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S K Wikel

Publications and source records attributed to S K Wikel.

14 recordsLinked to original sources

Modulation of host-immune responses by ticks (Acari: Ixodidae): effect of salivary gland extracts on host macrophages and lymphocyte cytokine production.

Ixodid tick infestation induces host acquired resistance, which involves immunoglobulin cell-mediated and complement-dependent effector pathways. Ticks have developed countermeasures to modulate host antiarthropod responses. Ixodid-mediated host immunomodulation results in vitro in reduced responsiveness to T-lymphocyte mitogens for cells obtained from infested hosts and impaired antibody responses to a thymic dependent antigen. Salivary gland extracts from days 0-9 of engorgement from unmated, female Dermacentor andersoni Stiles suppressed lymphocyte proliferative responses (LPS) to the T-cell mitogen Con A up to 68.4%, whereas responsiveness to E. coli LPS was enhanced. Cytokines assessed in this study included interleukin-1, IL-1, and tumor necrosis factor (TNF) alpha produced by macrophages, and interleukin-2, IL-2, and gamma interferon (IFN-G) secreted by T-lymphocytes. Salivary gland extracts prepared from tissues obtained on days 0-5 of engorgement suppressed IL-1 elaboration from 89.8% on day 0 through 37.5% on day 6. Levels of TNF were reduced from 40.7 to 94.6% throughout the course of the study. Production of IL-2 was suppressed by 14.1-31.9%, and IFN-G was reduced by 8.7-57.0%. Reduced IL-1 levels during the early phases of feeding indicated reduced host ability to activate T-lymphocytes and provide costimulatory, differentiation, and development signals for B-cells. Both IL-1 and TNF are endogenous pyrogens and activate polymorphonuclear leukocytes. Activities of TNF and IFN-G include antiviral properties and induction of expression of class I and II major histocompatibility complex molecules, which are critical components in the recognition of antigen by T-lymphocytes. The autocrine role of IL-2 in proliferation of T-lymphocytes is central to the development of immune reactivity involving T-cell regulation or effector functions or both. Reductions in cytokine levels would suppress immune responses directed toward immunogens introduced into the host during the course of tick feeding. These results indicates that immunomodulation of the host during tick feeding facilitates engorgement and pathogen transmission.

Animals

Murine immune responses and immunization against Polyplax serrata (Anoplura: Polyplacidae).

Mice with restricted grooming capabilities were infested with the solenophagous louse, Polyplax serrata (Burmeister). Louse burdens on Cox/Swiss and C3H/HeSN mice increased for approximately 1 mo, reaching burden/host weight ratios of 1.14 and 1.26 mg/g, respectively, followed by a steady decline. Fifty days after initial ectoparasite contact, both strains were resistant to lice. Resistance was anamnestic, lasting several months with second infestation weights reduced by 98 and 78% on Cox/Swiss and C3H/HeSN, respectively. Furthermore, mice were systemically resistant because infestations on naive body sites of resistant hosts were reduced by 59%. Host resistance was associated with the development of antilouse immune responses. After the first week of a primary infestation, the draining lymph nodes contained cells that proliferated in vitro to louse antigens. Skin responses to louse antigens were also detected: (1) delayed, (2) immediate and delayed, and (3) no significant reactivity on days 19, 34, and 54, respectively. The presence of systemic antilouse responses provided an immunologic basis for immunization against lice. Intradermal injections of soluble louse components reduced primary infestation weights by 62%. Immunized mice had immediate and delayed skin responses containing an inflammatory infiltrate 1 wk following immunization. This study, using the natural host of P. serrata, demonstrates an inducible, anamnestic immune component in louse resistance.

Animals

Ixodid-host immune interaction. Identification and characterization of relevant antigens and tick-induced host immunosuppression.

Ixodid ticks are the most important vectors of pathogens to domestic and wild animals. It is established that cattle and laboratory animal species acquire resistance to tick infestation; acquired resistance has an immunological basis consisting of cell-mediated, antibody-mediated and complement-dependent effector mechanisms. Even though acquired resistance to tick feeding is expressed, host immune competence is possibly impaired during the course of tick feeding. Ixodid-induced transient immunosuppression could possibly facilitate the transmission of vector-borne pathogens and/or enhance tick feeding capabilities in the presence of a host immune response to the hematophagous arthropod. Tick tissue extracts have been used to artificially induce resistance to ixodid feeding, and this has become an area of increasing interest as a possible strategy for tick control. It is essential to have defined antigenic molecules for analysis of host responses to infestation, characterization of immunopathologic processes and for vaccine development. This report focuses on attempts to identify, characterize and isolate tick immunogens. Protein immunoblotting, utilizing sera from animals of different genetic composition and infestation patterns, was used to detect a number of tick polypeptides which are reactive with sera of infested hosts. It is clear that infestation with one ixodid species stimulates antibodies reactive with molecules derived from the sensitizing species and/or tick species in the same genus or different genera. This approach is used to identify molecules that are good candidates for use in immunization studies and for analysis of mechanisms involved in acquisition and expression of resistance to tick feeding.

Animals

Langerhans cells trap tick salivary gland antigens in tick-resistant guinea pigs.

In the infested skin of tick-resistant guinea pigs, indirect immunofluorescence techniques have revealed that antigens from the ticks' salivary glands are associated with discrete dendritic cells in the epidermis. Evidence is presented to support the suggestion that these antigen-retaining cells are Langerhans cells.

Adenosine Triphosphatases

Acquired resistance to ticks: expression of resistance by C4-deficient guinea pigs.

Hartley and C4-deficient guinea pigs developed resistance to the ixodid tick. Dermacentor andersoni, after one infestation. Resistance was characterized by resistant animals of both groups allowing significantly fewer larvae (5--25%) to engorge during a second infestation than during an initial infestation (70--90%). Resistant animals in both groups developed cutaneous reactions at the site of tick attachment which were characterized by intraepidermal vesicles containing numerous basophils. In previous studies, tick-resistant Hartley guinea pigs depleted of complement by cobra venom factor were not able to express the resistance response and the skin reactions at the tick attachment sites were depleted of basophils. The use of cobra venom factor as an anti-complement probe could not distinguish the relative importance of the classical and/or alternate pathways of complement activation in the expression of tick resistance. The present study reports that C4-deficient guinea pigs, those with a total deficiency in the classical pathway of complement activation, but with an intact alternate pathway, can acquire and display tick resistance in a fashion similar to Hartley guinea pigs. This finding provides evidence that the alternate pathway of complement activation is important in the expression of tick resistance.

Animals

Resistance to tick-borne Francisella tularensis by tick-sensitized rabbits: allergic klendusity.

Mammals become hypersensitive to ticks that feed upon them. That hypersensitivity was thought responsible for an observation that a large number of Francisella tularensis-infected Dermacentor variabilis failed to infect a rabbit previously exposed to ticks of that species. In a series of tests of that hypothesis, rabbits sensitized to ticks were often significantly more resistant than control animals to tick-borne tularemia. The conditions that determine the klendusity are thought to be variable and complex but the phenomenon must be of importance in the epidemiology of some arthropod-borne agents.

Animals

Acquired resistance to ticks. III. Cobra venom factor and the resistance response.

Guinea-pigs developed resistance to larvae of the ixodid tick, Dermacentor andersoni, after one infestation. Resistant hosts were characterized by allowing significantly fewer larvae to engorge than non-resistant hosts. Larvae engorging on non-resistant hosts had a mean weight six times that of larvae obtained from resistant hosts at the end of a 5-day infestation. This immunologically based resistance was previously shown to have a cell-mediated and a humoral component. In an attempt to ascertain the role of complement in the resistance response, cobra venom factor (CoF) was administered to guinea-pigs producing prolonged (85--95 per cent) depletion of complement titres. CoF was administered during an initial infestation with tick larvae to determine if complement depletion altered the acquisition of tick resistance. CoF was also administered to tick-resistant hosts in an attempt to determine if the expression of tick resistance and the development of the basophil-packed lesion, characteristic of the tick-attachment site in resistant hosts, could be altered by complement depletion. CoF did not alter the acquisition of resistance when complement levels were reduced during a primary infestation. However, complement depletion of an animal which had acquired tick resistance blocked the expression of that resistance during a challenge infestation. In addition to increased numbers and weights of larvae engorging on tick-resistant animals depleted of complement, the basophil packed lesion at the tick attachment site was greatly reduced. Complement plays an important role in the expression of tick resistance in guinea-pigs.

Animals

Enigmatic resistance of sheep (Ovis aries) to infection by virulent Francisella tularensis.

Tularemia in range sheep is an occasional cause of severe economic loss from mortality and unthriftiness as well as a hazard to persons in contact with the animals. Epizootics are unpredictable and explosive, therefore, prophylaxis is more practical than therapy. Live vaccine of proven value in man and in beavers was inoculated into mature ewes and elicited antibodies without harm to the sheep. However, challenge of immunity was not possible because virulent Francisella tularensis in large doses did not cause significant mortality in healthy, well managed, unimmunized sheep. Evidence suggests that a complex of stresses such as inclement weather, lambing and concomitant ectoparasitism render sheep more susceptible to tularemia.

Animals

Acquired resistance to ticks. I. Passive transfer of resistance.

Guinea-pigs developed resistance to larvae of the ixodid tick, Dermacentor andersoni, after one infestation. Resistance was characterized by guinea-pigs allowing fewer larvae to engorge (5-15%) during a second exposure than during an initial infestation (70-90%). Larvae feeding on resistant hosts weighed less than larvae engorging on a host with no previous exposure to ticks. Evidence is presented which indicates that this resistance can be passively transferred with viable lymph node cells, but not with serum, from resistant guinea-pigs. Recipients of cells from such resistant animals allowed significantly fewer larvae to engorge than did controls previously unexposed to ticks. This was not so in recipients of immune serum. The protection provided by passive transfer of cells from a resistant donor was not as complete as the protection afforded by natural exposure.

Animals

Acquired resistance to ticks. II. Effects of Cyclophosphamide on resistance.

Guinea-pig developed resistance to Dermacentor andersoni larvae after one infestation. Cyclophosphamide administered in one dose (300 mg/kg) 48 hr prior to an initial infestation with larvae blocked the acquisition of resistance. When cyclophosphamide was given in a similar regimen to guinea-pigs which had already acquired resistance, the expressin of resistance was partially blocked. It was proposed that the blockage of the acquisition of resistance further confirmed the immunological nature of tick resistance. Partial blockage of the expression of resistance by cyclophosphamide substantiated the presence of a humoral component to the resistance mechanism. The presence of a cell-mediated component was previously well established.

Animals

Host immune response to northern fowl mite: immunoblot and lectin blot identification of mite antigens.

White leghorn hens were experimentally infested with northern fowl mites (Ornithonyssus sylviarum) and antibody responses to mite immunogens were monitored over 12 weeks. Mite burdens increased during the early phase of infestation and declined over the latter weeks of the study. Antigen was prepared from homogenized whole mites, which were then sonicated and extracted with non-ionic detergent. Antigen extract was fractionated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and antibody-reactive polypeptides were identified by immunoblotting. At the start of infestation, hens had natural, pre-existing antibodies that reacted with several mite-extract components. Individual hens had different natural antibody reactivities; however, all birds had immunoglobulins reactive with extract polypeptides of 117,000, 77,000 and 36,000 molecular weight. A variety of mite extract components reacted with hen antibodies generated in response to experimental infestation. The number of antibody-reactive mite polypeptides increased through week 8 of infestation and then decreased by week 12. Fifteen polypeptides of northern fowl mite extract were reactive with antibodies developed by the majority of infested birds. These commonly reactive polypeptides had molecular weights ranging from 40,000 to 160,000. Glycoconjugates of fractionated mite extract were identified by blotting with lectins that have different carbohydrate binding specificities. Also identified were lectins that bound extract components with the same molecular weights as those moieties complexed by immunoglobulins of infested birds.

Animals