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PubMedDate not supplied

A new experimental model of systemic connective tissue disease in immunized rabbit.

In rabbit, the immumizations with whole Mycobacterium Tuberculosis injected intradermally and its crude cytoplasmic W.S.E. injected intraarticulary induce not only a self-perpetuating synovitis in the stimulated knee but also chronic systemic lesions of connective tissue (non-stimulated knee, both shoulders, aortic artery adventitial valvular endocardium, liver, kidneys and lungs). W.S.E. stimulates precipitating antibody synthesis, skin reaction and lymphoblastic transformation of lymphocytes in vitro. Furthermore, rabbits develop tuberculin skin test and lymphocytic response to P.P.D. The intensity of inflammation in stimulated knee is in direct ratio to intensities of humoral and cellular immunological responses. On the contrary, the incidence of systemic lesions is in inverse ratio to immune responses and intensity of inflammation in stimulated knee.

Animals↗
PubMed1994

[Selected elements of biological activity of circulating immune complexes in serum of patients with atopic diseases. I. Ability to injure guinea pig tissue by injecting atopic patient plasma].

Serum level was measured of circulating complexes (SpA binding method-CIC/SpA) in pollen and house dust mite sensitive patients during specific immunotherapy. Histopathological changes in guinea pigs skin after the intradermal injection of patients serum have been studied. Differences were demonstrated in the observed patho-morphological changes in relation to CICs/SpA serum concentrations.

Allergens↗
PubMed1988

Tolerogenic activity of polymerized type II collagen in preventing collagen-induced arthritis in rats.

Rats were exposed parenterally or pergastrically to polymerized type II collagen (POLCII) and became resistant to the subsequent induction of disease with arthritogenic type II collagen (CII) administered intradermally in Freund's incomplete adjuvant (FIA). POLCII was prepared by cross-linking native soluble arthritogenic CII, from bovine nasal septal cartilage, with glutaraldehyde. POLCII injected intradermally in FIA did not induce arthritis. Animals treated in this manner were resistant for a period of at least 100 days to induced disease. The change in the properties of the CII from an arthritogen to a tolerogen was related to the amount of glutaraldehyde (used to polymerize the CII) which was assumed to control the extent of cross-linking of the CII. Highly cross-linked POLCII administered pergastrically, like soluble CII, was not arthritogenic but was tolerogenic, inducing a state of unresponsiveness to a challenge with arthritogenic CII. In general serum anti-CII antibody levels were higher in arthritic than in tolerized non-arthritic rats. It is concluded that the breaking of self-tolerance to CII depends upon its physical state. When polymerized and insoluble, a form analogous to that in which it exists naturally, it is tolerogenic.

Animals↗
PubMed2001

Functional caspase-1 is required for Langerhans cell migration and optimal contact sensitization in mice.

Langerhans cell (LC) migration from epidermis to draining lymph node is a critical first step in cutaneous immune responses. Both TNF-alpha and IL-1 beta are important signals governing this process, but the potential regulatory role of IL-1 alpha processing by caspase-1 is unknown. In wild-type (WT) mice, application of the contact allergens 2,4-dinitrofluorobenzine and oxazolone lead to a marked reduction in epidermal LC numbers, but in caspase-1-deficient mice this reduction was not observed. Moreover, although intradermal injection of TNF-alpha (50 ng) induced epidermal LC migration in WT mice, this cytokine failed to induce LC migration in caspase-1-deficient mice. Intradermal IL-1 beta (50 ng) caused a similar reduction in epidermal LC numbers in both WT and caspase-1-deficient mice, indicating that, given an appropriate signal, caspase-1-deficient epidermal LC are capable of migration. Contact hypersensitivity to both 2,4-dinitrofluorobenzine and oxazolone was inhibited in caspase-1-deficient mice, indicating a functional consequence of the LC migration defect. In organ culture the caspase-1 inhibitor Ac-YVAD-cmk, but not control peptide, potently inhibited the epidermal LC migration that occurs in this system, and reduced spontaneous migration of LC was observed in skin derived from caspase-1-deficient mice. Moreover, Ac-YVAD-cmk applied to BALB/c mouse skin before application of contact sensitizers inhibited LC migration and contact hypersensitivity in vivo. Taken together, these data indicate that caspase-1 may play a central role in the regulation of LC migration and suggest that the activity of this enzyme is amenable to control by specific inhibitors both in vivo and in vitro.

Administration, Cutaneous↗
PubMed1989

Effect of topically applied local anaesthesia on histamine flare in man measured by laser Doppler velocimetry.

The direct and indirect effects of histamine on the cutaneous microvasculature were measured by laser Doppler velocimetry. Histamine (6.51 x 10(-4) M) was injected intradermally into the forearms of eight healthy subjects following treatment with a topically applied local anaesthetic cream (EMLA) or equivalent placebo. The blood flow at the injection site (0 cm) and at 1 and 2 cm proximally was measured by laser Doppler velocimetry over 80 minutes. Analysis of the changes in magnitude of the hyperaemic responses with time showed no difference at the 0 and 1 cm sites, but a marked reduction was found at the 2 cm site following EMLA treatment (p less than 0.05). At all three sites the decay of the histamine-induced hyperaemia was faster following EMLA treatment than with placebo (p less than 0.04). The experiments showed that the indirect effect of histamine on the cutaneous microvasculature in the peripheral flare around the injection site was greatly diminished by prior application of EMLA cream and this supports the neurogenic hypothesis: pre-treatment with EMLA cream did not affect the development of hyperaemia and oedema at the site of histamine injection where the mediator acts directly on the cutaneous microvasculature.

Administration, Cutaneous↗
PubMedDate not supplied

YKL-39, a human cartilage-related protein, induces arthritis in mice.

OBJECTIVE: To determine whether YKL-39, a recently cloned secretory protein of articular chondrocytes, is arthritogenic in mice. METHODS: Recombinant YKL-39 (rYKL-39) was expressed and purified from E. coli. To induce arthritis in mice, rYKL-39 (1, 10 or 50 g in Freund's incomplete adjuvant) was injected into the right footpad of mice from four different strains (BALB/c, DBA/1J, C57BL/6 and ICR). The mice received a second immunization with rYKL-39 by intradermal injection into the root of the tail 10 days after the first immunization. Severity of arthritis was assessed by scoring each paw on a scale from 0 to 4. Sixty days after thefirst immunization, the mice were sacrificed and the joints were examined by immunohistochemistry and radiography. The anti-YKL-39 and anti type II-collagen (CII) antibody titres were also assayed using ELISA. RESULTS: Immunization with YKL-39 induced arthritis in all strains of mice tested, among which BALB/c was most susceptible. Histological examination showed synovial proliferation and irregularity of the cartilage surface in YKL-39-injected BALB/c mice. Moreover radiographic analysis revealed pathological changes in these mice. The YKL-39-immunised mice produced not only anti-YKL-39 antibody but also antibody against type II collagen, suggesting a spreading of autoimmunity after YKL-39. CONCLUSIONS: YKL-39, a cartilage-related protein, is found to induce arthritis accompanied by pathologic changes in bone and cartilage. A better understanding of the immune response against cartilage-related components including YKL-39 may help to elucidate the pathological processes of arthritic disorders.

Adipokines↗
PubMed2000

Role of P-selectin in the migration of neutrophils to chemoattractant-induced cutaneous inflammation in mice.

The role of P selectin in the accumulation of neutrophils at acute dermal inflammatory sites induced by chemoattractants, LTB4 and IL-8 was investigated in the mouse. A mouse P-selectin-human IgG chimera bound to mouse neutrophils in vitro in a calcium-dependent manner, as detected by flow cytometry. A rat monoclonal antibody (mAb) against mouse P-selectin, RB40.34 abolished P-selectin-IgG chimera binding to mouse neutrophils, but a control antibody did not. Intradermal injection of LTB4 at a dose of 100 ng/site caused neutrophil accumulation to increase by 3-4 fold, as detected by measuring myeloperoxidase activity. Neutrophil extravasation to perivascular tissue was detected by histochemical observation. The intravenous injection of RB40.34 or the specific LTB4 antagonist, SM-15178, at doses at 5 mg/kg attenuated the accumulation of neutrophils by 55.6% and 70.3%, respectively, but a control antibody showed no effect. Similarly, intradermal administration of IL-8 at a dose of 5 microg/site induced significant neutrophil migration into the interstitial tissue of the skin, as followed by measuring myeloperoxidase activity and histopathologic analysis. The intravenous injection of RB40.34 at a dose of 5 mg/kg reduced the neutrophil accumulation by 59.2% in contrast, a control antibody showed no effect. To our knowledge, this is the first direct demonstration that P-selectin plays a substantial role in LTB4- and IL-8-induced neutrophil accumulation in mouse skin.

Animals↗
PubMed1979

Collagen-induced arthritis in rats. Evaluation of early immunologic events.

When rats were injected intradermally with an oil emulsion of native type II collagen, they developed an inflammatory polyarthritis. The incidence and severity of arthritis increased as the amount of collagen injected was increased. Rats 4 1/2 weeks old were the most susceptible to the development of arthritis, whereas weanling and older animals were relatively resistant. There was no difference in incidence between males and females. Mononuclear cells from peripheral blood, lymph nodes, and spleen were cultured with type II collagen and responded maximally to a collagen concentration of 25 microgram/ml. The earliest detectable response was in peripheral blood mononuclear cell cultures obtained 6 to 8 days after immunization. The response of lymph node and spleen cells tended to lag behind that of peripheral blood cells at the earlier time intervals. Antibodies were detected in sera by hemagglutination at 8 days postimmunization. Quantitation of IgM and IgG antibodies by radioimmunoassay showed good correlation with hemagglutination titers and increased binding of collagen by both classes of antibody in arthritic as compared to nonarthritic animals. It is clear that the development of both humoral and cellular immunity to type II collagen is associated with the development of arthritis and may be important in the pathogenesis of this disease.

Age Factors↗
PubMed1994

Local analgesic and vascular effects of intradermal ropivacaine and bupivacaine in various concentrations with and without addition of adrenaline in man.

Ropivacaine, a new long-acting amino-amide local anaesthetic agent, and bupivacaine, in various concentrations with or without addition of adrenaline, were tested in a randomized, double-blind study using intradermal wheals. Ten non-smoking, healthy, young male volunteers participated. In series I plain solutions of ropivacaine (0.25%, 0.5%, 0.75% and 1%) and bupivacaine (0.25%, 0.5% and 0.75%) were injected intradermally and in series II the same concentrations, with the addition of adrenaline 5 ug.ml-1 (1:200,000), were used. The same volunteers took part in both series, with an interval of at least three weeks between the experiments. Saline was included as control in both series. Pin-pricking was used to assess the dermal analgesia. Plain solutions of ropivacaine produced significantly longer durations of dermal analgesia than did plain solutions of bupivacaine, in all tested concentrations. A significant increase in duration was seen for both local anaesthetics when adding adrenaline. Local vascular effects at the injected areas were determined by visual inspection (nil, pink, pale). Local blanching (pale) was significantly more frequent for plain solutions of ropivacaine, in all tested concentrations. Local redness (pink) was significantly more frequent with plain bupivacaine, in a dose-dependent relation. An initial redness was frequently observed for both local anaesthetics containing adrenaline, followed by blanching at most sites.

Adult↗
PubMed2001

Effects of intradermally administered plasmid deoxyribonucleic acid on ovine popliteal lymph node morphology.

In the last decade it has become apparent that bacterial deoxyribonucleic acid (DNA) is recognized as a "danger signal" by the mammalian immune system. To investigate this interaction, sheep were injected intradermally two centimeters distal to the lateral prominence of the fibular head with 400 microg of purified plasmid DNA. Over a 28-day period ultrasound measurements indicated a progressive increase in size of both plasmid and saline (controls) treated popliteal lymph nodes and at Day 30 macroscopic and histological measurements of the lymph nodes were determined. Compared with the contralateral control lymph nodes, plasmid exposed lymph nodes were heavier (2.8 +/- 0.1g vs. 2.0 +/- 0.6 g) and displayed prominent histological changes in the cortex and medulla. Average medullary cord thickness (114.2 +/- 25.2 microm) and the average distance across medullary sinuses (64.4 +/- 2.5 microm) were significantly greater after plasmid exposure relative to contralateral controls (62.7 +/- 14.9 microm and 36.5 +/- 1.0 microm, respectively). Total number of germinal centers (71.4 +/- 17.7) and the total area of germinal centers (4.0 +/- 1.3 mm(2)) within the cortex of popliteal lymph nodes exposed to plasmid were also significantly greater than the controls (40.4 +/- 11.4 and 1.6 +/- 0.5 mm(2), respectively). Our results demonstrate that a single exposure to plasmid DNA has long term effects on regional lymph node weight and morphology.

Animals↗
PubMed1969

Studies on the sensitization of animals with simple chemical compounds. XI. The fate of labeled picryl chloride and dinitrochlorobenzene after sensitizing injections.

The fate of (14)C-labeled allergens injected intradermally into guinea pigs, namely picryl chloride (PCl*) and 2:4 dinitrochlorobenzene (DNCB*), was followed during the induction period of delayed hypersensitivity. Both chemicals were applied in a single injection into one ear in amounts that approached their minimal sensitizing doses (PCl, 0.25 microg; DNCB, 5.0 microg). Radioactivity in the various tissues was determined by liquid scintillation counting after combustion of tissues to CO(2) and H(2)O. The injected allergens seemed to leave the injection site in three phases. A large proportion of allergen escaped rapidly from the ear, about 50% within 3 hr in the case of PCl, within 15 min for DNCB, the difference probably reflecting their unequal reaction constants. Initially there was a "half-life" escape in 2.5 hr with injected dosage of 0.25 microg PCl and in 18 hr for 5.0 microg DNCB. This escape occurred via the regional veins and not via the lymphatics. Radioactive decomposition products of the allergens were already present in the urine within 3-4 hr. After 6-8 hr, the half-life time of escape lengthened to approximately 28 hr for both allergens used in their respective initial dosages, holding up to 2 days after which there occurred still further slowing; between 2 and 4 days the time was about 43 hr for PCl, much longer (72-88 hr?) for DNCB, apparently reflecting different physicochemical properties of this second fraction. Sensitization seemed to be connected with the portion that was present between 12 hr and 4 days of the induction period. It is not known how far the escape of radioactivity during this period may represent gradual hydrolysis of attached picryl and dinitrophenyl groupings, respectively, to form picric acid and dinitrophenol. Gradual accumulation of the second fraction in the regional lymph nodes could definitely be excluded. It was noted that no hypersensitivity arose and essentially no depot of radioactivity existed between 12 hr and 4 days when DNCB was injected in a dose of 0.25 microg, owing to its ready escape from the ear; but 20 times as much DNCB caused sensitization and provided about the same fixed depot as 0.25 microg of picryl chloride. After delayed hypersensitivity had been established, traces of radioactivity were still measurable at the site. This third fraction, probably representing a different coupling product, escaped at a very low rate and was traceable up through several weeks. No demonstrable radioactivity could be detected in thymus, spleen, and mesenteric nodes when examined at short intervals between (1/2) min and 17 days. In analogy with findings on transplantation "immunity" and with studies reported in the following paper, the induction of delayed hypersensitivity can be explained by encounters between lymphoid cells and the hapten complex which is found present in the local site for 4 days, in agreement with Medawar's concept of peripheral sensitization.

Allergens↗
PubMed1993

Effects of intradermal lignocaine and mepivacaine on human cutaneous circulation in areas with histamine-induced neurogenic inflammation.

The vasoconstrictive potencies of lignocaine and mepivacaine were studied in human skin. Lignocaine 0.5%, 0.25% mepivacaine (both plain and mixed with adrenaline or ornipressin), and saline (control) were injected intradermally into skin areas with enhanced perfusion (1% histamine prick). Flux was determined by scanning laser Doppler flowmetry and the size of any eventual pallor was measured. The artificially enhanced flux was increased further by saline, but not altered by the local anaesthetics. Mepivacaine produced a small pallor. Both vasoconstrictors reduced flux significantly and produced a larger pallor. We conclude that both local anaesthetics have only a mild constrictive effect on precapillary vessels. Mepivacaine has, additionally, a constrictor effect on the postcapillary vascular bed, causing pallor. An effective precapillary constriction which reduces the capillary clearance of both local anaesthetics can be achieved only by addition of a vasoconstrictor.

Adult↗
PubMed1991

PMMA microspheres for intradermal implantation: Part I. Animal research.

In search of a biocompatible implant for the correction of small deficiencies within the dermal corium as in wrinkles and acne scars, polymethylmethacrylate (PMMA) microspheres, 10 to 63 microns in diameter, were dispersed in Tween 80 medium and injected intradermally and subdermally into the abdominal skin of rats. Histological examination of specimens for up to 7 months revealed a modest tissue reaction, forming a delicate fibrous capsule around each individual microsphere within 4 months. Foreign body giant cells were seen rarely (in up to 1.5% of all cells). No break-down, corrosion, or phagocytosis of the spheres was observed at 7 months. The Tween 80 dispersion medium did not produce any histologically detectable reaction. Because PMMA products (Paladon, Palacos) have been used in medicine for almost 50 years without causing biological degradation or cancer, the material may be applied safely in the form of microspheres (Arteplast) in corium and subcutis of human patients with wrinkles or acne scars.

Animals↗
PubMed2006

Imaging of lymphatic vessels in breast cancer-related lymphedema: intradermal versus subcutaneous injection of 99mTc-immunoglobulin.

OBJECTIVE: The disordered physiology that results from axillary lymph node clearance surgery for breast cancer and that leads to breast cancer-related lymphedema is poorly understood. Rerouting of lymph around the axilla or through new pathways in the axilla may protect women from breast cancer-related lymphedema. The aim of the study was to compare intradermal with subcutaneous injection of technetium-99m ((99m)Tc)-labeled human polyclonal IgG (HIG) with respect to lymphatic vessel imaging. MATERIALS AND METHODS: Six women with breast cancer-related lymphedema underwent unilateral upper limb lymphoscintigraphy, using a web space injection of (99m)Tc-labeled HIG, after intradermal and subcutaneous injections on separate occasions. Multiple sequential images were obtained of the affected upper limb and torso over 3 hr on each occasion. Accumulation of activity in blood was quantified from venous blood samples taken from the opposite arm. RESULTS: Imaging after intradermal injection clearly showed discrete lymphatic vessels in five of six patients, in contrast to imaging after subcutaneous injection, which did not show any discrete vessels in any patient. Intradermal injection resulted in more rapid visualization of cutaneous lymph rerouting than subcutaneous injection in six of six patients. Recovery of injected (99m)Tc-labeled HIG in venous blood was greater after intradermal injection in six of six patients. CONCLUSION: In patients with breast cancer-related lymphedema, lymphatic vessels are more clearly depicted after intradermal than subcutaneous injection as a result of direct access of radiotracer to dermal lymphatics. This finding has implications for imaging lymphatic vessel regeneration and lymph rerouting.

Adult↗
PubMed1993

Skin responses to bradykinin, kallidin, and [desArg9]-bradykinin in nonatopic and atopic volunteers.

BACKGROUND: Kinins are potent vasoactive oligopeptides that may act as mediators in a variety of inflammatory diseases of the skin by interacting with specific receptors designated B1 and B2. In this study we have investigated the structure-activity relationship of intradermally injected bradykinin, kallidin (lysine-bradykinin), and [desArg9]-bradykinin in atopic (n = 8) and nonatopic (n = 8) subjects. METHODS: On two separate occasions, each separated by a week, subjects randomly underwent intradermal challenge with incremental doses (0.5, 5, and 50 nmol) of either the B1-agonist [desArg9]-bradykinin, the B2-agonists bradykinin or kallidin, or vehicle placebo. In a separate randomized double-blind study we have also examined the effect of an orally administered antihistamine, terfenadine, on kinin-induced wheal and flare responses and their repeatability in a group of nine volunteers. The skin responses were monitored objectively by measurement of wheal and flare areas. RESULTS: Both bradykinin and kallidin induced a dose-dependent increase in wheal and flare areas in all subjects studied. Although the effects of the two lowest doses (0.5 and 5 nmol) of [desArg9]-bradykinin on skin responses were indistinguishable from those of placebo, this kinin at the highest dose administered (50 nmol) caused a significant increase in wheal and flare areas in all subjects studied. No difference could be identified in the skin responses to kinins between atopic and nonatopic subjects. In addition kinin-induced cutaneous responses were not altered by pretreatment with terfenadine. CONCLUSIONS: These in vivo structure activity studies suggest that in human beings the skin responses to kinins may be compatible with the stimulation of B2 receptors, which is unrelated to histamine release from cutaneous mast cells.

Adult↗
PubMed1991

Potent vasoactive properties of endothelin 1 in human skin.

The effect of the endothelial cell-derived peptide endothelin 1 was investigated in human skin. Intradermal injection of endothelin 1 (1-100 pmol) caused a dose-dependent area of pallor that was associated with a significant reduction in basal skin blood flow, measured by laser-Doppler blood flowmeter (with 1 pmol endothelin, P = 0.012, analysis of variance). The coadministration of endothelin 1 (1-100 pmol) with the neuropeptide vasodilator calcitonin gene-related peptide (CGRP) inhibited the vasodilator response to CGRP (10 pmol) by up to 82.7 +/- 9.2% (with 100 pmol endothelin, P less than 0.001). The response of the prostanoid vasodilator prostaglandin E2 (10 pmol) was inhibited by endothelin in a similar manner. In addition to the vasoconstrictor effects, endothelin 1 produced a dose-dependent flare that surrounded the area of pallor, and this was associated with a significant increase in blood flow (P less than 0.05) within the flare area. The H1 antagonist terfenadine (120 mg po) significantly reduced the flare area associated with endothelin 1: flare 5 min after intradermal endothelin (10 pmol, placebo treated), 668 +/- 405 mm2; terfenadine treated, 201 +/- 257 mm2 (P less than 0.05). The flare was also significantly attenuated when endothelin (10 pmol) was injected into local anesthetic-treated skin. Thus intradermal injection of endothelin in humans causes long-lasting vasoconstriction at the site of injection and a surrounding flare. Results suggest that the flare component is partially histamine dependent and the result of an axon reflex. This study demonstrates the potent activity of endothelin in human skin. It is possible that endothelin could be relevant to the local response of skin to injury.

Adult↗
PubMed2000

Computer-assisted infrared thermographic study of axon reflex induced by intradermal melittin.

The aim of the present study was to investigate whether melittin, the principal toxin of the honeybee (Apis mellifera) venom, can be used as an algogenic agent in the study of pain in humans. Five micrograms of melittin in 0.5 ml of saline was intradermally injected into the volar aspect of the forearm. Resultant pain was scored by a visual analogue scale (VAS), and skin temperature change was analyzed by means of a computer-assisted infrared thermography. Intradermal melittin temporarily produced severe pain, followed by a sustained increase in skin temperature. The skin temperature increase peaked in about 10 min and outlasted 1 h. Topical application of 10% lidocaine gel did not significantly suppress the melittin-induced pain, but markedly suppressed both the increase in the peak temperature and the area of temperature increase. In conclusion, 5 microg of melittin is sufficient to produce pain in humans and 10% lidocaine gel differentially decreases the melittin-induced axon reflex without any significant analgesic effect.

Administration, Topical↗
PubMed1966

The local training effect of secretory activity on the response of eccrine sweat glands.

1. The influence of repeatedly raising the body temperature by radiant heat to a level at which acclimatization to heat is normally acquired was investigated in two series of experiments, the first without the subjects sweating, the second with sweating.2. In a second investigation local sweat-gland activity was induced by drug injections on successive days without raising the body temperature.3. These experiments show that the increased sweating capacity characteristic of acclimatization to heat is a result of sweat-gland activity and does not appear to be induced by or to depend on an elevated body temperature.4. Secretory activity results in a loss of glycogen from sweat-gland cells on the first day of heat exposure but not after the glands have been ;trained' by acclimatization to heat.5. The state of acclimatization has no influence on the threshold concentration of acetylcholine required to elicit sweating when injected intradermally.

Acclimatization↗