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PubMed1992

Real-time measurement of microcirculation of skin by reflectance spectrophotometry.

A reflectance spectrophotometric measurement was developed to analyze the microcirculation of the skin in real time. The relative absorption (RA) spectra were obtained from skin tissue 10 times per second using a spectro-multi-channel-photodetector system. In this system, white light was projected onto the skin of the back of the anesthetized rat and the spectrum of the reflected light between 450 and 643 nm was analyzed. Two absorption peaks at wavelengths of about 540 and 577 nm were observed, corresponding to the absorption peaks in the oxyhemoglobin (HbO2) spectrum. Either phlebotomy or the i.v. injection of norepinephrine (NE) reduced the RA spectrum. Peaks of the reduction in spectrum [(RA spectrum before the treatment) - (RA spectrum after the treatment)] were observed at about 540 and 577 nm. Injection of NE (0.75-48 ng/100 g B.W., i.v.) reduced the RA value at 577 nm dose-dependently, suggesting a decrease in the skin blood flow due to vasoconstriction. In addition, the content of HbO2 and capillary permeation were measured at the same time after the i.v. injection of Evans blue (EB) dye. As indices of HbO2 content and capillary permeation, RA changes at 540 and 610 nm (the latter is an absorption peak in the EB spectrum) were measured in real time, respectively. Both RA values increased dose-dependently after the intradermal injection of histamine (0.3-100 micrograms/site), suggesting the presence of vasodilation and an increase in permeability. The time at which the RA value for HbO2 reached a maximum was shorter than that for EB. These observations suggest that the method described here can detect changes in the HbO2 content and permeation of skin microcirculation at the same time, and in real time.

Animals↗
PubMed1990

Evidence that a receptor-operated event on the neutrophil mediates neutrophil accumulation in vivo. Pretreatment of 111In-neutrophils with pertussis toxin in vitro inhibits their accumulation in vivo.

The role of neutrophil chemoattractant receptors in neutrophil stimulation in vitro is well established, however, the precise mechanisms underlying local neutrophil accumulation at inflammatory sites in vivo have not been defined. A fundamental question that remains open is whether chemoattractants act on the endothelial cell or the neutrophil to initiate the process of neutrophil migration in vivo. To address this question we have investigated whether neutrophil accumulation in vivo can occur if chemoattractant receptor occupancy is uncoupled from neutrophil stimulation. For this purpose we have used pertussis toxin (PT) as the pharmacologic tool. We have investigated the effect of in vitro pretreatment of rabbit neutrophils with PT on their responses in vitro and on their accumulation in vivo. Pretreatment of rabbit neutrophils with PT inhibited FMLP- and C5a-, but not PMA- induced increases in CD18 expression, neutrophil adherence, and degranulation in vitro. This pretreatment procedure with PT inhibited the accumulation of radiolabeled neutrophils in vivo in response to intradermally injected FMLP, C5a, C5a des Arg, leukotriene B4, IL-8, and zymosan in rabbit skin. Further, in contrast to the in vitro results, PT inhibited the PMA-induced 111In-neutrophil accumulation in vivo. Interestingly, pretreatment of neutrophils with PT also inhibited accumulation in response to intradermally injected IL-1, despite the reports that IL-1 lacks neutrophil chemoattractant activity in vitro. Although the experimental techniques used cannot distinguish the different stages of neutrophil migration involved, these results suggest that the accumulation of neutrophils induced by local extravascular chemoattractants in vivo depends on a pertussis toxin-sensitive receptor operated event on the neutrophil itself. Further, PMA and IL-1 may release secondary chemoattractants in vivo.

Animals↗
PubMed2002

Antigen-specific and persistent tuberculin anergy in a cohort of pulmonary tuberculosis patients from rural Cambodia.

Purified protein derivative (PPD) skin testing is used to identify persons infected with Mycobacterium tuberculosis (Mtb) and to assess cell-mediated immune responses to Mtb. However, lack of skin induration to intradermal injection of PPD or PPD anergy is observed in a subset of patients with active tuberculosis (TB). To investigate the sensitivity and persistence of PPD reactivity and its in vitro correlates during active TB disease and after successful chemotherapy, we evaluated the distribution of skin size induration after intradermal injection of PPD among 364 pulmonary TB patients in Cambodia. A subset of 25 pulmonary TB patients who had a positive skin reaction to mumps and/or candida antigens showed persistent anergy to PPD after successful completion of TB therapy. Strikingly, in vitro stimulation of T cells from persistently anergic TB patients with mumps but not PPD resulted in T cell proliferation, and lower levels of IL-2 and IFN-gamma and higher levels of IL-10 were detected in PPD-stimulated cellular cultures from PPD-anergic as compared with PPD-reactive pulmonary TB patients. These results show that anergy to PPD is antigen-specific and persistent in a subset of immunocompetent pulmonary TB patients and is characterized by antigen-specific impaired T cell proliferative responses and a distinct pattern of cytokine production including reduced levels of IL-2.

Adult↗
PubMed1997

Phase I/IB study of immunization with autologous tumor cells transfected with the GM-CSF gene by particle-mediated transfer in patients with melanoma or sarcoma.

The objective of this Phase I study is to assess the acute and long-term toxicities of intradermal vaccination of cancer patients with lethally-irradiated tumor cells that have been transfected by particle-mediated gene transfer (PMGT) with gold particles coated with human granulocyte-macrophage colony stimulating factor (GM-CSF) DNA in a plasmid expression vector. The GM-CSF DNA-coated gold particles are delivered to tumor cells using helium pressure with a hand held gene delivery device. Preclinical studies have demonstrated that vaccination of mice with irradiated, GM-CSF-transfected melanoma cells provided protection from subsequent challenges with non-irradiated, non-transfected tumor cells. Ongoing human tumor immunotherapy studies use patients' melanoma or renal carcinoma cells transfected with a retroviral vector containing GM-CSF cDNA as a vaccine to elicit anti-tumor immune responses. PMGT transfection, unlike retroviral transfection, does not require tumor cells to proliferate in vitro to undergo gene transfer. Instead, tumor tissue can be dissociated into small tissue clumps or cell aggregates and then immediately transfected using the gene gun. PMGT physically inserts the DNA without the need for cell surface interaction with viral components or exposure of the patient to viral antigens. As described in this protocol, fresh human sarcoma and melanoma specimens can be transfected with the GM-CSF DNA-coated gold particles with subsequent production of biologically active GM-CSF protein. In this study tumor tissue will be obtained from patients with melanoma or sarcoma. Tumor tissue will be dissociated, irradiated, and transfected with GM-CSF DNA by PMGT. In this ascending dosage study, two dose levels of GM-CSF DNA will be studied in 2 groups of 6 patients each. Patients will receive two intradermal injections of the irradiated, transfected tumor in a single extremity. On days 3 and 14 post-vaccination, patients will undergo surgical excision of the vaccination sites to assess GM-CSF production and infiltration of immune effector cells. On Day 25, patients will undergo DTH testing with intradermal injection in their opposite extremity of 5 x 10(6) irradiated non-transfected autologous tumor cells cryopreserved at the time of vaccine preparation. This injection site will be assessed on day 28 post-vaccination and surgical excision of the DTH testing site will be performed on day 28 if a positive reaction is noted. The patients will be observed for local and systemic toxicity on days 2, 3, 5, 8, 14, 25, and 28 after the vaccination. Restaging of the patients' disease and long term toxicity evaluation will be performed at 3, 6, and 12 months and then yearly.

Animals↗
PubMed1995

Assessment of cutaneous sensory and autonomic axon reflexes in rheumatoid arthritis.

OBJECTIVE: To assess sensory function in skin overlying the joints of patients with rheumatoid arthritis, in relation to the pain and tenderness which commonly arises in structures not directly involved in the inflammatory process. METHODS: An intradermal injection of capsaicin 0.05 microgram in 10 microliters was made over the wrists and forearms of 40 patients with rheumatoid arthritis and 46 control subjects. Axon reflex vasodilatation was measured using laser Doppler flowmetry. Cholinergic sympathetic function was assessed by measuring axon reflex sweating induced by a single intradermal injection of nicotine 0.5 microgram in 0.1 ml. RESULTS: Capsaicin induced axon reflex vasodilation over the wrists was found to decrease with age in normal subjects (r = -0.62, p < 0.001). In patients with rheumatoid arthritis, capsaicin induced axon reflex vasodilatation was significantly greater over the wrists, but not the forearms, when compared with age matched normal controls (p < 0.01). A minimal correlation between axon reflex vasodilatation and visual analogue pain score was apparent in the rheumatoid group (r = -0.37, p < 0.05). Nicotine induced sweating responses were similar in the rheumatoid and normal groups, and both showed a linear age related decline. CONCLUSIONS: The results show a selective increase of capsaicin induced vasodilatation in skin overlying joints in patients with rheumatoid arthritis. This suggests that the activity of a sub-population of periarticular small sensory fibres is altered, which may explain, at least in part, some of the clinical findings in this disorder.

Adult↗
PubMed1983

[Tuberculin screening and BCG vaccination in primary school children in the Bas-Rhin in 1976/1977].

A campaign of tuberculin testing in standard fashion, followed by BCG vaccination in those giving an inadequate reaction, was carried out on all children in the Bas-Rhin department in France in their first primary school year for the year 1976-1977. Of 15,560 pupils enrolled 64.5 percent had already had at least one BCG vaccination. 12,820 had the standard test, the remaining 2,740 were either absent or parents refused permission. 27.8 percent of those vaccinated had an indurated area of more than 4 mm diameter, compared to 7.4 percent among those not vaccinated. 9,517 children were vaccinated or revaccinated during the campaign, by means of scarification of intradermal injection. 4,472 had a standard post-vaccine test during the following school-year: a diameter of induration of 4 mm or less was found in 28.9 percent. The proportion varied according to the doctors who had vaccinated them but was lower among the children vaccinated by intradermal injection.

BCG Vaccine↗
PubMed1993

Airway allergy to trimellitic anhydride in guinea pigs: different time courses of IgG1 titer and airway responses to allergen challenge.

BACKGROUND: Trimellitic anhydride (TMA) is a low molecular weight chemical that may cause occupational asthma in human beings. The objectives of this study were to determine the time course of immune and airway responses to TMA in guinea pigs and to relate the immunologic response to the immediate responses in lung resistance (RL) and plasma exudation induced by allergen challenge. METHODS: We studied the effects of time course after sensitization on airway response to TMA in guinea pigs actively sensitized to free TMA, given by intradermal injection (0.1 ml of 0.3% TMA in corn oil). During weeks 1, 2, 3, 5, and 8 after sensitization, anesthetized animals were challenged with TMA conjugated to guinea pig serum albumin (TMA-GPSA), instilled via the airway route. Nonsensitized animals were challenged with the same amount of conjugate 4 weeks after intradermal injection of corn oil only. In the same animal, we measured both RL to monitor airflow obstruction and extravasation of Evans blue dye (20 mg/kg) to quantify airway plasma exudation. RESULTS: Instillation of TMA-GPSA (0.5%; 50 microliters) into the tracheal lumen caused a significant increase in RL, reaching a maximum at 2.5 minutes after the instillation in the 1-week group (9.0 +/- 5.9 cm H2O/ml/sec) and between 5 and 6 minutes in the 2-, 3-, 5-, and 8-week groups (9.4 +/- 4.8, 12.7 +/- 5.5, 3.7 +/- 1.1, and 1.7 +/- 0.2 cm H2O/ml/sec, respectively). The maximal increase in RL after the challenge in nonsensitized animals was 0.39 +/- 0.05 cm H2O/ml/sec. TMA-GPSA also produced significant extravasation of Evans blue dye at all airway levels in the sensitized groups, and the amount of dye in the peripheral airways was significantly greater than that in the trachea. Furthermore, the level of Evans blue dye in airway tissue increased with the time after sensitization, up to the latest time point tested (8 weeks). Specific IgG1 antibodies to TMA-GPSA demonstrated by ELISA were detected in all animals in the 3-, 5-, and 8-week groups, with maximal levels 5 weeks after sensitization. Specific IgG1 titers to TMA-GPSA significantly correlated with the level of Evans blue dye induced by challenge with TMA-GPSA but not with the increase in RL. CONCLUSIONS: Intradermal sensitization to free TMA induces specific airway allergy for a long period after sensitization. Specific IgG1 antibodies to allergen may influence allergen-induced plasma exudation rather than the airflow obstruction in this animal model of TMA-induced asthma.

Animals↗
PubMed2002

The effects of sympathectomy on capsaicin-evoked fos expression of spinal dorsal horn GABAergic neurons.

Electrophysiological studies have suggested that activity of spinal GABAergic interneurons can be enhanced following intradermal injection of capsaicin (CAP). This activity is proposed to be involved in the generation of dorsal root reflexes (DRRs) that contribute to neurogenic inflammation. We have recently reported that NMDA or non-NMDA antagonists by intrathecal pretreatment attenuate the increased Fos expression in spinal dorsal horn GABAergic neurons after intradermal injection of CAP in rats. Sympathetic efferents have been suggested to modulate inflammatory pain possibly by interactions with primary afferent terminals. In electrophysiological studies by our group, enhancement of the CAP-induced DRRs could be prevented by surgical sympathectomy and blocked by intraarterial pretreatment of the foot with alpha(1)- but not by alpha(2)-adrenoceptor antagonists. In order to determine morphologically if surgical sympathectomy changes the expression of Fos in GABAergic neurons in the lumbosacral spinal cord induced by CAP injection, further experiments were performed using immunofluorescence double-labeling staining at 30 min following CAP or vehicle injection into the glabrous skin of one hind paw of anesthetized rats both in sham-operated and sympathectomized animals. Our results showed that the proportion of Fos-positive GABAergic neuronal profiles was significantly increased following CAP injection (48.8+/-4.76%) compared to vehicle injection (23.8+/-5.1%) in laminae I-V on the ipsilateral side (P<0.05). However, when sympathetic efferents were removed surgically 7-10 days prior to the experiment (n=6), only 32.07+/-9.03% of GABA-immunoreactive neuronal profiles were stained for Fos following CAP injection, a significant reduction in the CAP-evoked Fos-staining of GABAergic neurons after surgical sympathectomy. These findings support our previous electrophysiological studies that GABAergic neurons take part in nociceptive processing within the spinal dorsal horn and suggest that sympathetic efferents may affect nociceptive transduction in the periphery.

Animals↗
PubMed2000

Influence of cellular ganglioside depletion on tumor formation.

BACKGROUND: Gangliosides are immunosuppressive cell surface molecules that are often present in high concentrations in and shed actively by tumor cells. These molecules inhibit the antitumor immune response that is implicated in tumor rejection. We therefore determined the ability of tumor cells pharmacologically depleted of gangliosides to form tumors in mice. METHODS: We tested a ganglioside-rich subline of B16 murine melanoma, MEB4, and MEB4 cells that had been depleted of endogenous gangliosides by incubation with 0.5 microM 1-phenyl-2-hexadecanoylamino-3-pyrrolidino-1-propanol, a specific inhibitor of the enzyme glucosylceramide synthase. Tumor formation was assessed twice a week for 10 weeks after the intradermal injection of tumor cells, and metastatic potential was assessed 4 weeks after tail vein injection of tumor cells. All P values are from two-sided tests. RESULTS: Reduction of the ganglioside content of MEB4 cells, which was not cytotoxic to cells and did not inhibit cell proliferation in vitro, markedly reduced their ability to form tumors. Only 40% of the mice given an intradermal injection of 10(5) ganglioside-depleted MEB4 cells developed tumors compared with 100% of the mice given an injection of 10(5) control MEB4 cells (P<.001). Ganglioside depletion also reduced metastasis: A mean of five pulmonary metastases was detected per mouse given an injection of 2 x 10(5) ganglioside-depleted MEB4 cells compared with a mean of 25 per mouse given an injection of 2 x 10(5) control MEB4 cells. CONCLUSION: Tumor cells with a pharmacologically decreased concentration of gangliosides produce fewer tumors in mice than do untreated cells, suggesting that pharmacologic depletion of gangliosides should be explored further as a therapeutic approach to cancer.

Animals↗
PubMed2002

Bradykinin sensitivity in primary open-angle glaucoma and normal-tension glaucoma patients.

PURPOSE: To report the reaction after intradermal injection of bradykinin in nonglaucoma, primary open-angle glaucoma, and normal-tension glaucoma subjects. DESIGN: Prospective comparative study. METHODS: The study participants were 14 healthy control subjects, 16 patients with primary open-angle glaucoma, and 15 patients with normal-tension glaucoma. In each participant, the wheal response to intradermal injection of 10 microg bradykinin in the volar forearm was measured by a masked observer. RESULTS: There was no significant difference in the wheal response to bradykinin between control subjects and primary open-angle glaucoma patients (P =.73) and between primary open-angle glaucoma patients and normal-tension glaucoma patients (P =.09). However, there was a significant difference in the wheal response to bradykinin between control subjects and normal-tension glaucoma patients (P =.04). CONCLUSIONS: These in vivo structure-activity studies may suggest abnormalities of the tissue kallikrein-kinin system in normal-tension glaucoma.

Adult↗
PubMed1986

Evidence that platelet activating factor may mediate some acute inflammatory responses. Studies with the platelet-activating factor antagonist, CV3988.

Platelet activating factor (PAF) has many proinflammatory properties. It is a polymorphonuclear leukocyte chemotactic factor, it aggregates platelets, increases vascular permeability, and is generated by inflammatory cells. To determine the possible in vivo role of PAF in inflammation, we examined the effects of the PAF antagonist and structural analogue, CV3988 on acute inflammatory responses in the skin of rabbits. Initial experiments indicated that CV3988 (10 mg/kg) was a specific inhibitor of PAF responses in vivo since it abolished neutropenia and thrombocytopenia induced by intravenous (iv) PAF infusion without effecting the response to f-met-leu-phe. In dermal inflammation, 125I-albumin, 111In-labeled platelets, 51Cr-labeled leukocytes, and 86RbCl were used to simultaneously quantitate protein exudation, platelet deposition, leukocyte accumulation, and blood flow in the lesions. CV3988 inhibited inflammatory responses to intradermal injection of PAF by 65 to 85% but it did not inhibit thrombin-induced platelet deposition or bradykinin and histamine-induced protein exudation. CV3988 treatment inhibited by 60 to 80% (p less than 0.01) the platelet deposition occurring at the peak of the reaction (1 1/2 hours) induced by the intradermal injection of zymosan, zymosan activated plasma, endotoxin, and the reversed passive Arthus reaction. Protein exudation was inhibited by 67 to 85% (p less than 0.1) and leukocyte accumulation was inhibited by 24 to 35% (p less than 0.05), but only in the zymosan and reversed passive Arthus reactions, respectively. Inflammatory hyperemia (increases blood flow) was not affected by CV3988 treatment. We conclude that in certain inflammatory reactions, PAF may mediate platelet deposition and protein exudation. The marginal effect of CV3988 on leukocyte accumulation suggests that the leukotactic activity of PAF is relatively less important in vivo.

Acute Disease↗
PubMed1994

Interleukin-1 alpha mediates phorbol ester-induced inflammation and epidermal hyperplasia.

The topical application of the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) to murine skin produces acute inflammatory and hyperplastic responses that have been associated with the promotion stage of skin carcinogenesis. It has been shown in a previous study that TPA induces the expression of the highly inflammatory cytokine, interleukin (IL) -1 alpha, in the epidermis of SENCAR mice. The goal of this study was to investigate the role of IL-1 alpha in several TPA-induced responses in skin. Topical application of TPA (1 microgram) enhanced the production of immunoreactive IL-1 alpha protein, primarily associated with the suprabasal keratinocytes. IL-1 alpha intradermally injected in the dorsal surface significantly increased (P < 0.001) vascular permeability at low concentrations (1-1000 microU) and increased (P < 0.001) inflammatory cell infiltration and epidermal hyperplasia at higher concentrations (10(3) U). TPA produced fourfold increases in vascular permeability as measured by Evans blue dye leakage; this effect was prevented by intradermal injection of anti-IL-1 alpha antibody (25-75 micrograms). Furthermore, injected anti-IL-1 alpha antibody significantly reduced (P < 0.001) TPA-induced inflammatory cell infiltration and epidermal hyperplasia. This study suggests that IL-1 alpha directly or indirectly mediates the inflammatory and hyperplastic responses elicited by topical treatment with TPA.

Analysis of Variance↗
PubMed1998

Intravenous immunoglobulin in autoimmune chronic urticaria.

Histamine releasing autoantibodies play a central role in the pathogenesis of chronic urticaria (CU) in approximately 30% of affected patients. We investigated the therapeutic effect of high-dose intravenous immunoglobulin (IVIG) on disease activity in patients with severe CU of autoimmune aetiology. Autoimmune urticaria was diagnosed by the development of a weal-and-flare reaction to the intradermal injection of autologous serum and by serum-induced histamine release from the basophil leucocytes of healthy donors in vitro. Ten patients with severe, autoimmune CU, poorly responsive to conventional treatment, were treated with IVIG 0.4 g/kg per day for 5 days. The outcome on cutaneous wealing and itch was monitored using urticaria activity scores, visual analogue scales and autologous intradermal serum tests. Clinical benefit was noted in nine of 10 patients: three patients continue in prolonged complete remissions (3 years follow-up), two had temporary complete remissions, and symptoms in four patients improved subsequent to treatment. There was significant improvement in the urticaria activity scores and visual analogue scores at 2 (P < 0.01) and 6 weeks (P < 0.01) post-IVIG compared with the baseline values (Wilcoxon matched pairs). The diminution in urticarial activity in the majority of patients corresponded with a reduced weal-and-flare response to the intradermal injection of autologous post-treatment serum compared with the pretreatment serum. Minor side-effects were common, but there were no serious or long-term adverse effects. IVIG represents a novel therapeutic option in selected patients with recalcitrant CU associated with histamine releasing autoantibodies.

Adult↗
PubMed1989

Interactions between the tachykinins and calcitonin gene-related peptide lead to the modulation of oedema formation and blood flow in rat skin.

1. The mechanisms involved in tachykinin-induced oedema were investigated in rat skin and interactions between the tachykinins and calcitonin gene-related peptide (CGRP) were studied. 2. Intradermal injections of the tachykinins, substance P, neurokinin A and neurokinin B, stimulated local oedema formation which was in each case potentiated by co-injection of the vasodilator CGRP. Oedema induced by substance P, in the presence and absence of CGRP, was significantly inhibited by pretreatment of rats with a combination of the histamine H1 antagonist, mepyramine, and the 5-hydroxytryptamine antagonist, methysergide. Oedema induced by neurokinin A or B was not inhibited by this pretreatment. 3. Intradermally-injected CGRP induced a long lasting increase in local blood flow, which was measured with a laser Doppler blood flow meter. The simultaneous injection of substance P, but not of the structurally-related neurokinins, caused a loss of the prolonged vasodilator activity of CGRP. 4. These results show that oedema induced by substance P is partially dependent on mast cell amines and that only substance P causes a loss of the prolonged vasodilator activity of CGRP. 5. We suggest that the ability of substance P to prevent the persistent vasodilator activity of CGRP may be a direct consequence of substance P-induced activation of mast cells.

Animals↗
PubMed2000

Regulation of epidermal Langerhans cell migration by lactoferrin.

Lactoferrin (LF) is a member of the transferrin family of iron-binding glycoproteins to which several anti-inflammatory functions have been ascribed. LF has been shown to down-regulate expression of the pro-inflammatory cytokine tumour necrosis factor-alpha (TNF-alpha), although the possibility has been raised that the activity of LF in this regard was indirect and secondary to its ability to bind to and inactivate the bacterial lipopolysaccharide (LPS) used to induce cytokine production. However, the identification of putative membrane receptors for LF raises the possibility that the interaction of LF with its receptor may be one important route through which this protein exerts anti-inflammatory activity. In the present investigations the biological properties of LF have been examined in a model of cutaneous immune function where the allergen-induced migration of epidermal Langerhans cells (LC) from the skin and their subsequent accumulation as dendritic cells (DC) in skin-draining lymph nodes are known to be dependent upon the de novo synthesis of TNF-alpha, but independent of exogenous LPS. Consistent with the protein having direct anti-inflammatory properties, it was found that the intradermal injection of recombinant murine LF (either iron-saturated or iron-depleted LF) inhibited significantly allergen (oxazolone) -induced LC migration and DC accumulation. That these inhibitory effects were secondary to the inhibition of local TNF-alpha synthesis was suggested by the findings that first, LF was unable to inhibit LC migration induced by intradermal injection of TNF-alpha itself, and second, that migration stimulated by local administration of another epidermal cytokine, interleukin 1beta, which is also dependent upon TNF-alpha production, was impaired significantly by prior treatment with LF. Finally, immunohistochemical analyses demonstrated the presence of LF in skin, associated primarily with keratinocytes. Collectively these data support the possession by LF of direct immunomodulatory and/or anti-inflammatory activity, probably associated in this case with inhibition of cytokine production. Furthermore, the results suggest that as a constituent of normal skin, LF may play a role in homeostatic regulation of cutaneous immune function.

Allergens↗
PubMed1980

Native type II collagen-induced arthritis in the rat. I. Incidence and humoral response to collagen.

An acute inflammatory arthritis has been induced in 76% of rats injected intradermally with native bovine type II collagen emulsified in Freund's complete (CFA) or incomplete (ICFA) adjuvant. The arthritis became chronic in 14 out of 31 rats, and ear and tail lesions were noted in some rats. No arthritis was induced by native type I collagen, denatured type II collagen, rabbit IgG, or buffer alone injected intradermally with adjuvant. Using a solid-phase radioimmunoassay for serum antibodies we have shown that IgM and IgG levels to native bovine type II collagen were significantly higher in arthritic than nonarthritic rats. Antiglobulin antibody levels were not raised in arthritic rats. Equivalent antibody levels to native type II collgen were obtained whether this antigen was emulsified in ICFA or CFA. However, native type I collagen produced high antibody levels only when emulsified in CFA, indicating a difference in the immunogenicity of these collagens. These studies suggest that native type II collagen possesses arthritogenic properties in the rat and that humoral immunity may play a role in the induction of this arthritis.

Animals↗
PubMed2004

Sentinel lymph node biopsy in breast cancer: results of intradermal periareolar tracer injection and follow-up of sentinel lymph node-negative patients.

Several methods are in use for identification of the sentinel lymph node (SLN) in breast cancer. We set up the hypothesis that intradermal (i.d.) infra-areolar injection of technetium-99m in combination with i.d. injection of patent blue dye lateral to the areola can identify the same lymph node as peritumoral injection, regardless of the location of the tumour. Each of 50 patients with breast cancer (group I) received an i.d. injection of technetium-99m 1cm caudal to the areola. After induction, blue dye was injected intradermally 1cm lateral to the areola. These patients underwent axillary dissection regardless of their lymph node status. The SLN was identified in 96% of these patients. One of them had axillary lymph node metastases even though the SLN was negative (6%). Further 82 patients (group II) underwent SLN identification and removal without further axillary dissection. The duration of mean follow-up for these patients was 28 months (16-39 months). One patient developed axillary recurrence (1%) 24 months after the initial operation. Intradermal periareolar tracer injection is an accurate method of locating the sentinel node. Long-term follow-up of patients who had negative sentinel nodes and did not undergo axillary dissection revealed a low axillary recurrence rate.

Adult↗
PubMed1982

Mechanism of ionophore A23187 induction of plasma protein leakage and of its inhibition by indomethacin.

Calcium ionophore A23187 produced a dose-dependent increase in plasma protein leakage on intradermal injection in rats. Studies with mepyramine and cyproheptadine indicated that histamine and 5-hydroxytryptamine (5-HT) partially contribute to the ionophore action and experiments with compound 48/80 supported these findings. Depletion of plasma kininogen levels with cellulose sulphate administered indomethacin inhibited the ionophore response in a dose-dependent manner. The inhibition was not reversed by intradermally injected prostaglandin E2 (PGE2) in doses up to 50 ng/site, suggesting that PGE2 also may not be an important mediator. It is proposed that the ionophore produces plasma protein leakage by an indirect (through histamine and 5-HT release) and a direct action on vascular endothelial cells and that indomethacin antagonises both actions by inhibiting calcium transport processes.

Animals↗