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B Hammerberg

Publications and source records attributed to B Hammerberg.

16 recordsLinked to original sources
PubMed1991

Inhibition of antigen-driven proliferative responses and enhancement of antibody production during infection with Brugia pahangi.

Long standing Brugia pahangi infections in seven dogs, restricted to one rear limb popliteal lymph node and its afferent ducts, were monitored with regard to proliferative responses and antibody production specific for a PBS extract of B. pahangi (BpA) by cells from infected and uninfected lymph nodes and by PBL. Five of 10 dogs were negative for proliferative responses to BpA in node cells from infected limbs, yet they had positive PBL responses, and another was negative in both node cells and PBL. Production of BpA-specific antibody was detected in cultures of node cells from infected limbs of 9 of 10 dogs, but only in two cultures of node cells from uninfected limbs and not at all in PBL cultures. Three dogs with responsive node cells produced the least amount of anti-BpA antibody in culture. Injections of B. pahangi adult worm excretory/secretory products (ES), totaling 1 mg over 48 h, into the limb of the original infections in seven dogs, resulted in inhibition of Ag-driven proliferation by cell populations previously responsive to BpA. There was a loss of PBL responsiveness by all but one infected dog and a loss of node cell response by the two dogs previously responsive in infected and uninfected nodes. This loss of responsiveness lasted at least 28 days in three dogs. There was no evidence of suppression of responses to mitogens either before or after ES injection. In contrast, BpA-specific antibody production was greatly increased in node cells from infected limbs injected with ES. Similar injections into the uninfected limbs of two infected dogs produced no change of proliferative responses or of antibody production in the uninfected node. These results indicate that ES can modulate immune cell, Ag-driven proliferation, and simultaneously enhance antibody production in previously infected nodes. This may promote parasite survival by inhibiting cellular attack based on delayed-type hypersensitivity while directing immune responses toward production of antibodies that are less damaging to the adult helminth.

Animals↗
PubMed1990

Taenia taeniaeformis: evasion of complement-mediated lysis by early larval stages following activation of the alternative pathway.

Activation of the alternative pathway of complement by T. taeniaeformis oncospheres and early stage metacestodes, although a factor in host defense against primary infection, does not directly lead to the killing of the parasite larvae observed prior to day 6 post-infection in innately resistant BALB/cByJ inbred mice. Immunogold labelling techniques clearly demonstrated tegument-associated C3 on in vitro-activated oncospheres incubated with non-immune mouse sera. However, C5, a protease necessary for the assembly of the membrane attack complex, was not detected. Early stage larvae cultured from in vitro-activated oncospheres escaped membrane damage and survived incubation in non-immune sera from both BALB/cByJ and taeniid-susceptible C3H/HeDub mice. Comparisons of cobra venom factor-treated and untreated C5-deficient B10.D2osn mice revealed no significant differences in parasite burden and local eosinophil infiltration at 6 days post-infection, suggesting that the terminal arm of the complement system is necessary for the previously reported role of complement in resistance to primary infection in BALB/cByJ and C3H/HeDub mice. An in vivo test of chemotaxis indicated that although both complement-intact mouse strains examined responded to intraperitoneal injections of inulin, there were lower numbers of eosinophils in C3H/HeDub mice than in BALB/cByJ mice, perhaps pointing to possible mouse strain differences in C5a generation/catabolism or eosinophil ability to respond to C5a. Lectin-binding studies showed an affinity of PNA for the exposed surface of taeniid oncospheres and 4-day post-infection metacestodes; however, binding of lectin to the carbohydrate moiety did not inhibit complement activation.

Animals↗
PubMed1990

Effect of depletion of L3T4+ cells on resistance to early primary infection of mice with Taenia taeniaeformis.

The role of L3T4+ T lymphocytes in early primary infection with the metacestode of T. taeniaeformis was investigated by selective removal of these cells in vivo by parenteral injections with the rat monoclonal antibody (MAb) GK1.5 directed against the L3T4 molecule. Comparisons between treated and non-treated BALB/cByJ mice, normally resistant to infection with T. taeniaeformis, demonstrated that the treated mice had a greater percentage of viable parasites in the livers. Eosinophils were prominent in the region immediately surrounding parasite larvae in control mice, whereas treated mice showed virtually no eosinophil infiltration. Additionally, fewer tissue macrophages were evident near parasite larvae in the treatment group when compared to controls. The more susceptible C3H/HeDub strain mice demonstrated similar responses following treatment with the MAb, including diminished parasite killing and limited inflammatory cell infiltration. When C3H/HeDub mice were injected with the cytotoxic agent vinblastine sulfate, which has been shown to diminish Lyt-2+ suppressor cell activity, these mice remained unable to mount a strong local cellular response to the larval parasite. It is suggested that L3T4+ T lymphocytes play a crucial role in the innate resistance to T. taeniaeformis infection during the first 6 days post-infection. Effects seen following vinblastine treatment may be a result of drug-induced alterations in leukocyte chemotaxis, toxicity to other effector T cell populations, or a specific depletion of a functional Lyt-2+ T cell population that is required in addition to L3T4+ T cells for the expression of resistance to primary infection with T. taeniaeformis.

Animals↗
PubMed1990

Selective breeding of dogs for segregation of limb edema from microfilaremia as clinical manifestations of Brugia infections.

Three generations of beagles were monitored for microfilaremia (mf) and clinical disease during repeated infection with Brugia pahangi and were selectively bred for offspring manifesting limb edema and low or amicrofilaremia. A high microfilaremic female mated to a high microfilaremic male produced 7 pups, 6 of which maintained mf greater than 1,000/ml for greater than 2 years after 5 monthly infections of 10 infective larvae each. An uninfected female mated to another high mf male produced 5 pups, 4 of which did not exceed 1,000 mf/ml 7 months after initiation of the repeating infection regimen; 1 of these remained amicrofilaremic after 2 additional challenges. Neither the parents nor the offspring from these matings manifested chronic limb edema. Two matings were conducted with offspring from the microfilaremic female by breeding siblings with the lowest mf and breeding siblings with the highest mf. The high mf siblings produced 4/5 offspring manifesting chronic limb edema (greater than or equal to 7 months duration) and either no mf (in 2 dogs) or less than 100 mf/ml after the repeating infection regimen. The lower mf siblings produced 5 offspring, all with greater than 1,000 mf/ml 6 months after the initiation of the repeating infection regimen; none manifested edema. Comparisons of IgG antibody levels, specific for extracts of adult worms, showed no consistent differences between these 2 litters of dogs that could be associated with limb edema or mf when monitored for 16 months; however, the onset of lymph node enlargement was much earlier in the group of dogs manifesting limb edema than in the other litter.

Animals↗
PubMed1989

Protective immunity against Brugia malayi infective larvae in mice. II. Induction by a T cell-dependent antigen isolated by monoclonal antibody affinity chromatography and SDS-PAGE.

A mAb directed against filarial worm secretory/excretory product and reactive with Brugia malayi larval worm surface was used in conjunction with preparative SDS-PAGE to isolate protective Ag from extracts of adult B. malayi. The IgM mAb OVH bound to a repeating carbohydrate epitope present in adult, infective, and fourth stage larvae and microfilariae of B. malayi, and on the surface of fourth stage larvae. Ag bearing this epitope were also present in the sera of hosts infected with a variety of helminths, including Brugia, Onchocerca, Dirofilaria, and Paragonimus. Affinity chromatography of SDS extract of adult Brugia, using mAb OVH immobilized on agarose beads, isolated several Ag that separated into multiple protein staining bands on SDS-PAGE. In comparing SDS-PAGE-fractionated Ag from the crude SDS extract with fractionated mAb OVH-isolated Ag for the ability to protect BALB/c mice from challenge with B. malayi-infective larvae, it was found that of the mAb OVH-isolated Ag only those at a molecular mass of 26 to 32 kDa were protective while the original SDS extract yielded protective Ag at the following molecular mass: greater than 200, 170 to 200, 40 to 44, 33 to 36, 23 to 28, 20 to 22, and 17 to 19 kDa. Although Ag isolated by mAb OVH were highly protective, they failed to induce high antibody levels against the immunogen or SDS extracts compared to crude SDS extract immunized mouse sera, as determined by immunoblot and ELISA. Transfer of nylon wool non-adherent T cells from BALB/c mice immunized with the 26- to 28-kDa fraction of mAb OVH-isolated Ag to naive mice just before challenge with infective larvae of B. malayi resulted in a 70% reduction in larvae recovered 14 days after challenge.

Animals↗
PubMed1989

Protective immunity against Brugia malayi infective larvae in mice. I. Parameters of active and passive immunity.

Protective immunity against infective larvae of Brugia malayi was studied in different strains of mice using various sources of antigens. The following strains of mice were susceptible to infective larvae development for 2 weeks after primary ip challenge: BALB/c, C3H/HeJ, C3H/NeN, C3H/HeJms, C57BL/6Jms, and DDD. In comparison to gerbils, BALB/c mice developed stronger resistance to infective larvae after immunization with irradiation attenuated larvae or with killed microfilariae (mf). However, killed mf failed to enhance resistance in C3H/HeJ mice, although C3H/HeN mice were strongly protected and C3H/HeJms mice were protected to a lesser degree by this antigen. Extracts of mf with phosphate buffered saline and sodium dodecyl sulfate both induced high levels of resistance in BALB/c mice. Transfer of resistance from BALB/c mice immunized with attenuated infective larvae to naive mice was accomplished at a high level at protection with nylon wool nonadherent spleen cells (T cells) but not with adherent cells treated with anti-Thy 1.2 serum and complement. In contrast, sera from immunized mice were much less protective.

Animals↗
PubMed1988

Taenia taeniaeformis: cellular reconstruction of athymic mice and role of L3T4+ helper T lymphocytes in the early infection.

The role of T helper lymphocytes (L3T4+) in the early response to Taenia taeniaeformis metacestodes was investigated. Athymic BALB/c-nu/nu mice (susceptible) were inoculated intraperitoneally with the following cell populations from congenic BALB/c-nu+ + mice (resistant): (a) whole spleen single cells, (b) thymus single cell suspensions, or (c) spleen cells pretreated with anti-L3T4 monoclonal antibody before the injection. The mice were given 3 weekly injections of cells and then infected orally with 300 eggs 7 days after the last injection. Cryostat sections of the liver from the infected mice were examined at 6 days postinfection (PI) for parasite viability, the numbers of eosinophils, and L3T4+ T lymphocytes present within 100 micron of the parasite and for the presence of biotin in hepatocytes (involved in biosynthesis of fatty acids) around the parasite. The success of the cellular reconstitution of athymic mice with the lymphoid cells was measured by a T-cell mitogenic assay with concanavalin A (ConA). The cellular reconstitution of athymic mice with a mixture of lymphoid cells from the spleen and thymus of BALB/c-nu/ + mice resulted in both parasite death and eosinophil infiltration. Reconstitution with mature splenic cells alone resulted in a greater parasite killing and eosinophil infiltration as compared to reconstitution with thymic cells. The better reconstitution with splenic cells was reflected in a greater mitogenic response to ConA.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Dynamics of immune responses related to clinical status in Brugia pahangi-infected dogs.

Clinical signs of lymph node enlargement, limb edema, lymph duct fibrosis, and microfilaremia were monitored in dogs with chronic Brugia pahangi infections. During the study a single rear limb of each dog was reinfected with multiple low doses of infective larvae. The changing immune responses to parasite antigens prepared from three sources--Brugia pahangi adult worm homogenate extract, adult worm excretory-secretory products, and microfilaria excretory-secretory products--were monitored by Western blot ELISA of antigens fractionated on sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) and by microtiter plate ELISA. Assays were used to detect antibodies in both the the IgG and IgE classes. A wide range of clinical manifestations was demonstrated in response to reinfection: asymptomatic, amicrofilaremic; asymptomatic, microfilaremic; acute short duration node enlargement and/or limb edema with microfilaremia; and chronic limb edema, amicrofilaremic. On microtiter plate ELISA, the dogs demonstrating the highest anti-adult worm homogenate titers were amicrofilaremic and were asymptomatic or developed chronic limb edema, dogs with high anti-mf ES titers were persistently amicrofilaremic, and the most marked increases against all three antigen sources upon reinfection occurred in low or amicrofilaremic dogs. Quantitative changes in antibody levels against the three crude antigen sources following reinfection were often paralleled by distinct changes in recognition of specific bands of antigens fractionated by SDS-PAGE.

Animals↗
PubMed1986

Pathophysiology of nematodiasis in cattle.

Recent detailed studies of the physiologic changes occurring in cattle infected with some of the common gastrointestinal nematodes have shown that the weight loss and reduced carcass values resulting from these infections are a consequence of major alterations in host metabolism. Dramatic changes in protein metabolism were consistently found to involve decreased muscle synthesis and increased urinary nitrogen excretion. Because of the well-recognized loss of plasma proteins into the gut lumen and cellular damage at the mucosa occurring during nematode infections of the abomasum and duodenum, it has been assumed that protein was being lost in feces or not absorbed; however, this loss has proved not to be as significant as postabsorptive protein catabolism in these infections. Only when the colon and cecum are involved in protein-losing infections is the loss of protein into the feces significant. The mechanisms by which gastrointestinal nematode infections result in such altered host metabolic states are not known, but suggestions have been made that parasites directly or indirectly alter gut hormone levels. Gut hormone changes may also be responsible for diarrhea and anorexia. Another mechanism of altering metabolism has been proposed for chronic parasitisms that stimulate macrophages. Macrophages produce a peptide called cachectin, and cachectin is thought to mediate protein and lipid catabolism. This mechanism obviously could be contributing to weight loss and anorexia whenever nematodes cause sufficient macrophage activation, including during lungworm infections, which do not have enteric involvement.

Animals↗
PubMed1978

Interaction between Taenia taeniaeformis and the complement system.

Factors present in the cystic bladder fluid of metacestodes of Taenia taeniaeformis and released by these parasites maintained in vitro were shown to interact with the C system in vitro and in vivo. This interaction resulted in the depletion of hemolytic C in normal sera of several species, the generation of anaphylatoxin-like activity in vitro, the conversion of C3, and the production of vascular permeability changes in vivo. The substances appeared to initiate C fixation nonimmunologically via both the alternative and classical pathways. Intravenous administration of parasite factors in rats led to profound depression of circulating C levels and the rats did not become refractory to this effect after repeated dosing over a 3-week period. Circulating levels of hemolytic C were not altered in infected rats over the first 8 weeks of infection. C-dependent inflammatory responses in the skin of rats were inhibited in animals given i.v. doses of parasite factors. The possibility is raised that local consumption of C around the metacestode in vivo could contribute to its successful evasion of inflammation and immune rejection during infection.

Animals↗
PubMed1977

Uptake of colostral immunoglobulins by the suckling rat.

The sequential appearance of immunoglobulins was studied in serum samples from rats during the suckling period. At birth both IgG1 and IgG2 were present, but IgM was not detected until the 7th day and IgA until the 17th day. No intestinal transmission of intact homologous IgA was demonstrable after oral administration of radiolabelled preparations (125I) of either serum or colostral IgA to suckling rats. When 125I labelled IgG 2a+b rat immunoglobulins were given orally there was a selective transport of the slower moving subclass from the gut into the serum. The rat appeared to differ from several other species in which some intestinal absorption of passively transferred IgA by the newborn has been demonstrated. It was suggested that retention of colostral and milk IgA in the intestine may serve to enhance local defense mechanisms in the newborn rat.

Animals↗
PubMed1977

Activation of complement by hydatid cyst fluid of Echinococcus granulosus.

Factors present in hydatid cyst fluid of Echinococcus granulosus were found to interact with complement from several species. This nonimmunologic fixation resulted in the depletion of hemolytically active complement from fresh guinea pig serum, the conversion of human C3 to an electrophoretically faster species and the genration of smooth muscle contracting substances, analogous to anaphylatoxins, in normal rat serum in vitro. Vascular permeability changes were produced in vivo in rats and humans after intradermal inoculation of complement interacting fractions of hydatid fluid. It is suggested that these factors may contribute to the pathogenesis of the shock syndrome which follows intravenous administration of hydatid fluid in normal animals, and to the nonspecificity of immunodiagnostic skin tests for hydatid infection in man and animals.

Anaphylatoxins↗
PubMedDate not supplied

The lymphatic pathology of chronic Brugia pahangi infection in the dog.

The dog infected with Brugia pahangi is an excellent model for studying the clinical and immunological pathogenesis of lymphatic filarial infection and disease. Dogs demonstrated a range of clinical changes including varying levels of microfilaraemia, episodic lymphadenopathy, lymphangitis, and limb oedema similar to the clinical spectrum reported in man. Histologically, tissues from parasite-infected dogs were characterized by fibrosis of the lymph nodes and their afferent and efferent lymphatic ducts in the infected limbs. Some nodes were atrophied while others were characterized by reactive hyperplasia. Duct walls of some afferent lymphatics were thickened with a mononuclear inflammatory infiltrate. Parasite antigen deposition was detected in the subcapsular sinuses and middle of germinal centres of infected popliteal lymph nodes, using an immunohistochemical technique.

Animals↗