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PubMed2003

Peripheral norepinephrine exacerbates neuritis-induced hyperalgesia.

Inflammation of a peripheral nerve (neuritis) causes mechanical and thermal hyperalgesia in the region in which the inflamed nerve innervates. We investigated whether peripherally applied norepinephrine (NE) would exacerbate mechanical hyperalgesia in rats with neuritis. After inflammation of the left L5 spinal nerve with complete Freund's adjuvant, the foot withdrawal thresholds to mechanical stimuli applied to the affected hind paw (mechanical thresholds) were decreased significantly, indicating the development of mechanical hyperalgesia. An intradermal injection of NE to the affected paw further aggravated mechanical hyperalgesia transiently (1-3 days) and then recovered to the pre-NE injection levels afterwards. This responsiveness to NE (adrenergic sensitivity) was observed not only while rats were showing inflammatory hyperalgesia but also after recovering from it. The effect of NE on mechanical hyperalgesia was mediated by both peripheral alpha(1)- and alpha(2)-adrenoceptors. Immunohistochemical study of the previously inflamed nerve showed that proinflammatory cytokine tumor necrosis factor immunoreactivity was significantly higher in the rats showing adrenergic sensitivity compared to rats without adrenergic sensitivity. The data thus suggest that peripheral NE, when released in an excessive amount from the sympathetic nervous system, might play an important role in the aggravation of pain in neuritis.

Adrenergic alpha-Agonists↗
PubMed2000

Biochemical and biological characterization of neutrophil chemotactic protein, a novel rabbit CXC chemokine from alveolar macrophages.

The role of interleukin-8 (IL-8) and related CXC chemokines has been demonstrated in many human diseases. However, more profound studies, e.g., by blocking the effect of these inflammatory mediators, request animal models and hence the identification of all human counterparts for commonly used laboratory animals. In this study, we describe the identification of a novel neutrophil chemotactic protein (NCP) of the rabbit. Intact and NH(2)-terminally truncated NCP forms and IL-8 were isolated from LPS-stimulated rabbit alveolar macrophages and purified to homogeneity by a four-step purification procedure. Determination of the complete primary structure of NCP by mass spectrometry and NH(2)-terminal sequencing of natural protein revealed high structural homology with human epithelial cell-derived neutrophil attractant-78 (ENA-78) and granulocyte chemotactic protein-2 (GCP-2), two related ELR(+)CXC chemokines. Intact NCP(1-76) was found to be 10-fold less potent than truncated NCP(7, 8-76) at inducing neutrophil chemotaxis. NCP(7,8-76) was equally potent as intact rabbit IL-8 at chemoattracting human neutrophils and at inducing calcium fluxes in rabbit neutrophils, 1 ng/mL being the minimal effective concentration. However, like IL-8, NCP failed to induce monocyte or eosinophil migration at 300-fold higher concentrations. IL-8 desensitized the calcium increase induced by NCP and vice versa. Finally, intradermal injection of NCP induced a dose-dependent and significant infiltration of neutrophils in mice skin. It can be concluded that NCP is a novel rabbit CXC chemokine that is, like IL-8, implicated in animal models used to study various human disorders in which neutrophils play an important role.

Amino Acid Sequence↗
PubMed1997

Characterization of synthetic human granulocyte chemotactic protein 2: usage of chemokine receptors CXCR1 and CXCR2 and in vivo inflammatory properties.

Human granulocyte chemotactic protein 2 (GCP-2) has originally been isolated from cytokine-stimulated osteosarcoma cells as a chemokine coproduced in minute amounts together with interleukin 8. Human GCP-2 (75 residues) was synthesized on a 0.25-mmol scale using Fmoc chemistry. After disulfide bridge formation and purification, monomeric GCP-2 was recovered as a 6-kDa protein; the pure synthetic protein showed a molecular mass of 8076 Da as determined by matrix-assisted laser desorption/ionization mass spectrometry (MALDI-MS). The exact amino acid sequence of synthetic GCP-2 was confirmed by Edman degradation. Synthetic GCP-2 was an equally active (minimal effective concentration of 1-3 nM) chemoattractant for neutrophilic granulocytes as was natural 75-residue GCP-2. At concentrations up to 30 nM, synthetic GCP-2 did not stimulate eosinophil, monocyte, or lymphocyte chemotaxis. GCP-2 induced a dose-dependent increase in [Ca2+]i in neutrophils, 1 nM being the minimal effective concentration. The GCP-2-induced [Ca2+]i increase was completely prevented by pertussis toxin. Prestimulation of neutrophils with equimolar concentrations of purified natural IL-8, GROalpha, GROgamma and ENA-78 abolished the [Ca2+]i increase in response to 1 nM GCP-2. Alternatively, the [Ca2+]i rise induced by these CXC chemokines was inhibited by pretreatment of neutrophils with GCP-2. GCP-2 stimulated [Ca2+]i increases in CXCR1- and CXCR2-transfected cells, demonstrating that GCP-2 binds to both IL-8 receptors. Intradermal injection of synthetic GCP-2 resulted in a dose-dependent neutrophil accumulation and plasma extravasation in rabbit skin. To provoke this skin reaction, GCP-2 (10 pmol/site) was nearly as effective as IL-8, indicating that it is an important complementary mediator of the inflammatory response.

Amino Acid Sequence↗
PubMed1999

Intradermal DNA immunization: antisera specific for the membrane lectin MR60/ERGIC-53.

The trafficking of intracellular membrane proteins in Golgi apparatus, endoplasmic reticulum or intermediate compartment has not yet been fully elucidated. The human MR60/ ERGIC-53 and the rat p58 proteins are one such protein; and to study them in cell-free and in situ systems, high quality monospecific antisera are required. Highly specific antisera have been obtained after immunization of mice with plasmids containing a gene encoding either the full length or a truncated protein. The best results were obtained after intradermal injections of a plasmid encoding a truncated protein comprising both the luminal carbohydrate recognition domain and the stem down to a cysteine residue close to the C-terminal end, but neither the transmembrane nor the cytosolic domains. Such antisera have a very high titer and are very efficient tools to visualize the MR60 protein in situ or to selectively precipitate the MR60 proteins from a whole cell lysate.

Animals↗
PubMed2000

Localized in vivo genotypic and phenotypic correction of the albino mutation in skin by RNA-DNA oligonucleotide.

We recently demonstrated that an RNA-DNA oligonucleotide corrected a point mutation in the mouse tyrosinase gene, resulting in permanent and inheritable restoration of tyrosinase enzymatic activity, melanin synthesis, and pigmentation changes in cultured melanocytes. In this study, we extended gene correction of melanocytes from tissue culture to live animals, using a chimeric oligonucleotide designed to correct a point mutation in the tyrosinase gene. Both topical application and intradermal injection of this oligonucleotide to albino BALB/c mouse skin resulted in dark pigmentation of several hairs in a localized area. The restored tyrosinase enzymatic activity was detected by dihydroxyphenylacetic acid (DOPA) staining of hair follicles in the treated skin. Tyrosinase gene correction was also confirmed by restriction fragment length polymorphism analysis and DNA sequencing from skin that was positive for DOPA staining and melanin synthesis. Localized gene correction was maintained three months after the last application of the chimeric oligonucleotides. These results demonstrated correction of the tyrosinase gene point mutation by chimeric oligonucleotides in vivo.

Administration, Cutaneous↗
PubMed2000

Resolution of cutaneous inflammation after local elimination of macrophages.

We constructed an immunotoxin, composed of an antibody directed against the high-affinity IgG receptor CD64 and Ricin-A, with the aim of resolving chronic inflammation through elimination of activated macrophages. In vitro, this immunotoxin proved very efficient in inducing apoptosis in activated macrophages, leaving resting and low CD64-expressing macrophages unaffected. We examined the activity of our immunotoxin in a sodium lauryl sulfate (SLS)-induced cutaneous inflammation model, using transgenic mice expressing human CD64. Upon intradermal injection of the immunotoxin (IT), cutaneous inflammation resolved in 24 h. This was demonstrated histologically by clearance of all CD64-expressing macrophages, followed by clearance of other inflammatory cells. Clinical parameters associated with inflammation, such as local skin temperature and vasodilation, also decreased.

Animals↗
PubMed1973

Immunotherapy for acute myelogenous leukaemia.

One hundred and seven untreated patients with acute myelogenous leukaemia (AML) were admitted to St Bartholomew's Hospital between 10 October 1970 and 31 January 1973. Before receiving drugs to induce remission they were allocated alternatively into 2 groups to decide their remission treatment-a group to receive chemotherapy alone and a group to receive the same chemotherapy with immunotherapy. The patients were then given induction chemotherapy and 45 of them attained complete remission. All patients in remission then received chemotherapy consisting of 5 days treatment every 28 days. Patients receiving immunotherapy were also given multiple weekly intradermal injections of irradiated stored AML cells and Glaxo B.C.G. using a Heaf gun. There were 19 patients in the group which received only chemotherapy during remission; 7 of these patients remain alive (median survival after attaining remission 303 days) and only 5 are still in their first remission (median remission length 188 days). Twenty-three patients were allocated to receive immunotherapy during remission in addition to chemotherapy and 16 remain alive (median 545 days) and 8 are in their first remission (median 312 days). The difference in survival of the two groups is significant with a P value of 0·003.

Adolescent↗
PubMed1998

Alleged allergy to local anaesthetic drugs.

OBJECTIVE: To identify the true nature of an acute reaction in 25 patients initially diagnosed as allergic to local anaesthetic drugs. SETTING: University General and Dental Hospitals. INTERVENTIONS: Detailed review of each patient's previous exposure to local anaesthetic drugs and of the history of the acute event was followed up with challenge testing by intradermal injection. RESULTS: One patient was subsequently found to be genuinely allergic to a local anaesthetic drug of the amide type. A wide range of conditions had actually precipitated the other adverse reactions, but all could be classified under three major headings: an immunological condition to a different antigen; a manifestation of anxiety; or an iatrogenic problem. CONCLUSION: Local anaesthetic allergy is rare, but does occur. All reactions to local anaesthetic drugs must be assessed carefully and specialist referral may be appropriate.

Acute Disease↗
PubMed2004

Membrane type-1 matrix metalloproteinase promotes human melanoma invasion and growth.

Membrane type-I metalloproteinase (MT1-MMP) is a transmembrane metalloproteinase that is critical for tumor cell invasion. MT1-MMP can degrade extracellular matrix (ECM) proteins directly and/or indirectly by activating soluble MMPs such as pro-MMP-2. Although MT1-MMP is upregulated in malignant melanoma, the biological consequences of elevated MT1-MMP expression for tumor progression are not entirely understood. In the current study, we have utilized the Bowes melanoma line for evaluating MT1-MMP in invasion and growth. Our studies extend the earlier observations to demonstrate that MT1-MMP expression in Bowes melanoma cells promotes selective invasion into matrigel but not matrices consisting of type-I collagen. Furthermore, MT1-MMP expressing melanoma cells exhibit increased migration in response to laminin 1 but not to type-I or type-IV collagen. MT1-MMP expression results in enhanced 3 dimensional growth in agarose gels and in long-term cultures within matrigel. The hydroxymate inhibitor BB94 inhibits MT1-MMP enhanced invasion and growth in 3 dimensional culture systems, but had no effect on increased motility. We demonstrated that MT1-MMP expression significantly facilitated tumorigenicity and growth by intradermal injection. The results suggest a more general role for elevated MT1-MMP in promoting both the selective invasion and increased growth of malignant melanoma in vivo.

Animals↗
PubMed2002

Histopathological findings in rabbits after experimental acute exposure to the Loxosceles intermedia (brown spider) venom.

Loxoscelism, the term used to describe envenomation with brown spiders, is characterized by a dermonecrotic lesion at the bite site. In the present investigation we submitted albino rabbits to an acute experimental envenomation protocol using Loxosceles intermedia (brown spider) venom, with in order to determine the pathogenesic features of the lesion induced by this spider, which is the cause of several accidents throughout the world. Rabbits received intradermal injections of the venom and were monitored over the first 4 h, and then at 12 h and 1, 2 and 5 days after envenomation. Histological specimens from 3 rabbits per time point were collected from euthanized animals and processed for histological examination by light microscopy. Major findings observed during the first 4 h were oedema, haemorrhage, degeneration of blood vessel walls, plasma exudation, thrombosis, neutrophil accumulation in and around blood vessels with an intensive diapedesis, a diffuse collection of inflammatory cells (polymorphonuclear leucocytes) in the dermis, and subcutaneous muscular oedema. Over the following hours and up to 5 days after envenomation the changes progressed to massive neutrophil infiltration (with no other leucocytes) into the dermis and even into subcutaneous muscle tissue, destruction of blood vessels, thrombosis, haemorrhage, myonecrosis, and coagulative necrosis on the 5th day.

Animals↗
PubMed1999

Identification of arthritogenic adjuvants of self and foreign origin.

The lack of defined triggers for human inflammatory joint diseases warrants efforts to identify candidate molecules. For this task, it may be an important lead that nonspecific activation of the immune system can precipitate arthritis in rats. Consequently, arthritis-prone rat strains were used to search for disease-triggering factors among molecules which initially induce innate defence reactions rather than specific immune responses. A variety of immunological adjuvants were investigated by intradermal injection into DA and LEW.1AV1 rats and monitoring of clinical signs for 30 days. Several arthritogenic cell-wall structures from yeast and bacteria were identified, such as beta-glucan, lipopolysaccharide and trehalosedimycolate. The test procedures also revealed arthritogens of chemical origin, such as dioctadecyldiammoniumbromide (DDA = C38H80NBr) and heptadecane (C17H36). Furthermore, it allowed the precise definition of arthritogenic determinants of lipids, since C16H34 induced arthritis, whereas the closely related linear hydrocarbons C16H32, C16H33Br and C15H32 did not. The observed pathogenicity of organic lipids raised the question of whether endogenous lipids can also precipitate arthritis. Indeed, this was true for the cholesterol precursor squalene (C30H50). In conclusion, this article describes the rational use of arthritis-prone rat strains to identify arthritogenic factors of both foreign and self origin. Although structurally unrelated, the pathogenic molecules defined here share the feature of being nonspecific triggers of the immune system. This consolidates a general principle for the induction of adjuvant arthritis which may provide clues to the aetiology of human arthritides, including rheumatoid arthritis.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed2002

Treatment of axillary hyperhidrosis with botulinum-A toxin.

BACKGROUND: Severe axillary hyperhidrosis is a source of great embarrassment and considerable emotional stress to individuals afflicted with this condition. Existing topical and surgical therapies are either ineffective or associated with unacceptable morbidity. We attempt to determine the effect of botulinum-A toxin (Dysport) in the treatment of axillary hyperhidrosis. PATIENTS AND METHODS: After visualization of hyperhidrosis using the iodine-starch test, 10 patients with axillary hyperhidrosis underwent intradermal injection with 125 units of Dysport on each axilla. Patients were observed for 7 months after treatment. RESULTS: The treatment was well tolerated without side-effects. All patients experienced relatively complete anhidrosis of the axillary skin after about 1 week for periods ranging from 4 to 7 months. CONCLUSIONS: Botulinum-A toxin may offer a fast, safe, and highly effective therapeutic option for severe hyperhidrosis.

Adult↗
PubMed1998

Ultraviolet radiation induced suppression of Mantoux reactions in humans.

The effects of low dose ultraviolet (UV) radiation on delayed type hypersensitivity responses to tuberculin purified protein derivative were investigated in 17 healthy, Mantoux-positive volunteers. Suberythemal and erythemal doses of solar simulated UV from a fluorescent lamp source were delivered to the subjects' lower backs daily for five consecutive days. Mantoux testing with intradermally injected purified protein derivative was then performed at both the irradiated sites and an adjacent, unirradiated site, and the Mantoux induced erythema was quantitated 72 h later with a reflectance erythema meter. In comparison with the unirradiated Mantoux sites, Mantoux induced erythema was significantly reduced at the irradiated test sites. In six subjects, we compared the effects of chronic versus short term UV irradiation on the Mantoux reaction. These volunteers were irradiated on one side of their lower backs with the 5 d UV protocol, and on the other side of their backs for 4 or 5 wk. In all but one subject, the short irradiation protocol induced greater suppression of Mantoux responses than prolonged UV exposure. We conclude that even suberythemal doses of UV significantly reduce delayed type hypersensitivity responses to purified protein derivative, and that an adaptive mechanism appears to counteract the immunosuppressive effects of chronic irradiation.

Adult↗
PubMed2001

Interleukin-16 supports the migration of Langerhans cells, partly in a CD4-independent way.

Migration of cutaneous dendritic cells is essential for the induction of primary immune responses. Chemotaxis plays an important part in guiding migrating cells through the skin. Therefore, we investigated the influence of interleukin-16, a potent chemoattractant, on the migratory properties of cutaneous dendritic cells. Interleukin-16 added to murine and human skin explant cultures, enhanced emigration of Langerhans cells as well as dermal dendritic cells out of the skin. In contrast to tumor necrosis factor-alpha, intradermally injected interleukin-16 did not reduce the density of Langerhans cells suggesting a chemotactic rather than a mechanistic migration-inducing effect of interleukin-16. In support of these findings, the known migration-promoting effect of tumor necrosis factor-alpha in skin explant cultures could be neutralized by anti-interleukin-16 antibody and vice versa, indicating different but cooperative ways of action for both cytokines. In whole skin explant cultures blocking of the interleukin-16 effect was also achieved with a monoclonal antibody against CD4, the receptor for interleukin-16. In contrast, in cultures of murine epidermis alone no blocking by anti-CD4 became obvious and in CD4-deficient mice Langerhans cell migration in response to interleukin-16 was maintained. This suggests that another receptor for interleukin-16 might be operative for Langerhans cells in the mouse epidermis. Finally, we detected interleukin-16-positive cells in the dermis of skin explants, tumor necrosis factor-alpha-treated and contact allergen-treated skin. Taken together, it seems likely that locally secreted interleukin-16 might serve to enhance the migration of cutaneous dendritic cells and optimize the response to foreign antigen encountering the skin.

Animals↗
PubMed2002

Long-term quantitative benefits of botulinum toxin type A in the treatment of axillary hyperhidrosis.

BACKGROUND: Although axillary hyperhidrosis is readily treated with botulinum toxin, the time course of benefits is not well established. OBJECTIVE: To quantify the long-term effectiveness of botulinum toxin type A (BTX-A) for the treatment of axillary hyperhidrosis. METHODS: This was a double-blind, placebo-controlled study. Eighteen patients received intradermal injections of either 100 U BTX-A (50 U/ml/axilla) or placebo. Sweating per surface area was quantified monthly for 5 months. RESULTS: The BTX-A group had an average reduction in sweat production of 91.6% at 2 weeks (from 5.03 ml/min/m(2) to 0.42 ml/min/m(2), P <.05). The average reduction over 5 months was 88.2%. At the end of the study, only 1 of 12 BTX-A-treated patients had returned to baseline sweat production. CONCLUSION: These quantitative results demonstrate that BTX-A is a safe and effective treatment for axillary hyperhidrosis and that the benefits last for at least 5 months.

Adolescent↗
PubMed1990

A double-blind study of symptom provocation to determine food sensitivity.

BACKGROUND: Some claim that food sensitivities can best be identified by intradermal injection of extracts of the suspected allergens to reproduce the associated symptoms. A different dose of an offending allergen is thought to "neutralize" the reaction. METHODS: To assess the validity of symptom provocation, we performed a double-blind study that was carried out in the offices of seven physicians who were proponents of this technique and experienced in its use. Eighteen patients were tested in 20 sessions (two patients were tested twice) by the same technician, using the same extracts (at the same dilutions with the same saline diluent) as those previously thought to provoke symptoms during unblinded testing. At each session three injections of extract and nine of diluent were given in random sequence. The symptoms evaluated included nasal stuffiness, dry mouth, nausea, fatigue, headache, and feelings of disorientation or depression. No patient had a history of asthma or anaphylaxis. RESULTS: The responses of the patients to the active and control injections were indistinguishable, as was the incidence of positive responses: 27 percent of the active injections (16 of 60) were judged by the patients to be the active substance, as were 24 percent of the control injections (44 of 180). Neutralizing doses given by some of the physicians to treat the symptoms after a response were equally efficacious whether the injection was of the suspected allergen or saline. The rate of judging injections as active remained relatively constant within the experimental sessions, with no major change in the response rate due to neutralization or habituation. CONCLUSIONS: When the provocation of symptoms to identify food sensitivities is evaluated under double-blind conditions, this type of testing, as well as the treatments based on "neutralizing" such reactions, appears to lack scientific validity. The frequency of positive responses to the injected extracts appears to be the result of suggestion and chance.

Double-Blind Method↗
PubMed2001

Intradermal administration of a killed Mycobacterium vaccae suspension (SRL 172) is associated with improvement in atopic dermatitis in children with moderate-to-severe disease.

BACKGROUND: Although a doubling in the prevalence of atopic disease, including atopic dermatitis, in the Western world over the last few generations has been paralleled by a marked reduction in infectious diseases, especially tuberculosis, it is unclear whether this increase in atopy is causally related to reduced exposure to mycobacteria. OBJECTIVES: The aim of this study was to determine whether administration of mycobacterial antigens to atopic individuals might ameliorate their disease. METHODS: Forty-one children aged 5 to 18 years with moderate-to-severe atopic dermatitis were enrolled in a randomized, double-blind, placebo-controlled trial, where they were given either one intradermal injection of killed Mycobacterium vaccae (SRL 172) or buffer solution (placebo). Changes in skin surface area affected by dermatitis and dermatitis severity score were assessed before treatment and at 1 and 3 months after treatment. RESULTS: Children treated with SRL 172 showed a mean 48% (95% CI, 32%-65%) reduction in surface area affected by dermatitis compared with a mean 4% (95% CI, -29% to 22%) reduction for the placebo group (P <.001) and a median 68% (interquartile range, 46%-85%) reduction in dermatitis severity score compared with 18% (interquartile range, -2% to 34%) for the placebo group (P <.01) at 3 months after treatment. There were no untoward effects of the treatment, apart from a local reaction in 13 of the 21 children, which occurred 1 month after SRL 172 administration and settled spontaneously. CONCLUSION: SRL 172 was associated with an improvement in the severity of the dermatitis in children with moderate-to-severe disease.

Adolescent↗
PubMed2000

A simplified cyclic adenosine monophosphate-mediated sweat rate test for quantitative measure of cystic fibrosis transmembrane regulator (CFTR) function.

OBJECTIVE: Sweat production is stimulated by both cholinergic and beta-adrenergic pathways in the sweat gland secretory coil. beta-Adrenergic pathway-mediated sweating is absent in cystic fibrosis (CF) because cyclic adenosine monophosphate (cAMP)-mediated chloride transport through the cystic fibrosis transmembrane regulator (CFTR) is disrupted. We report the development of a rapid, reproducible, macroscopic, and quantitative methodology to test the hypothesis that beta-adrenergic sweat rate discriminates among 3 different CFTR phenotypes-CF, heterozygote CF carriers, and non-CF. STUDY DESIGN: Intradermal injection of a mixture of 50 micromol/L isoproterenol, 5 mmol/L aminophylline (to potentiate the beta-adrenergic stimulation), and 140 micromol/L atropine (to block potential cholinergic stimulation) in lactated Ringer's solution was performed in duplicate on one forearm. A single injection of 0.5 mmol/L methacholine to stimulate sweat production by the cholinergic pathway was performed on the other forearm. Sweat rate was determined as the amount of sweat collected on filter paper over 20 minutes. RESULTS AND CONCLUSIONS: Median cAMP-mediated sweat rates were 1.45 mg/20 min (CF, n = 29), 2.55 mg/20 min (CF heterozygote carriers, n = 30), and 3.65 mg/20 min (non-CF, n = 30) and were significantly different in all 3 groups (P =.0001, Kruskal-Wallis test). Methacholine-stimulated sweat rates were similar for all 3 groups. The cAMP-mediated sweat rate test may be a useful endpoint for studies of new agents to increase the function of CFTR.

Adolescent↗