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Query: UMLS:C0851341 (infestation)
 10,121 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cattle and laboratory animal species-acquired resistance to tick infestation has an immunological basis involving antigen presenting cells, B-lymphocytes, T-lymphocytes, and cytokines. Tick infestation has been shown to impair guinea pig antibody responses to a thymic-dependent antigen and in vitro responsiveness of lymphocytes to T-cell mitogens. Tick salivary gland extracts inhibited in vitro proliferative responses of normal murine lymphocytes to the T-cell mitogen concanavalin A (Con A) and enhanced reactivity of normal B-lymphocytes to the mitogen E. coli lipopolysaccharide (LPS). Salivary gland extracts collected daily during engorgement were shown to inhibit normal murine macrophage elaboration of interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF) as well as murine T-lymphocyte production of interleukin-2 (IL-2) and interferon-gamma (IFN-G). Peripheral blood mononuclear cells collected from purebred Bos indicus and B. taurus were significantly inhibited in their in vitro responses to Con A by salivary gland extracts prepared daily from female Dermacentor andersoni stiles during the course of engorgement. Percentage of suppression of Con A responsiveness was similar for both B. indicus and B. taurus cells. The overall responsiveness of B. indicus derived T cells is significantly greater than that of similar cells from B. taurus, when mean counts per minute of methyl-tritiated-thymidine incorporation were compared for both groups. Cells of B. indicus origin were 34.5% more reactive. In vitro responsiveness of the same cell populations to LPS were significantly enhanced by the presence of tick salivary gland extracts. B. indicus lymphocyte reactivity to LPS was significantly greater (42.9%) than that of similar B. taurus cells in the absence of salivary gland extracts. B. indicus and B. taurus macrophage elaboration of IL-1 were suppressed in a similar manner by tick salivary gland extracts prepared on days 5-9 of engorgement. B. indicus macrophages produced more IL-1 than similar cells of B. taurus origin either in the presence (45.6%) or absence (43.0%) of LPS. Macrophages derived from both genetic backgrounds were significantly suppressed in their LPS induced production of TNF in the presence of tick salivary gland extracts collected on days 0-9 of engorgement. B. indicus might be able to develop more vigorous immune responses to foreign immunogens presented to the animal during tick feeding.
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PMID:Effects of Dermacentor andersoni (Acari: Ixodidae) salivary gland extracts on Bos indicus and B. taurus lymphocytes and macrophages: in vitro cytokine elaboration and lymphocyte blastogenesis. 761 25

In this study we compared the ability of lymphocytes taken from axillary and brachial lymph nodes of BALB/c mice that had been infested once three times with 15 nymphal Ixodes ricinus ticks, to produce interleukin-4 (IL-4) and interferon-gamma (IFN-gamma) after in vitro stimulation with concanavalin A (Con A). They released high levels of IL-4 and low levels of IFN-gamma. An increase of IFN-gamma between the first and the third tick infestation was observed. Salivary gland extracts from female I. ricinus ticks induced specific in vitro proliferation of lymphocytes from infested mice. IL-4 production was correlated with the salivary gland extracts' ability to stimulate tick-specific lymphocyte proliferation. Its levels remained high from the first to the third infestation. IFN-gamma production was not necessarily associated with tick salivary gland antigen stimulation. In BALB/c mice, anti-tick immune response induction is regional and the contribution of other similar secondary lymphoid organs is negligible. Only cells from the lymph nodes which drained the tick-fixation site proliferated in vitro in the presence of tick antigens, and when stimulated with Con A produced IL-4 and IFN-gamma.
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PMID:In vitro production of interleukin-4 and interferon-gamma by lymph node cells from BALB/c mice infested with nymphal Ixodes ricinus ticks. 763 13

Immune and inflammatory responses occurring during dermal infestation by larvae of Lucilia cuprina can retard larval growth and development. This study examined the effect of 4 classes of humoral inflammatory mediators on larval growth in an in vitro assay. Mediators of plasma leakage (histamine, bradykinin, platelet-activating factor and serotonin), leucocyte chemotactic agonists (activated complement, leukotriene B4 and interleukin-8), effector molecules of immune responses (interleukin-1 beta, tumour necrosis factor-alpha and interferon-gamma) and endotoxin all failed to inhibit larval growth. In contrast, immunoglobulins isolated from immune serum caused marked retardation of larval growth. The results suggest that humoral mediators of inflammatory and immune responses do not play a role in immune defence against Lucilia cuprina.
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PMID:The effect of immune and inflammatory mediators on growth of Lucilia cuprina larvae in vitro. 791 57

Human African trypanosomiasis (HAT) is caused by infestation with a flagellate protozoan, the trypanosome which is inoculated by the bite of the tsetse fly Glossina. The particular ecological conditions of parasites and vectors are such that the disease is only found in the intertropical regions of Africa. Although there are many species of trypanosomes, only two, belonging to the brucei group are likely to lead to HAT. These two species are quite similar morphologically but have different pathogenicity. Trypanosoma brucei gambiense found in West and Central Africa leads to a chronic form of the disease or sleeping sickness. T. b. rhodesiense leads to a more virulent and acute condition, although for each species of trypanosome there are strains of different virulence, which account, at least in part, for the interindividual variability in the clinical course. Immediately after penetration into the human organism, the trypanosome multiplies at the point of inoculation, producing a local inflammatory reaction. It then invades the whole organism, and the central nervous system (CNS). The involvement of the CNS leads to an irreversible demyelinating process ending by death without treatment. Apart from the initial stages, it is not easy to determine the phase of the disease that the patient is presenting. The parasite can escape the host immune response by varying the surface glycoprotein coat. Variable surface glycoproteins (VSG) are strongly antigenic and lead to great antibody response with immune lysis. But, some heterologous antigenic variants can survive to repopulate blood and other tissues. This mechanism of antigenic variation is under parasite genetic control. The trypanosome can release numerous pathogenic substances which cause alterations in cytokine/prostaglandin network. A 41-46 kDa molecule termed trypanosome-released lymphocyte trigerring factor may selectively activate CD8+ T cells to produce interferon-gamma which then activates macrophages but also promotes parasite growth. Activated macrophages release tumor necrosis factor alpha and nitric oxide (NO) which are trypanostatic static and other cytokines and prostanglandins. These macrophage relased substances enhance the immunosuppression and alter the blood brain barrier (BBB). So, trypanosomes and inflammatory cells can invade the CNS leading to a progressive meningoencephalitis with typical perivascular cuffings which explain neurological disorders and neuroendocrine alterations. The inflammatory cells (lymphocytes, astrocytes, glial cells) produce cytokines, NO and other mediators and enhance the CNS immunopathological process. The peri-ventricular regions, the tuberoinfundibula and thalamic-hypothalamic regions, are particulary involved. These disturbances lead to a progressively complete disruption of the normal sleep-waking cycle. Antibodies anti-CNS components (galactocerebrosides, neurofilaments, tryptophane) are also described in sera and cerebrospinal fluid (CSF) of HAT patients. Their presence may be due to cross reactions with comon epitopes between host and trypanosomes which can lead to a self-propagating autoimmune reaction, which accounts for the marked demyelination found in the late stage of the disease. The diagnosis of CNS involvement in not easy to establish in the early neurological phase in the absence of neurological signs and in absence of great chnages in CSF. This is an important problem because it is the basis to apply existing available drugs. pentamidine and suramin are effective only in early stages of the disease when CNS is not invaded. Melarsoprol is effective in all-stages: this is the drug of choice when CNS is involved. Unfortunaley, melarsoprol is toxic and, in 5% of treated patients, this drug can lead to arsenical encephalopathy which is often fatal. In the continuing search for new antitrypanosonal drugs, biochemical peculiarities of the trypanosome are used as drug garget, especially glycolysis, trypanothione, sensibil
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PMID:[Human African trypanosomiasis]. 895 90

BALB/c mice infested three times with nymphs or larvae of Ixodes ricinus ticks do not acquire resistance as assessed by evaluation of both tick attachment and the weight of engorged nymphs or larvae. Tick challenge causes a gradual increase in total IgE antibody production from the first to the third infestation. Anti-tick IgG antibodies are never detected. When the mice are treated with anti-interleukin-4 (anti-IL-4) or anti-interferon-gamma (anti-IFN-gamma) monoclonal antibodies (mAbs) 1 day before each infestation, they produce fewer or more IgE antibodies, respectively. No effect is observed on IgG antibodies. In IL-4-deficient mice, no IgE or IgG antibody is produced. However, these treatments and the use of IL-4-deficient mice have no negative effect on either tick attachment or the weight of engorged nymphs or larvae. Treatment with anti-IL-4 mAb and the use of IL-4-deficient mice inhibits and abolishes the switching of IgE, respectively, but these are apparently not sufficient to shift the response toward Th1 cells.
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PMID:Susceptibility of BALB/c mice to nymphs and larvae of Ixodes ricinus after modulation of IgE production with anti-interleukin-4 or anti-interferon-gamma monoclonal antibodies. 961 Jun 36

Several studies have revealed that T lymphocytes and cytokines play a crucial role in determining the outcome of parasitic infections in terms of protective immunity. In this study we found that Rhipicephalus sanguineus tick saliva stimulates transforming growth factor-beta (TGF-beta), and reduces interleukin-12 (IL-12) secretion by cells from normal C3H/HeJ mice. Moreover, murine lymph node cells harvested 6 days after the fourth infestation with ticks presented an 82.4% decrease in their proliferative response to concanavalin A (Con A) compared with the response of control cells. In addition, lymph node cells cultured in the presence of Con A showed a T-helper 2-type (Th2-type) cytokine profile, represented by augmented IL-4 and IL-10 and TGF-beta. On the other hand, the IL-2, interferon-gamma (IFN-gamma) and IL-12 synthesis was significantly inhibited. These results indicate that ticks may modulate the host's immune response through saliva injection. Considering that C3H/HeJ mice develop no protective immunity to R. sanguineus infestation, our results suggest that tick-induced Th2-type cytokines and a decreased proliferative response probably lead the host to a susceptible state to both tick and tick-transmitted pathogens.
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PMID:Successive tick infestations selectively promote a T-helper 2 cytokine profile in mice. 1023 25

Schoeler, G. B., Manweiler, S. A., and Wikel, S. K. 1999. Ixodes scapularis: Effects of repeated infestations with pathogen-free nymphs on macrophage and T lymphocyte cytokine responses of BALB/c and C3H/HeN mice. Experimental Parasitology 92, 239-248. Ixodes scapularis is the principal vector in the United States of Borrelia burgdorferi, the causative agent of Lyme borreliosis, the human granulocytic ehrichiosis agent, and Babesia microti. Infestation with I. scapularis nymphs has previously been shown to modulate host T lymphocyte cytokine production. Tick-induced host immunomodulation is increasingly recognized as a contributing factor in successful transmission and/or establishment of tick-borne pathogens. This study was conducted to determine the effects of repeated infestations with pathogen-free I. scapularis nymphs on the production of the macrophage cytokines interleukin (IL)-1beta and tumor necrosis factor-alpha and the T lymphocyte cytokines IL-2, IL-4, IL-10, and interferon-gamma in both BALB/c and C3H/HeN mice. The pattern of T lymphocyte cytokine production was evaluated to determine if repeated tick infestation polarizes the immune response toward a Th-1 or Th-2 cytokine profile. Female BALB/c and C3H/HeN mice were infested one to four times with pathogen-free I. scapularis nymphs, with a 14-day tick-free period between each exposure. After each infestation, tick biology parameters were measured and macrophage and T lymphocyte cytokine production was assessed. Elaboration of T lymphocyte and macrophage cytokines was quantitated by antigen capture enzyme-linked immunosorbent assay. Acquired resistance to I. scapularis feeding was not developed by either mouse strain. Significant differences in cytokine production were observed between infested and noninfested mice, as well as between the two mouse strains, following tick infestation. Infestation of both strains with pathogen-free I. scapularis results in a polarization of the host immune response toward a Th-2, anti-inflammatory pattern, with a corresponding suppression of Th-1 responses.
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PMID:Ixodes scapularis: effects of repeated infestations with pathogen-free nymphs on macrophage and T lymphocyte cytokine responses of BALB/c and C3H/HeN mice. 1042 52

Scabies is a contagious skin disease of humans and many other species of mammals. Previous studies suggested that the balance between the Th1 and Th2 immune responses may influence the outcome of a scabies infestation in a sensitized host. Therefore, in this study, we examined the T-helper cell cytokine profiles of splenocytes and lymph node cells in BALB/c mice that were immunized with scabies extract (primary response), infested with scabies mites (primary response), or immunized and then infested (secondary response). Lymphocyte cytokine expression was analyzed by flow cytometry after staining for intracellular cytokines. Immunization with scabies extract induced production of interferon-gamma (IFNgamma) (Th1 response) by both spleen and lymph node cells. Mice that were infested with scabies increased production of interleukin-4 by lymph node cells and of IFNgamma by splenocytes. Mice that were first immunized and then infested with mites increased production of IFNgamma by both spleen and lymph node cells. However, this increased level of IFNgamma was only about half of that induced by immunization alone. These results suggest that live scabies mites produced something that inhibited IFNgamma production in the lymph nodes of scabies-immunized mice. Our data also indicate that lymphocytes in the spleen and lymph nodes can present different cytokine response profiles.
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PMID:Skewed Th1/Th2 immune response to Sarcoptes scabiei. 1535 58

The aim of the investigation was to study the specific features of in vitro cytokine production in response to specific parasitic antigens, mycobacterial antigen, and nonspecific mitogens in patients with chronic opithorchiasis who had varying infestation rates. There was a considerable increase in the mononuclear cell production of interleukin-4 and interleukin-10 after specific Opisthorhis antigen stimulation with purified tuberculin derivate or the mitogen conconavalin A in opisthorchiasis patients having varying infestation rates as compared with appropriate parameters in healthy individuals. The production of these cytokines in opisthorchiasis patients with a high infestation rate (Group 2) was significantly higher than that in those with a low infestation rate (Group 1). The mononuclear cell production of interferon-y in the culture stimulated by specific Opisthorhis antigens, tuberculin, or phytohemagglutinin in opisthorchiasis patients with a high infestation rate (Group 2) was not only much lower than that in the control group, but also as compared with the appropriate parameters in Group 1 patients. Thus, the mononuclear cell-stimulated production of cytokines in vitro in patients correlates with the rate of infestation. The highest mononuclear cell production of interleukin-4 and interleukin-10 and the highest suppression of interferon-gamma secretion are characteristic of the patients who have high infestation rates, suggesting the predominance of the type 2 response ofT helper cells.
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PMID:[Cytokine production in relation to the rate of infestation in patients with chronic opisthorchiasis]. 2061 19

The transmission of scabies occurs with the burrowing of Sarcoptes scabiei var. hominis mites into the skin. Infestation invariably leads to the development of localized cutaneous inflammation, pruritus and skin lesions. Classical transmission studies document an initial increase in S. scabiei numbers subsequent to primary infestation with a gradual reduction as host immunity develops. However, certain individuals fail to control infection and develop severe crusting of the skin, accompanied with extremely high mite burdens, elevated antibody levels and eosinophilia. These individuals have the nonhealing form of the human disease known as crusted scabies. The genetic predisposition for susceptibility or resistance to S. scabiei infection in humans is hypothesized to correlate with the dominance of an IgE-driven Th2 response in severe disease or an interferon-gamma-dominated Th1 response that promotes parasite control. However, recent data reveals complexities in cytokine regulation in the skin and the mechanisms of acquired resistance and immune escape. In this review, we consider the recent immunological and biomolecular advances in understanding the human host immune response to S. scabiei infestations in the context of earlier studies and attempt to reconcile apparent differences and emphasize those aspects of the Th1/Th2 model that are supported or refined.
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PMID:The immunology of susceptibility and resistance to scabies. 2062 8


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