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PubMed1975

Phytohemagglutinin (PHA) skin test in patients with sarcoidosis.

A group of 17 patients with histologically confirmed sarcoidosis were examined for the presence of anergy and the intracutaneous response to 2 mug of purified phytohemagglutinin (PHA); lymphocytes of 15 of these patients were studied for in vitro blastic response to PHA-M. Although 8 of the patients were anergic and 8 had impaired in vitro response to PHA, all patients showed a normal response to intradermal injection of PHA. It was concluded that patients with sarcoidosis have an intact intradermal response to PHA, suggesting that the anergy seen in this disease results from impaired initiation of the delayed hypersensitivity reaction and not from impaired mononuclear cell responsiveness. The PHA skin test may be a useful adjunct in the evaluation of anergic patients.

Humans↗
PubMed1981

Testicular function of actively immunized male rats with LH releasing hormone (LHRH): a possible role of prolactin on regulation of spermatogenesis.

The effect of testosterone propionate (TP) on the recovery of spermatogenesis was compared in 3 types of experimentally induced gonadotropin-deficient rats; 1. hypophysectomized rats, 2. rats actively immunized to LHRH and 3. hypophysectomized and immunized rats bearing a pituitary isograft. In order to immunize animals to LHRH, deamidated LHRH conjugated with BSA (LHRH-BSA) was injected intradermally to male rats 4 times at 2 week intervals and additional booster injections continued once a month. Anti-LHRH titer was the highest on the 12th week and the titer remained at a relatively high levels thereafter. A remarkable decrease in testicular weight and testosterone production was achieved in 10 weeks associated with a drop in serum LH and FSH levels. In long term immunized rat (LIM rats) which had been immunized for more than 3 months, testicular atrophy advanced to a similar extent to that in long term hypophysectomized rats (HX rats). The administration of TP (1 mg/day) sc for 30 days restored spermatogenesis in LIM rats. The simultaneous administration of anti-LH and -FSH sera in addition to TP did not affect the restoration of spermatogenesis in LIM rats. The same TP treatment in HX rats, however, failed to restore spermatogenesis. Spermatogenesis was reinitiated after TP treatment if immunized-hypophysectomized rats received a pituitary isograft. Though the serum PRL level in LIM rats was one fifth of that in normal rats, a 2.5-fold rise in the PRL level was observed after TP treatment. These results suggest that PRL is involved in the process of spermatogenesis.

Animals↗
PubMedDate not supplied

Effects of a 1 per cent hydrocortisone conditioner on the prevention of immediate and late-phase reactions in canine skin.

Ten laboratory beagles were used to determine whether a 1 per cent hydrocortisone conditioner applied topically for three consecutive days would inhibit IgE-mediated immediate and late-phase reactions induced in their skin. The trial was blinded, controlled with the product's vehicle and designed with a crossover. It consisted of three phases: one period without treatment (control phase) and two periods of treatment with either the active ingredient or the vehicle. Immediate and late-phase reactions were induced by the intradermal injection of rabbit anti-canine IgE polyclonal antibodies. Twenty minutes after the intradermal challenge, the diameter of the wheal, but not the erythematous flares, were significantly reduced after the application of the active product. In contrast, IgE-mediated cutaneous late-phase reactions, evaluated by measurements of dermal thickness and eosinophil counts six hours after challenge and the numbers of dermal CD3-positive T lymphocytes after 24 hours, were not reduced by its application.

Administration, Cutaneous↗
PubMed1974

Vascular leakage through intraendothelial channels induced by cholera toxin in the skin of guinea pigs.

Guinea pigs were injected intravenously with Evans blue solution (1/2), 1, 5 and 22 hours after intradermal injection of Vibrio cholerae 569B toxin. Then they were fixed by perfusion with diluted Karnovsky's aldehyde mixture 1(1/2), 5, 10, 15 and 90 minutes later. In some cases, horseradish peroxidase was mixed in the dye solution, and chopped tissue slices were incubated histochemically. Dermal blood vessels from these samples were examined under the electron microscope. The fine structure of the endothelial junctions remained unchanged as compared with controls. However, extended rough surfaced endoplasmic reticulum was observed in the endothelial cells at 30 minutes after the toxin injection, when cutaneous bluing was not marked yet. At 22 hours after toxin injection, endothelial perikarya were filled with prominent Golgi complexes, multivesicular bodies and systems of caveolae and vesicles which coalesced, forming intraendothelial channels after diaphragms disappeared. Endothelial fenestrae were numerous in the attenuated portions.

Animals↗
PubMed1997

The expression of murine cutaneous late phase reaction requires both IgE antibodies and CD4 T cells.

BACKGROUND: Exposure of atopic patients to a specific allergen evokes an immediate response which is followed, in many cases, by a late phase reaction (LPR) some hours later. Here we have examined the immunological mechanisms required for the expression of cutaneous LPR in mice. METHODS: BALB/c mice were immunized by i.p. injection of ovalbumin (OVA) and alum actively or by i.v. injection of anti-OVA IgE monoclonal antibody (mAb) passively. After challenge by intradermal injection of OVA into ears, the changes in ear thickness, the number of eosinophils, and the levels of IL-4 and IFN-gamma protein at the site of antigen challenge were examined. RESULTS: Actively immunized mice developed a biphasic response at the site of OVA injection, while mice passively immunized with IgE anti-OVA mAb displayed a strong early response but no LPR. Cell transfer experiments using BALB/c nu/nu mice revealed that both OVA-specific IgE mAb and OVA-primed CD4 T cells were required to evoke LPR. Moreover, LPR was associated with increased levels of IL-4 production concomitant with reduced IFN-gamma production and was abolished by pretreatment with anti-IL-4 neutralizing mAb. CONCLUSION: It is suggested that murine cutaneous LPR against OVA is a type 2 inflammatory response in which both IgE antibodies and CD4 T cells play an obligatory role.

Animals↗
PubMed1986

Histologic response to intradermal Zyderm and Zyplast (glutaraldehyde cross-linked) collagen in humans.

Biopsies were periodically taken over 6 months from sites injected intradermally with purified bovine collagen, Zyderm collagen implant, and a similar collagen, cross-linked with glutaraldehyde, Zyplast implant. The ultimate fate of the implants differed. Zyderm collagen was dispersed among host collagen fibers and gradually lost the appearance of a cohesive implant. By 90 days, the injected material could not be detected and was presumably resorbed, without becoming colonized by host fibroblasts. In contrast, the cross-linked implant remained as distinct foci for 3 to 6 months accompanied by massing of fibroblasts around the periphery. These fibroblasts subsequently invaded the implant and provoked an inflammatory reaction which replaced the implant by new host collagen. The fine collagen bundles in parallel arrays along with many small blood vessels were deposited in the site formerly occupied by the implant. These findings indicate that Zyplast collagen might provide longer-lasting correction of soft tissue defects.

Absorption↗
PubMed1997

Immunostimulatory effects of a plasmid expressing CD40 ligand (CD154) on gene immunization.

Interaction of CD40 with its ligand (CD154) can induce CD40-bearing APCs to express immune stimulatory accessory molecules that facilitate immune recognition. We evaluated whether a plasmid vector encoding CD154 (pCD40L) could influence the immune response to a transgene protein encoded by coinjected plasmid DNA. We found that coinjection of pCD40L in BALB/c mice enhanced the Ab response to beta-galactosidase induced by i.m. or intradermal injection of placZ, a plasmid DNA vector encoding beta-galactosidase. Furthermore, i.m. or intradermal coinjection of pCD40L with placZ enhanced the generation of CTL specific for P815 cells transfected with placZ. This study indicates that pCD40L can serve as a genetic adjuvant capable of augmenting humoral and cellular immune responses to Ags encoded by plasmid DNA expression vectors.

Adjuvants, Immunologic↗
PubMed2005

A new dendritic cell vaccine generated with interleukin-3 and interferon-beta induces CD8+ T cell responses against NA17-A2 tumor peptide in melanoma patients.

Dendritic cells derived from monocytes cultured in the presence of type I interferon were found to induce efficient T cell responses against tumor antigens in vitro. We vaccinated eight stage III or IV melanoma patients with dendritic cells generated with interferon-beta and interleukin-3, activated by poly I: C, and pulsed with the tumor-specific antigen NA17.A2. This dendritic cell vaccine was well-tolerated with only minor and transient flu-like symptoms and inflammatory reactions at the injection sites. In most patients, isotopic imaging documented dendritic cells (DC) migration from the intradermal injection site to the draining lymph nodes. Finally, mixed lymphocyte-peptide culture under limiting dilution conditions followed by tetramer labeling indicated that three out of eight patients mounted a CD8 T cell response against the NA17.A2 antigenic peptide. We conclude that DC generated in type I-IFN represent an interesting alternative to DC generated in IL-4 and GM-CSF for cancer immunotherapy.

Adult↗
PubMed1998

Effect of granulocyte macrophage-colony stimulating factor on Langerhans cells in normal and healthy atopic subjects.

Granulocyte macrophage-colony stimulating factor (GM-CSF) is a multipotent cytokine produced by many cutaneous cell types including keratinocytes. Langerhans cells (LC) represent the major antigen-presenting cells in skin, and in vitro studies demonstrate that GM-CSF is of pivotal importance in LC. Healthy volunteers (n = 3 non-atopic, n = 3 with atopy) received recombinant human GM-CSF (0. 05 microg/mL) by intradermal injection for 3 days to the same site. Diluent was injected in a similar manner as control. Biopsies were taken 24 h after the final injection and examined immunohistochemically for LC and inflammatory cell markers. Compared with control sites, intradermal GM-CSF resulted in shortening of dendritic cell processes and redistribution of LC in the epidermis; numbers of CD1a + cells in the epidermis were significantly decreased (P < 0.005), while those in the dermis were significantly increased (P < 0.05) following intradermal GM-CSF when compared with controls. Double labelling studies on epidermal CD1a + cells indicated de novo expression of intercellular adhesion molecule (ICAM)-1 and increased expression of HLA-DR following GM-CSF (P < 0. 005, P < 0.005, respectively). Additional findings included a marked mixed inflammatory cell infiltrate in the dermis and increased expression of the endothelial cell adhesion molecules E-selectin and ICAM-1. These data indicate that in normal human skin, GM-CSF induces changes in the phenotype and distribution of CD1a + cells consistent with LC functional maturation and exit from the epidermis to the dermis. As these events are central to the initiation of cutaneous inflammation, GM-CSF may potentially play a critical role in the pathogenesis of inflammatory dermatoses.

Adolescent↗
PubMed1978

Identification of systemic phototoxic drugs by human intradermal assay.

An improved method is presented for the detection of systemically administered photosensitizing drugs in humans. Test agents were injected intradermally in physiologic saline and then exposed to broad spectrum radiation from a Xenon solar simulator. Several clinically recognized photosensitizers were identified by this technique. The activating spectrum depended on the test drug. Sulfonamides and vinblastin were activated by sunburning erythemic radiation (UV-B), while tetracyclines, nalidixic acid and phenothiazines by near UV (UV-A), and chlorothiazide by both. It is suggested that intradermal phototesting offers a means of verifying the phototoxic potential of agents suspected clinically of provoking a photosensitivity eruption.

Adult↗
PubMed1980

Eosinophil response in guinea pig skin to a low molecular weight eosinophil chemotactic factor extracted from livers of mice with schistosomiasis.

A low-molecular weight eosinophil chemotactic factor (ECF-G), isolated and partially purified from livers of mice with schistosomiasis, was injected intradermally into guinea pigs. Biopsies obtained were studied for inflammatory cell accumulation in the injected sites and compared with those in the control sites injected with phosphate buffered saline. Tissue eosinophilia was seen as early as 1 hr after injection of ECF-G, but not in the control site. The increase of eosinophilia appeared biphasic with peaks at 6 and 24 hr. Mast cells increased in both ECF-G and saline injected sites and the increase was still found at 120 hr after injection. Neutrophils also increased in both ECF-G and saline injected sites but disappeared within 48 hr. These findings indicate that ECF-G is a tissue and species nonspecific eosinophil chemotactic factor, and injection of ECF-G initiates interaction of eosinophils and mast cells in the skin.

Animals↗
PubMed2004

Early delayed-type hypersensitivity eosinophil infiltrates depend on T helper 2 cytokines and interferon-gamma via CXCR3 chemokines.

We investigated the role of T helper (Th)1- and Th2-type cytokines in delayed-type hypersensitivity to soluble protein antigens elicited early postimmunization. Mice were sensitized by intradermal injection without adjuvants, or subcutaneously with complete Freund's adjuvant, and subsequently ear challenged intradermally. As soon as day 3, antigen-specific eosinophil-rich responses were elicited in wild-type mice, but not in T-cell receptor-alpha-/- mice without adjuvant. Draining lymph node T cells stimulated with antigen secreted interleukin (IL)-4, IL-5 and interferon-gamma (IFN-gamma). IFN-gamma-dependent specific immunoglobulin G (IgG)2a and IL-4-dependent IgG1 were also generated. Delayed-type hypersensitivity ear swelling and local eosinophil recruitment were decreased in IL-5-/-, IL-4-/- and signal transducer and activator of transcription-6 (STAT-6)-/- mice, and with anti-IL-4 treatment of wild-type mice, suggesting Th2 mechanisms. Interestingly, responses were also decreased in IFN-gamma-/- mice, and IFN-gamma protein and the IFN-gamma-inducible CXC chemokine, IP-10, were present in 24-hr ear tissue extracts, suggesting Th1 effects. Finally, ear swelling, total histology and eosinophils were decreased in mice deficient in CXCR3, the chemokine receptor for IP-10. These results suggest that both a Th2-like (IL-5, IL-4 and STAT-6) and a Th1-like (IFN-gamma, IP-10, CXCR3) pathway contribute to eosinophil recruitment in early delayed-type hypersensitivity.

Animals↗
PubMed1971

Mediators of the inflammation induced in the rat paw by carrageenin.

1. The time course of oedema formation in rats caused by injection of carrageenin into the paw was followed for 5.5 hours. Intact or adrenalectomized rats which had previously been injected with ellagic acid or saliva to reduce considerably the concentration of blood kininogens, or with methysergide to antagonize 5-hydroxytryptamine (5-HT) showed a reduced inflammatory response. It was concluded that kinins and 5-HT contributed significantly to oedema formation during this period.2. Mepyramine alone had no effect on oedema formation, but in combination with ellagic acid treatment, with or without methysergide, it caused a reduction suggesting that histamine played a minor role in oedema formation during the first 3 hours.3. Vascular permeability studies indicated that injection of ellagic acid did not interfere with the normal responses in skin to intradermal injections of histamine, 5-HT, bradykinin or compound 48/80. Mepyramine and methysergide, at the doses used in the carrageenin experiments, completely antagonized histamine and 5-HT, respectively, and did not affect the skin responses of bradykinin.4. Treatment in vivo with ellagic acid or rat saliva was equally effective in reducing plasma kininogen concentrations by an amount equivalent to more than 10 times the quantity of substrate 1 measured by Gautvik & Rugstad (1967).5. Rat saliva, but not ellagic acid, lowered complement levels by approximately 20%.

Animals↗
PubMed1974

Reactions in the periodontium to continuous antigenic stimulation in sensitized gnotobiotic rats.

The purpose of our experiment was to evaluate the destructive potential of a strain of Actinomyces viscosus on the periodontium of sensitized rodents, describing the induced lesions on the basis of quantitative cytology. The experimental design comprised in principle the following procedures. Young germfree rats were immunized either by intravenous or intradermal injections with heat-killed cells of A. viscosus Ny 1 or sham immunized intradermally with physiological saline. After a period suitable for activation of the humoral and cell-mediated immune systems, Ny 1 was monoassociated in all animals by oral implantation. During the ensuing 42 days the animals were allowed to react against the continuous peripheral oral antigen challenge. Since A. viscosus is known as a heavy dental plaque-forming organism, the animals could be expected to develop local immunopathological lesions in the periodontal tissues. These lesions were then studied by quantitative cytology after sampling procedures allowing optimal tissue preservation. The degree of bone loss observed in all treatments was unrelated to the destructive capacity of the infiltrates, suggesting the presence of distinct mechanisms responsible for the activation of osteoclasts and factors interfering with fibroblast activity. Although the cellular composition of the infiltrated tissues was analyzed at the end of the experiment only, distinct stages of the lesions in the different treatments allowed reconstruction of the sequence of events. After an acute inflammatory phase, a classic delayed hypersensitivity reaction developed which was transformed after some time by a large superimposed plasma cell accumulation. The particular but undefined immune status was the significant factor determining the final type of peripheral infiltrative reaction.

Actinomyces↗
PubMed1976

Cutaneous granulomatous response to BCG cell walls with reference to cancer immunotherapy.

A chronic inflammatory response produced by cell walls of Mycobacterium bovis strain BCG associated with microscopic oil droplets (BCG CW-O) was studied with reference to the tumor-regressing ability of this preparation. When BCG CW-O was injected intradermally in the footpads of guinea pigs, intense inflammation developed at the site of injection and in the draining popliteal lymph node. This was characterized histologically as granulomatous inflammation. The intensity of the response was related to the dose of BCG CW-O. Cell walls without oil produced the same type of inflammation but much less in degree. Data are presented that demonstrate the immunological nature of this response and classify it as a cell-mediated immune reaction. Ramifications of this chronic inflammatory reaction occurring at the site of a tumor are discussed.

Animals↗
PubMed1983

Work in progress: radionuclide imaging of indium-111-labeled eosinophils in mice.

Eosinophils isolated from peritoneal exudates were labeled with indium-111-oxine and injected intravenously into sensitized mice. They became localized at sites of inflammation produced by intradermal injections of schistosomal antigen or Toxocara canis larvae, whereas labeled neutrophils did not. Intense uptake of eosinophils by normal spleen, liver, and bone marrow was noted, with tracer distribution effectively complete by 5 hours after injection. Indium-111-eosinophil studies appear to be quite sensitive to parasitic inflammatory reactions; in contrast, nonspecific inflammation such as that induced by turpentine causes localization of eosinophils, but to a lesser extent. This technique may be useful in the study of parasitic and allergic disease.

Animals↗
PubMed2006

Immunologic responses against hydrolyzed soy protein in dogs with experimentally induced soy hypersensitivity.

OBJECTIVE: To assess whether dogs with experimentally induced type I hypersensitivity against soy protein would respond to soy hydrolysate and develop cutaneous or gastrointestinal tract reactions after intradermal and oral challenge exposure. ANIMALS: 12 naïve Beagle pups (9 sensitized and 3 control dogs). PROCEDURE: 9 dogs were sensitized against soy protein by administration of allergens during a 90-day period. After the sensitization period, serum concentrations of soy-specific IgE were determined and an intradermal test was performed to confirm the dogs were sensitized against soy protein. An intradermal challenge test and an oral challenge test with native and hydrolyzed soy protein were conducted on 6 sensitized and 2 control dogs. RESULTS: High serum concentrations of soy-specific IgE and positive results for the intradermal test were observed for the 9 sensitized dogs after completion of the sesitization process. Sensitized dogs challenge exposed with hydrolyzed soy protein had a reduced inflammatory response after intradermal injection and no clinical response after an oral challenge exposure, compared with responses after intradermal and oral challenge exposure with native soy protein. CONCLUSIONS AND CLINICAL RELEVANCE: Soy-sensitized dogs did not respond to oral administration of hydrolyzed soy protein. Thus, hydrolyzed soy protein may be useful in diets formulated for the management of dogs with adverse reactions to food.

Animals↗
PubMed2000

Inhibition of aminopeptidase P potentiates wheal response to bradykinin in angiotensin-converting enzyme inhibitor-treated humans.

Bradykinin is a nonapeptide that contributes to the cardioprotective effects of angiotensin-converting enzyme (ACE) inhibitors. During ACE inhibition, an increased proportion of bradykinin is degraded through non-ACE pathways. Studies in animals suggest that aminopeptidase P (EC 3.4.11.9) may contribute to the metabolism of bradykinin. The purpose of the present study was to determine the contribution of aminopeptidase P to the degradation of bradykinin in humans in the presence and absence of ACE inhibition. To do this, we measured the wheal response to intradermal injection of bradykinin (0, 1, or 10 nicrog) in the presence or absence of intradermal administration of the specific aminopeptidase P inhibitor apstatin (5 or 10 microg) and oral administration of the ACE inhibitor quinapril (10 mg) in six healthy subjects. Both bradykinin (ANOVA; F = 101.18, P <.001) and apstatin alone (F = 7.01, P =.049) caused a wheal of dose-dependent size. There was no significant interaction between apstatin and bradykinin (F = 4.94, P =.175). Pretreatment with 10 mg of quinapril significantly shifted the dose-response curve for bradykinin to the left (effect of quinapril; F = 77.96, P <.001) and there was significant interaction between quinapril and bradykinin (F = 7.82, P =.041). The effect of quinapril was significantly potentiated by coinjection of 10 microg of apstatin (effect of apstatin; F = 21.60, P =.006), such that there was significant interactive effect of quinapril and apstatin (F = 20.83, P =.006) on the wheal response to bradykinin. Collectively, these data suggest that aminopeptidase P plays a minor role in the degradation of bradykinin in human skin in the absence of ACE inhibition but contributes significantly to the degradation of bradykinin in the presence of ACE inhibition.

Adult↗