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Results for “host manipulation”

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PubMed1990

Recent advances in rumen microbial ecology and metabolism: potential impact on nutrient output.

Feedstuffs consumed by ruminants are all initially exposed to fermentative activity in the rumen prior to gastric and intestinal digestion. The extent and type of transformation of feedstuffs thus determines the productive performance of the host. Research on rumen microbial ecology and metabolism is essentially a study of the interactions between the host, microorganisms present, substrates available, and end products of digestion. Furthermore, the interactions of the normal microbial flora with the host can be manipulated to improve the efficiency of nutrient utilization in ruminant animals. Three important areas of ruminal fermentation will be reviewed, N metabolism, fiber degradation, and biotransformation of toxic compounds. The extent of protein degradation and the rate of uptake of resultant peptides and ammonia are extremely important factors in determining the efficiency of N utilization by rumen bacteria and, therefore, the relative amounts of microbial or bypass protein available to the host. Strategies aimed at identifying and characterizing rate-limiting enzymes of cellulolytic bacteria are essential in elucidating mechanisms involved in ruminal fiber degradation. Results obtained with ruminococci will be described. The detoxification of phytotoxins by passage through the gastrointestinal tract of ruminants is a process deserving special attention and several examples will be presented. Opportunities for manipulation of rumen fermentation are good. However, successful manipulation and full exploitation depend on a through understanding of the mechanisms involved.

Animal Feed↗

PubMed2003

Regulation of human short-term repopulating cell (STRC) engraftment in NOD/SCID mice by host CD122+ cells.

OBJECTIVE: NOD/SCID and NOD/SCID B2m(null) mice are used for the in vivo study of human hematopoietic stem cells (HSC). A previously unrecognized HSC in cord blood, termed short-term repopulating cell (STRC), has been identified using NOD/SCID B2m(null) mice. However, only low levels of STRC engraft in NOD/SCID mice, presumably due to their higher levels of NK cell activity. The objective of these studies was to deplete NK cells both by genetic manipulation of the hosts and by antibody depletion of cell populations that may regulate engraftment with human STRC. METHODS: C57BL/6-SCID mice and immunodeficient NOD mice genetically deleted in NK cell activity were injected intravenously with human cord blood cells to quantify STRC engraftment. Cohorts of these mice were also treated with anti-NK1.1 or anti-CD122 (IL-2r beta-chain) antibodies. RESULTS: Human STRC fail to engraft in C57BL/6-SCID mice treated with anti-NK1.1 or with anti-CD122 antibody that targets mouse NK and myeloid cells. NOD/SCID mice, NOD-Rag1(null) mice, and NOD-Rag1(null)Pfp(null) mice that are genetically deleted in NK cell cytotoxic activity support only low levels of STRC engraftment. In contrast, STRC engraft at high levels in all three strains of immunodeficient NOD mice treated with anti-CD122 antibody. CONCLUSION: Injection of anti-CD122 antibody leads to high levels of STRC engraftment in immunodeficient NOD mice, but not in C57BL/6-SCID mice. These data document that depletion of NK cells is required, and that additional murine host innate immune factors, presumably myeloid cells, are important in regulating human STRC engraftment.

Animals↗

PubMed1999

Titres of juvenile hormone I, II and III in Spodoptera littoralis (Noctuidae) from the egg to the pupal moult and their modification by the egg-larval parasitoid Chelonus inanitus (Braconidae).

Physico-chemical analysis of juvenile hormones (JHs) of Spodoptera littoralis revealed highest quantities in the second half of embryonic development and in newly hatched 1st instar larvae. At these stages, mostly JH II, JH I and little JH III were found, while in later stages only JH II and JH III were found. Titres fluctuated in a similar manner in all larval instars, being lowest during the moults. In last (=6th) instar larvae, JHs disappeared in the late feeding-digging stage and again increased in the early prepupal stage. Parasitisation with Chelonus inanitus, a solitary egg-larval parasitoid which induces in its host the precocious onset of metamorphosis in the 5th instar, did not alter JH homologue composition but led to a disappearance of JHs in the 5th instar. Implantation of a parasitoid larva into early 5th instar larvae containing polydnavirus/venom caused a drop in the JH titre which indicates that the parasitoid larva plays an important role in the manipulation of the host's JH titre. In the parasitoid larva, only JH III was found; titres were highest in the 2nd larval instar, a stage when the host is in the 5th instar and contains almost no JHs. Thus, JHs of the parasitoid and the host fluctuate in an independent manner.

Journal Article↗

PubMed1986

Biologic control of cancer. The James Ewing lecture.

There is abundant clinical and laboratory evidence that host defenses are a significant factor in the progression and the control of cancer. The host immune system plays the major role, primarily through cell-mediated responses to the neoplastic threat. Great progress has been made in evaluating immune competence, although the specific defects have not been identified in all patients. The history of immunotherapy includes numerous trials, with few successes and many failures. Advances in knowledge and technology, however, indicate that efforts to manipulate and strengthen host defenses have great potential in the fight against cancer.

Adult↗

PubMed1990

Cardiac transplantation in the rat. II. Alteration of the severity of donor graft arteriosclerosis by modulation of the host immune response.

Cardiac transplantation between inbred rat strains that differ for weak histocompatibility antigens is associated with the development of arteriosclerosis in the arteries of the donor graft myocardium. The lesions are seen in donor/recipient pairs that differ for both MHC and non-MHC histocompatibility antigens that apparently stimulate a low-level, chronic rejection of the donor heart graft. The arteriosclerosis associated with this chronic rejection consists of a diffuse, concentric proliferation of the intima and pathologically resembles the lesions observed in the coronary arteries of long-term human cardiac graft recipients. We have recently examined the influence of positive and negative manipulation of the host immune response on the development of the graft arteriosclerosis. Our results demonstrate that delayed harvest of the cardiac grafts or immunization with donor skin grafts or splenic lymphocytes increases the sensitivity of the recipient to the donor heart grafts--and, under conditions that allow for the long-term survival of the graft--increases the severity of the arteriosclerotic lesions. Alternatively, suppression of the host immune responses with cyclosporine or FK506, substantially reduces the arteriosclerotic changes. These results suggest that control of accelerated graft arteriosclerosis in long-term human cardiac recipient may require more careful and effective immunosuppression of the allograft reaction.

Animals↗

PubMed2006

Resistance of Leishmania donovani to sodium stibogluconate is related to the expression of host and parasite gamma-glutamylcysteine synthetase.

Sequencing studies showed that the gamma-glutamylcysteine synthetase (gamma-GCS) heavy chain genes from sodium stibogluconate (SSG)-resistant (SSG-R) and SSG-susceptible (SSG-S) Leishmania donovani strains were identical, indicating that SSG resistance was related to quantitative differences in gamma-GCS expression rather than gene interstrain polymorphisms. In vitro infection of murine macrophages with the SSG-R strain, but not the SSG-S strain, down regulated expression of host gamma-GCS, which would result in a reduction in intramacrophage glutathione (GSH) levels and promote an oxidative intramacrophage environment. This would inhibit, or minimize, the reduction of SSG pentavalent antimony to its more toxic trivalent form. Macrophage studies showed that the SSG-R strain expressed higher levels of gamma-GCS compared to the SSG-S strain, which would result in higher GSH levels, giving increased protection against oxidative stress and facilitating SSG efflux. However a similar differential effect on host and parasite gamma-GCS expression was not obtained when using tissues from infected mice. In this case gamma-GCS expression was organ and strain dependent for both the host and the parasite, indicating that environmental conditions have a profound effect on gamma-GCS expression. Consistent with the proposed mechanism from in vitro studies, increasing tissue GSH levels in the presence of SSG by cotreatment of L. donovani-infected mice with SSG solution and GSH incorporated into nonionic surfactant vesicles was more effective in reducing liver, spleen, and bone marrow parasite burdens than monotherapy with SSG. Together, these results indicate that SSG resistance is associated with manipulation of both host and parasite GSH levels by L. donovani.

Animals↗

PubMed2006

[How the bovine viral diarrhea virus outwits the immune system].

The interaction of bovine viral diarrhea virus (BVD virus) with its host has several unique features, most notably the capacity to infect its host either transiently or persistently. The transient infection stimulates an antiviral immune reaction similar to that seen in other transient viral infections. In contrast, being associated with immunotolerance specific for the infecting BVD viral strain, the persistent infection differs fundamentally from other persistent infections like those caused by lentiviruses. Whereas the latter are characterized by complex viral evasion of the host's adaptive immune response by mechanisms such as antigenic drift and interference with presentation of T cell epitopes, BVD virus avoids the immune response altogether by inducing both humoral and cellular immune tolerance. This is made possible by invasion of the fetus at an early stage of development. In addition to adaptive immunity, BVD virus also manipulates key elements of the host's innate immune response. The non-cytopathic biotype of BVD virus, which is capable of persistently infecting its host, fails to induce type I interferon. In addition, persistently infected cells are resistant to the induction of apoptosis by double-stranded RNA and do not produce interferon when treated with this pathogen-associated molecular pattern (PAMP) that signals viral infection. Moreover, when treated with interferon, cells persistently infected with non-cytopathic BVD virus do not clear the virus. Surprisingly, however, despite this lack of effect on persistent infection, interferon readily induces an antiviral state in these cells, as shown by the protection against infection by unrelated viruses. Overall, BVD virus manipulates the host's interferon defense in a manner that optimises its chances of maintaining the persistent infection as well as decreasing the risks that heterologous viral infections may carry for the host. Thus, since not all potential host cells are infected in animals persistently infected with BVD virus, heterologous viruses replicating in cells uninfected with BVD virus will still trigger production of interferon. Interferon produced by such cells will curtail the replication of heterologous viruses only, be that in cells already infected with BVD virus, or in cells in which the heterologous virus may replicate alone. From an evolutionary viewpoint, this strategy clearly enhances the chances of transmission of BVD virus to new hosts, as it attenuates the negative effects that a global immunosuppression would have on the survival of persistently infected animals.

Animals↗

PubMed2001

Toxocara in the mouse: a model for parasite-altered host behaviour?

The objective of this paper is to critically evaluate the significance of parasite-altered host behaviour in the Toxocara mouse model particularly in the light of the Manipulation Hypothesis. Murine behaviours were examined in both outbred and inbred strains of mice infected with different doses of Toxocara canis ova. Behaviours investigated included activity, exploration, response to novelty, anxiety, learning, memory and social behaviour. Subsequent modifications to the behaviour of infected mice were investigated with respect to dose administered and larval accumulation in the brain. There was substantial variation in the number of larvae recovered from brains of individual mice, which received similar doses of Toxocara ova. Furthermore, the numbers of larvae recovered at different doses differed significantly between an outbred and inbred strain of mouse. Alterations in infected host behaviour occurred and were related to the number of larvae recovered from the brain. For social behaviour in outbred mice, a high infection in the brain reduced levels of aggressive behaviour and increased levels of flight and defensive behaviours. In contrast, outbred mice with a low infection in the brain displayed a greater level of risk behaviour in respect of predator odour and the light/dark box compared to control or high infection mice. Post-infection, outbred mice were more immobile whereas inbred mice showed reduced immobility and increased digging and climbing. Impaired learning ability was observed in outbred mice with moderate and high levels of infection in the brain compared to control and low infection mice. Toxocara infection has an impact upon a diverse range of murine behaviours with little evidence for a specific and hence an adaptive alteration. Many of the effects on murine host behaviour by Toxocara are likely to be pathological side effects of infection rather than as a consequence of adaptive host-manipulation. Observed changes in murine behaviour may be relevant to human toxocariasis.

Animals↗

PubMed2001

Progenesis and reduced virulence as an alternative transmission strategy in a parasitic trematode.

The complexity of the life-cycle of many parasitic helminths has driven the evolution of several well-documented adaptations serving to facilitate the completion of each difficult step in the cycle. In some trematode taxa, selection has even favoured the truncation of the life-cycle: progenetic larval stages (metacercariae) are capable of producing eggs inside their usual intermediate hosts, eliminating the need to be transmitted by predation to a definitive host. In some species, progenesis is shown by all individuals, whereas in other species both the normal and truncated life-cycles coexist in the same populations. Here, the strategies chosen by normal and progenetic metacercariae of the trematode Coitocaecum parvum are investigated and compared. Normal metacercariae, i.e. metacercariae that only develop into adults following ingestion by a suitable fish definitive host, were not capable of manipulating the behaviour of their amphipod intermediate host in ways that could facilitate their capture by fish. These metacercariae were associated with increased mortality in amphipods. Progenetic metacercariae, on the other hand, showed lower virulence levels than normal metacercariae. At the time of their death, amphipods harbouring progenetic metacercariae contained close to the maximum number of eggs that can be produced by progenetic metacercariae, suggesting that the parasite lowers its virulence to keep its host alive long enough to maximize egg output. The maintenance of the 2 strategies in the C. parvum population suggests that they may have equal fitness payoffs: progenesis and low virulence guarantee the production of at least some eggs, whereas the normal life-cycle and its associated higher virulence in the intermediate host provides a low probability of much higher fecundity.

Animals↗

PubMed1997

Liver-directed gene transfer in non-human primates.

To develop a primate model for liver-directed gene therapy, we studied several gene transfer vehicles and routes in eight rhesus monkeys (Macaca mulatta). For this purpose, we used first-generation, replication-deficient adenoviral vectors carrying the Escherichia coli lacZ gene (Ad.CMVlacZ) or a lacZ-containing plasmid (pCMV beta) with lipofectamine for transfection. The reporter gene construct was infused into either the portal vasculature, common bile duct, or saphenous vein. Adenovirus-mediated gene transfer via the portal vein resulted in expression of lacZ in over 70% of hepatocytes by days 3-7, but was accompanied by acute hepatitis. Adenovirus-mediated gene transfer via the common bile duct resulted in lacZ expression in less than 10% of hepatocytes and was accompanied by portal inflammation. The animals mounted a significant immune response, as demonstrated by adenoviral antigen-induced T-cell proliferation and production of neutralizing anti-adenovirus antibodies and antibodies to E. coli beta-galactosidase (beta-Gal). Activation of the immune response was associated with rapid decrease of the reporter gene by days 13-21. Lipofectamine-mediated gene transfer was inefficient, and no lacZ expression in the liver was detected. To limit the host immune response, 4 animals were immunosuppressed by cyclophosphamide/prednisone and then infused with the Ad.CMVlacZ via the portal vein or the saphenous vein. The monkeys showed sustained expression of lacZ for up to 35 days with no evidence of inflammation. The primates transduced via the saphenous vein showed a level of beta-Gal expression in the liver similar to that of the portal vein-infused animals. In conclusion, adenovirus-mediated gene transfer to non-human primate livers via the portal vein or saphenous vein is efficient, but it results in transient expression and is accompanied by an immune response to both vector and transgene products and acute hepatitis, whereas lipofectamine-mediated transfer is inefficient. Manipulation of the host immune response may expand potential applications of adenoviral vectors for liver-directed gene transfer.

Adenoviridae↗

PubMed1996

Use of transient CD4 lymphocyte depletion to prolong transgene expression of E1-deleted adenoviral vectors.

E1-deleted adenoviral vectors are increasingly being utilized for in vivo gene transfer. The potential use of these vectors is limited by transient expression of the transgene and a markedly reduced rate of transduction following readministration, presumably due to a host immune response to the vector. We hypothesized that CD4+ lymphocytes are necessary to generate an immune response to these vectors and that administration of a depleting anti-CD4 antibody (GK1.5) might prolong transgene expression in vivo. We found that pretreatment of mice with a single injection (transient depletion) or weekly injections of GK1.5 (persistent depletion), markedly prolonged expression of an adenovirus-encoded tumor necrosis factor (TNF) inhibitor or luciferase gene compared to controls. Moreover, mice treated with GK1.5 showed no antiadenoviral antibody response to repeat administration of the vector and a second adenoviral transgene could be expressed in these animals. However, control mice developed a significant neutralizing antibody response that prevented transgene expression with administration of a second adenovirus. These findings demonstrate that manipulation of the host immune response may expand potential applications of gene transfer utilizing adenoviral vectors.

Adenovirus E1 Proteins↗

PubMed2005

Cost induced by viral particles manipulating superparasitism behaviour in the parasitoid Leptopilina boulardi.

Vertically transmitted symbionts can be maintained in a host population only if they do not reduce host fitness, unless they compensate by manipulation of their host's reproduction or have alternative mode of transmission. In Leptopilina boulardi, a parasitoid of Drosophila larvae, some females are infected by viral particles showing both maternal and horizontal transmission. Horizontal transmission occurs when larvae from infected and uninfected individuals of L. boulardi compete in the same host. This situation is facilitated by the increasing tendency to accept already parasitized hosts that viral infection induces in L. boulardi females. Estimation of the adaptive significance of this behavioural modification requires measuring the effect of viral presence on other parasitoid physiological features. Here, we show that viral infection in females imposes no cost on adult survival, a low cost on developmental rate and tibia length, and leads to a strong reduction of locomotor activity. Surprisingly, infected females show higher egg load which could be accounted for by a redirection of energy allocation to egg production. The high intensity of superparasitism in infected females induced a dramatic decrease in pre-imaginal survival of the parasitoid's offspring, representing a potential indirect cost of infection. Low overall pathogeny induced by viral particles appears to be well suited to both transmission modes, both of them requiring females ability to locate and (super)parasitize hosts.

Animals↗

PubMed2003

Down-regulation of CD46 by piliated Neisseria gonorrhoeae.

Human membrane cofactor protein (CD46) protects host cells against complement attack and may function as a receptor for pathogenic Neisseriae. We assessed CD46 expression in the human cervical cell line ME-180 after exposure to Neisseria gonorrhoeae. Piliated but not nonpiliated gonococci adhered to cells and produced up to an 80% reduction in CD46 surface expression by 6 h that persisted for at least 24 h. This response required a minimum multiplicity of infection of 10 and was not prevented by antibodies to CD46. CD46 down-regulation was not attributable to intracellular retention or a global or specific shutdown of mRNA or protein synthesis. Substantial quantities of CD46 were found in the supernatants, indicating a specific shedding of this protein. Adherent gonococci lacking the pilus retraction protein PilT did not down-regulate CD46 but de-repression of pilT expression restored CD46 down-regulation. After experimental infection of human volunteers with a gonococcal variant incapable of inducing CD46 down-regulation, variants of this strain were reisolated that exhibited CD46 down-regulation. Pilus-mediated interactions of gonococci with human epithelial cells results in a pathogen-induced manipulation of the host cell environment in which a membrane protein is removed from epithelial cells by liberation into the surrounding milieu.

Antigens, CD↗

PubMed1993

Functional activity of intrahippocampal septal grafts is regulated by catecholaminergic host afferents as studied by microdialysis of acetylcholine.

Previous microdialysis experiments have shown that acetylcholine (ACh) release from septal grafts in the hippocampus of awake rats is influenced by the behaviour of the animals, which strongly suggests that the host brain can exert a regulatory control over the activity of the grafted neurons. Since the activity of the normal septo-hippocampal cholinergic system is likely to be regulated, in part, by brainstem catecholaminergic afferents, we wished to study the effect of catecholaminergic drugs on ACh release in the hippocampus reinnervated by septal grafts. Rats were subjected to a unilateral aspirative fimbria-fornix (FF) transection and grafted with tissue from the fetal septal-diagonal band area, either as a cell suspension injection into the depth of the hippocampus or as a solid implant in the FF lesion cavity. Microdialysis of ACh release was carried out 17-20 months after transplantation in awake, freely-moving animals. The reduction in steady-state ACh overflow induced by the FF lesion (-81%) was restored to normal or above normal levels in rats with either solid or suspension grafts. In normal rats, systemic administration of apomorphine (2.0 mg/kg, s.c.) or amphetamine (2.5 mg/kg, i.p.) caused a 3.7 (+189%) or 7.8 (+301%) pmol/15 min increase in ACh overflow compared to the previous baseline level, respectively. The drug-induced increases in ACh levels in the FF-lesioned controls was substantially lower than normal (86-89% reduction). Both apomorphine and amphetamine resulted in an approximately two-fold increase in hippocampal ACh release in rats with suspension grafts. These responses were significantly increased over those seen in rats with FF lesions only, but they tended to be lower and more variable than normal. Rats with solid septal grafts responded significantly stronger than FF lesion controls to amphetamine with two-fold increased ACh overflow, whereas the response to apomorphine was less clear-cut. Pretreatment with the catecholamine synthesis blocker alpha-methyl-p-tyrosine (AMPT; 200 mg/kg x 3) did not affect steady-state or apomorphine-stimulated release of ACh in any of the groups, whereas the effect of amphetamine was abolished in both normal and grafted rats. The results suggest that ACh release derived from septal grafts in the hippocampus, similar to the normal septo-hippocampal system, can be affected by manipulations of the host catecholaminergic systems. This mechanism may, at least in part, underlie the ability of the host brain to influence and control the activity of grafted cholinergic neurons.

Acetylcholine↗

PubMed1988

Time course of neocortical graft innervation by AChE-positive fibers.

Acetylcholinesterase (AChE)-containing axons are the only extrinsic fibers projecting to the adult cortex that readily innervate embryonic cortical grafts up to normal densities without prior manipulation of the host brain. In the present paper we compare the time course of AChE-positive fiber innervation in the normal mouse cortex with that seen in neocortical grafts by using AChE histochemistry as a marker for presumed cholinergic fibers. Donor tissue was taken at two different stages of gestation; before (embryonic days 12-14, or E12-14) and after (E17-19) the cortical plate is formed. Three features are analyzed: 1) the distribution and density of AChE-containing fibers, 2) the presence of AChE-positive cells, and 3) the distribution of butyrylcholinesterase (BuChE)-positive elements. The modification of Koelle's method used for AChE localization showed AChE-positive fibers in developing parietal neocortex as early as E18-19. The distribution of AChE-labeled fibers in the normal cortex achieves the mature pattern by the end of the third postnatal week. The rate of innervation of transplants takes longer and depends on the age of the donor tissue. Tissue from both donor ages first showed AChE-positive fibers crossing the host-transplant interface by 7 days postsurgery. E17-19 tissue approaches the density of AChE-positive fibers in the normal adult cortex by 15 weeks after grafting, whereas the E12-14 donor tissue does not approach normal innervation densities until after 20 weeks. While the degree of innervation in the E12-14 donor tissue never equalled the surrounding adult cortex within our range of survival times, a few of the E17-19 transplants did develop densities equal to that of the host cortex. AChE-positive cells are first detectable in the normal parietal cortex on the day of birth, peak by the end of the first postnatal week, and then decline in number to the low levels of the mature cortex after the second postnatal week. Grafted cells in E12-14 tissue stain lightly for AChE by 7 days postsurgery, achieve maximal densities by 3 weeks, and become markedly reduced in number and density by 10 weeks. Cells in E17-19 tissue are lightly reactive by 7 days postsurgery, reach maximal numbers by 2 weeks postsurgery, and become similar in number and density to those seen in the mature cortex after 4 weeks. The appearance of BuChE-reactive blood vessels, neurons, and glia in both normal development and in the transplants is described and discussed.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholinesterase↗

PubMed2002

Behavioural dominance and Taenia crassiceps parasitism in BALB/c male mice.

Behavioural dominance relationships in mouse populations are based upon fighting and antagonistic behaviour. Social rank is affected by the physiological states present in the mice. Experimental infection by Taenia crassiceps cysticerci induced physiological disorders and disrupted the dominant-subordinate status. Infected male mice showed strong perturbations in territorial behaviour and aggressiveness. Infected dominant male mice did not show a significant reversal of dominance order compared to uninfected mice. In addition, during confrontation between naive infected and healthy mice, infected animals more often assumed a subordinate status than healthy ones. The effects of the infection by T. crassiceps were more likely to prevent adult male mice from becoming behaviourally dominant than to reverse existing dominance relationships. The results are discussed on the basis of the parasite manipulation hypothesis and host optimal foraging and decision-making theories.

Animals↗

PubMed1995

Rejection of mesencephalic retinal xenografts in the rat induced by systemic administration of recombinant interferon-gamma.

Previous studies have shown that mesencephalic retinal xenografts can be induced to undergo rejection following various systemic and local manipulations of the host immune system. In each of these paradigms, the development of major histocompatibility complex (MHC) antigen expression on cells in and around the graft is correlated with the onset of rejection. We therefore examined the effect on graft viability of systemic administration of high-dose interferon-gamma a potent inducer of MHC antigen expression on cells within the brain. Postnatal Day 1 (P1) Sprague-Dawley rats received mesencephalic grafts of Embryonic Day 13 CD-1 mouse retina. Beginning at P30, one group of rats received daily injections of rat recombinant interferon-gamma intraperitoneally; litter-matched control animals received injections of vehicle alone. Rats were sacrificed on P51. Each of the animals with detectable grafts that had received interferon-gamma showed a strong rejection response characterized by perivascular cuffing with mononuclear cells in and around the graft and infiltration of the graft and the surrounding host brain by lymphocytes and MHC class I- and class II-antigen positive cells resembling reactive microglia. In contrast, only 2 of the 11 control grafts showed evidence of rejection. The rejection rate in the interferon-treated group was significantly higher than in the control group (Fisher's exact test, P = 0.0012). These results suggest that interferon-gamma is involved in the initiation and/or subsequent maintenance of the rejection response to cross-species transplants.

Animals↗

PubMed1994

Tick ecology.

The availability and expediency of acaricides for the control of ticks, together with the development of vaccination procedures against tick-borne diseases as a matter of priority, initially preceded information gained from research on tick ecology. The establishment of acaricide resistance, the increasing cost of chemical control and the data on production loss as an integral part of tick infestation are factors which led to the incorporation of ecological principles into tick control. Continuing research on the life processes of ticks as well as on their interaction with hosts and the environment, initiated producer manipulation of acaricide application frequencies, habitat manipulation techniques and the use of host immunity which are important for the establishment of economically suitable strategies of tick control. The role of tick ecology in establishing these concepts and its influence on current tick research is examined.

Animals↗