during immune development. Here, we review the damage response mechanisms operating on DNA double strand breaks and their function during development of the immune response. We discuss disorders that are associated with immunodeficiency and defective responses to the presence of DNA double strand breaks.

Animals↗
PubMed2002

Genetic and management factors that influence the susceptibility of cattle to Mycobacterium bovis infection.

Genetic variation in the susceptibility of cattle to Mycobacterium bovis infection exists in differences between families and species, but not breeds. Susceptibility to M. bovis infection increases with age of cattle. Natural exposure to M. bovis or environmental mycobacteria may assist in the development of specific immunity, but there is no direct evidence for such immunological priming of tuberculosis resistance in cattle. This has, however, been demonstrated in humans and other animals. Since non-specific mechanisms have a role in protective immunity, developing an effective vaccine will be difficult, even though some protection of other species has been achieved. Immunological suppression in the periparturient period can produce anergic reactors, which may act as a constant source of infection for cattle-to-cattle transmission. Circumstantial evidence suggests that an adequate intake of mineral, vitamin and protein reduces the susceptibility of cattle. Although weather patterns have been implicated in the susceptibility of herds to M. bovis infection, there is insufficient information to determine the risk factors precisely. It is concluded that some reduction in the susceptibility of cattle to M. bovis infection can be achieved by modifications to the management system to minimize risk factors, but that a considerable amount of further research is required.

Age Factors↗
PubMedDate not supplied

Second generation effects of maternal ethanol consumption on immunity to Trichinella spiralis in female rats.

The deleterious effects of maternal ethanol consumption on neonatal immune development and early immune responses has been well documented. However, the effects of such neonatal exposure to maternally consumed ethanol on the neonates' immune responses in their adult life, especially in combination with additional ethanol exposure, has received little attention. For these experiments, female rats were fed on either 6% ethanol or pair-fed isocaloric control Lieber-DeCarli liquid diets for 30 days prior to, and during, pregnancy and lactation. One day after weaning their pups, the mothers were infected with 1000 Trichinella spiralis larvae, and maintained on diets for an additional 20 days. At this time, they were challenged with 2000 T. spiralis larvae, killed 3 days later, and their immune status determined. These animals served as the first generation alcohol animals. Their female offspring served as the experimental second generation animals. These animals received maternal ethanol during pregnancy and lactation and control diet during their juvenile period (from weaning to 90 days of age). They were then subjected to a schedule of ethanol or pairfeeding, identical to the first generation dams. Two groups of second generation animals were established: Group 1 was exposed to ethanol during their dam's pregnancy and lactation periods only, with no subsequent ethanol treatment; Group 2 received ethanol during their dam's pregnancy and lactation periods and then again throughout their adult experimental period. Our previous studies showed only minimal changes following a secondary challenge in T. spiralis-immunized rats; however, neonates born to alcohol-consuming mothers did show some depressed secondary immune responses when challenged soon after weaning. We chose to use a secondary immune challenge to assess further immune alterations in second generation adult animals. No differences between any of the ethanol and pair-fed groups were observed in intestinal worm burdens, which is similar to data previously reported for adult alcohol-consuming animals. However, second generation group 2 animals demonstrated significantly reduced proliferation responses to T. spiralis antigen and Concanavalin A (Con A) stimulation relative to the ethanol first generation and to the second generation Group 1 animals. This group also demonstrated significantly lower absorbencies in the ELISA assay for specific IgM and IgG anti-T. spiralis antibodies than the pair-fed, ethanol first and second generation Group 1 animals. The proportion of total T cells and cytotoxic T cells was significantly lower and the proportion of natural killer cells was elevated in both second generation ethanol Groups 1 and 2 relative to the ethanol first generation and pair-fed groups. In addition, Group 2 second generation animals showed significantly lower proportions of total leukocytes and T cells than Group 1 second generation animals. Although secondary immune responses to T. spiralis infection were not altered in rats exposed to ethanol only as adults, exposure to maternal ethanol does affect some specific immune responses in second generation adult life and maternal exposure may exert cumulative immune effects in concert with later consumption of ethanol by offspring born to alcoholic mothers.

Age Factors↗
PubMed1979

Immunological and serological diversity of Neisseria gonorrhoeae: identification of new immunotypes and highly protective strains.

Gonococci, irrespective of serotype or immunotype, varied significantly in their capacity to induce immunity in animal models, and in vitro serological relatedness did not always insure in vivo cross-protection. By using a serum bactericidal assay followed by in vivo cross-protection studies, new immunotypic strains which were highly protective were identified from cultures isolated in different geographical areas and from patients with various clinical manifestations. Beta-lactamase production and gonococcal immunotype did not appear as related characteristics in that certain penicillin-sensitive strains were highly effective in immunizing animals against infection with beta-lactamase producers. The findings of this study emphasize the importance of using appropriate biological tests and strains for the investigation of gonococcal immunity and vaccine development. Immunization with a combination of a few major gonococcal immunotypic immunogens may provide substantial protection against the majority of penicillin-sensitive and beta-lactamase-producing gonococci. Investigation of isolated immunotypic immunogens is in progress.

Animals↗
PubMed1980

Experimental infection of the respiratory tract with Mycoplasma pneumoniae.

M. pneumoniae, a common human respiratory pathogen, has been studied experimentally for years using intranasal inoculation of the golden Syrian hamster. Because of recent evidence outlining the role in pulmonary immune development of particle size and depth of mycoplasma deposition in the hamster lung, we developed an aerosol chamber for the reproducible aerosolization of radiolabeled M. pneumoniae. Organisms were labeled to high specific activity by the incorporation of 3H-oleic acid and aerosolized under airflow and humidity conditions creating a mean particle diameter of 2.0 micrometers. Under these conditions, viable mycoplasmas were reproducibly and evenly distributed to all major lobes of the lung. Examination of radioactive clearance and organism viability within the lung during the first 48 hr after aerosolization have suggested a minimal role for macrophage mycoplasmacidal activity and a more prominent role for ciliary clearance. Data from aerosol infections of hamsters with radio-labeled M. pneumoniae should provide a unique opportunity to examine in a highly controlled manner the effects of air pollutants on the initial stages of infection as well as effects on the development of pulmonary immunity and histologic alterations.

Aerosols↗
PubMed1991

Don't kill the parasite: control the disease.

It is clear from both laboratory and clinical studies that the blood-stage malaria parasite does not itself directly cause most of the serious complications of the disease, with the possible exception of anaemia. For example, T cell- deprived mice with lethal infections survive longer and mice can be protected against early death by vaccines that appear not to affect parasitaemia. In certain cases antibodies to TNF have the same effect. Clinically it has been known for over 50 years that children in endemic areas develop immunity to the serious toxic aspects of malaria several years before their parasitaemias start to fall. Recent work on the induction of cytokines such as tumour necrosis factor (TNF) by exoantigens of the blood-stage parasite and on the role of cytokines in this and other toxic diseases suggests that an appropriate vaccine might induce antibody that blocks the effect of the exoantigens, thus conferring on young children the anti-disease immunity that normally takes years to appear. Such vaccines might be less hampered by the antigenic variation that makes anti-parasite immunity slow to develop. Characterisation of the molecules involved is a high priority.

Animals↗
PubMed1990

In vivo administration of anti-asialo-GM1 antibody enhances splenic clearance of Listeria monocytogenes.

Resistance of mice to infection by Listeria monocytogenes involves a biphasic response. The first phase consists of the first 48 h after infection, during which there is multiplication of Listeria in the liver and spleen of infected mice. In these nonimmune mice, macrophages and polymorphonuclear leukocytes are the effector cells involved in controlling multiplication. In the second phase, cell-mediated immunity develops, beginning on day 2, during which multiplication of Listeria is prevented by macrophages possessing increased microbicidal activity that is mediated through the action of lymphokines released by immunologically committed T lymphocytes. The purpose of the present study was to define a role for natural killer (NK) cells in natural resistance to Listeria during the first 48 h after infection, prior to the development of specific immunity. Splenic NK cell activity was enhanced following a sublethal intravenous injection of viable Listeria as early as 24 h after injection and remained elevated throughout the nonimmune phase of infection. Interestingly, treatment of mice with anti-asialo-GM1 significantly enhanced the ability of mice to clear Listeria from the spleen relative to infected controls possessing intact NK cell populations. This was evidenced by 23-fold fewer bacteria obtained from the spleens of anti-asialo-GM1-treated mice. In addition, Percoll-enriched NK cell populations obtained from 48-hour Listeria-infected mice do not exhibit in vitro listericidal activity. These observations suggest a regulatory role of NK cells in resistance against Listeria and preclude a role for NK cells in direct cytolysis. Perhaps these cells modulate the immune response to Listeria by down-regulating the activity of the immune cells crucial to listerial resistance.

Animals↗
PubMed1986

[Immunogenicity of a chemical typhus vaccine and of a corpuscular radioantigen obtained from Rickettsia prowazekii].

The protective activity of chemical typhus vaccine and R. prowazekii corpuscular radioantigen (CRA) was studied. Guinea pigs were immunized with doses of 32 and 48 antigenic units. Antibody production was assayed in the complement fixation test. On days 7, 15, 21, 30 and 60 after immunization the animals were challenged with R. prowazekii introduced in an amount of 10(5) minimum embryonal infective doses (MEID). On day 30 some of the animals were challenged with 10(3) MEID of R. typhi. The results demonstrated that both preparations were highly immunogenic and capable of protecting most of the animals from 10(5) MEID of R. prowazekii. Immunity developed earlier after immunization with CRA. The guinea pigs immunized with CRA, purified in percoll density gradient, and challenged with 10(3) MEID of R. typhi on day 30 showed a high level of cross immunity. In all control animals high fever and periorchitis were observed.

Animals↗
PubMed1995

Vaccination routes that fail to elicit protective immunity against Schistosoma mansoni induce the production of TGF-beta, which down-regulates macrophage antiparasitic activity.

C57BL/6 mice immunized intradermally (i.d.) with bacillus Calmette Guerin (BCG) plus killed skin-stage schistosomula are protected against subsequent infection with Schistosoma mansoni, whereas immunization by i.v. or i.m. routes is not protective. Moreover, previous immunization via the nonprotective i.v. route interfered with the ability to subsequently induce protection by i.d. vaccination, suggesting that inhibitory responses are invoked. Given the evidence that activated macrophages (M phi) play a role as effector cells in protection against schistosomiasis, we investigated the ability of spleen cells from protected and nonprotected immunized mice to produce M phi activating and deactivating cytokines. Exposure to supernatant fluids (SNs) from Ag stimulated spleen cells of i.d., but not i.v. or i.m., immunized mice activated inflammatory M phi for in vitro killing of schistosome larvae, through a mechanism dependent on both IFN gamma and TNF-alpha. No evidence was observed for the preferential induction of the M phi activating Th1 cytokines IFN-gamma and IL-2 in i.d. immunized mice, nor did spleen cells from nonprotected animals produce higher levels of the Th2 associated cytokines IL-4 and IL-10, which are known to prevent M phi activation. TGF-beta was, however, detected in SNs from unprotected mice. Moreover, the M phi inhibitory activity detected in these SNs was heat stable and neutralized by anti-TGF-beta Abs, suggesting that production of TGF-beta is at least partially responsible for the failure of i.m. and i.v. immunized mice to develop immunity to S. mansoni. Thus, the induction of down-regulatory cytokines may be an important factor limiting the efficacy of certain vaccination protocols.

Animals↗
PubMed1977

Glomerular lesions in argyric NZB/NZW mice.

Glomerular basement membranes showed strong silver labelling on electron microscopy in NZB/NZW mice fed 12 mmol AgNO3 for 6 weeks at ages from 1-7 months. Although some silver granules were seen within mesangial immune deposits following their concurrent deposition, silver was usually deposited in electron-lucent areas around pre-existing deposits, or formed a boundary to an expanded mesangium when immune deposits subsequently developed. Immune deposits in capillary loops occurred on the outer or inner aspect of the zone of silver labelling.

Animals↗
PubMed1997

T cell immunity in malaria.

Immunity to malaria is a complex process. In malaria endemic areas, sustained clinical immunity develops gradually. Protective immunity to malaria comprises both antibody-dependent and antibody-independent effector mechanisms. Although, the relative roles of B and T cells differ in different malaria systems and different stages of the parasite, T cells are essential for the induction and maintenance of immunity against malaria. T cell-derived soluble factors are believed to be important mediators of cellular effector mechanisms. The efficacy of an antigen as a malaria vaccine depends to a great extent on the T cell recognition sites and the nature of the responses induced by these determinants. In order to select suitable epitopes in an immunogen, an understanding of the definition of antigenic sites recognized by T cells and characterization of the nature of the T cell responses induced in malaria endemic populations is important.

Animals↗
PubMedDate not supplied

[The character of development of the immune response to sheep erythrocytes and parallel responses to exo- and endobiotics].

The immune response to sheep erythrocytes (SE) is usually used as the indicator system in screening of immunotropic compounds. We had shown earlier that a rapid immune reaction develops in response to a chemical compound (drug). It is characterized by an increase in the number of antigen-recognizing and antigen-producing lymphocytes and their blast forms, titers of antibodies specific of the introduced compound and endobiotics mobilized under its effect.

Animals↗