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PubMed2003

In vivo alteration of the keratin 17 gene in hair follicles by oligonucleotide-directed gene targeting.

Using intradermal injection of a chimeric RNA-DNA oligonucleotide (RDO) or a single-stranded oligonucleotide (ssODN) into murine skin, we attempted to make a dominant mutation (R94p) in the conserve alpha-helical domain of keratin 17 (K17), the same mutation found in pachyononychia congenichia type 2 (PC-2) patients with phenotypes ranging from twisted hair and multiple pilosebaceous cysts. Both K17A-RDO and -ssODN contained a single base mismatch (CGC to CCC) to alter the normal K17 sequence to cause an amino acid substitution (R94P). The complexes consisting of oligonucleotides and cationic liposomes were injected to C57B1/6 murine skin at 2 and 5 day after birth. Histological examination of skin biopsies at postnatal day 8 from several mice showed consistent twisted hair shafts or broken hair follicles at the sebaceous gland level and occasional rupture of the hair bulb or epidermal cyst-like changes. In the injected area, the number of full anagen hair follicles decrease by 50%. Injection of the control oligonucleotide, identical to K17A-RDO but containing no mismatch to the normal sequence, did not result in any detectable abnormality. The frequency of gene alteration was lower than 3%, according to the restriction fragment length polymorphism (RFLP) analysis of the genomic DNA isolated by dissection of hair follicles from slides. Although intradermal injection of K17A-RDO or K17-ssODN caused a dominant mutation in K17 affecting hair growth and morphology, these phenotypic changes were transient either due to the compensation of K17 by other keratins or the replacement of the mutated cells by normal surrounding cells during hair growth.

Animals↗
PubMedDate not supplied

Time-dependent differences in the vasopermeability response to intradermal peptidoleukotrienes.

The time course of extravascular albumin accumulation responses elicited by the leukotrienes LTC4, LTD4, LTE4, and histamine in the skin were compared in the conscious guinea pig. During the initial 15-min period, comparison of the dose-response curves revealed that histamine produced a much larger increase in extravascular albumin content than any of the leukotrienes. One hour after intradermal injection and at subsequent time intervals, the response to LTD4 had increased in magnitude so that it equaled the response produced by histamine. This was apparent from comparison of the time courses of extravascular albumin accumulation for intermediate doses of LTD4 and histamine and also from comparison of dose-response relationships at 4 h post intradermal injection. In contrast to LTD4, the magnitude of the microvascular permeability responses to LTC4 and LTE4 remained relatively small even over an extended time scale. Although histamine produced a large initial response, this also remained essentially unchanged over a 4-h period. It appears that LTD4 may produce a unique, time-dependent cutaneous microvascular permeability response and measurements over 15-30-min periods may underestimate its activity as a vasopermeability factor. The time-dependent effects of LTD4 on albumin extravasation cannot be ascribed to leukocyte infiltration into the skin since LTC4, LTD4, and LTE4 were entirely without effect in this regard.

Albumins↗
PubMed1982

In vivo modification of delayed type hypersensitivity by small molecular weight components derived from human leucocytes: partial purification of components causing amplification of response.

Human leucocyte dialysates contain components which, when injected intradermally in combination with an antigen to which the recipient displays prior sensitivity, produces an accelerated and intensified delayed hypersensitivity response. These components which we have termed leucocyte amplifiers, can be partially purified by gel filtration on Sephadex G-10 followed by high pressure reverse phase chromatography. The amplifiers do not produce an inflammatory reaction when injected intradermally by themselves. Amplifying effects were not observed when analogous sub-fractions prepared from erythrocytes or platelets were employed in the same manner. The leucocyte amplifiers were not able to transfer a new sensitivity to a non-sensitive recipient.

Antigens↗
PubMed1996

Priming of eosinophil recruitment in vivo by LPS pretreatment.

Eosinophils are important inflammatory cells in allergic diseases. Recent evidence suggests that priming mechanisms in the blood may be important for effective eosinophil recruitment to sites of allergic inflammation. We have investigated whether priming an inflammatory site could enhance eosinophil recruitment in vivo. Pretreatment of skin sites in the guinea pig with a low dose (30 ng) of LPS, which had little effect on eosinophil accumulation alone, enhanced by up to threefold the 111In-eosinophil accumulation in response to a passive cutaneous anaphylactic reaction and to intradermally injected eosinophil chemoattractants (leukotriene B4, PAF, and C5ades Arg). In contrast, LPS pretreatment did not enhance accumulation of 111In-neutrophils. Priming was seen only with a 1-h pretreatment time and was not associated with an increase in local edema or a change in cutaneous blood flow. It was independent of local protein synthesis, as assessed using cycloheximide, and was unaffected by a PAF antagonist, a 5-lipoxygenase inhibitor, and the IL-1 receptor antagonist. The priming response was, however, reduced by co-injection with the LPS of TNFR-IgG, but not of CD4-IgG. Blockade of CD18 showed this adhesion molecule to be critical for eosinophil accumulation, and LPS-primed sites were inhibited as effectively as nonprimed sites. In conclusion, low dose LPS pretreatment of guinea pig skin sites primes for eosinophil accumulation induced by intradermally injected inflammatory mediators and cutaneous anaphylactic reaction. This may be an important process by which eosinophil recruitment is modulated in vivo.

Animals↗
PubMed1991

Estimation of immunity in the developing calf: cellular and humoral responses to keyhole limpet haemocyanin.

The efficacy of keyhole limpet haemocyanin (KLH) as a test antigen was determined in calves. Humoral and cellular (in vivo and in vitro) responses were compared. Calves were immunized with KLH at either 3 weeks or up to 5 months of age and immune responses were subsequently tested. Class and subclass antibody responses were detected by ELISA, lymphocyte blastogenesis was measured using a whole blood culture technique (LTT) and skin sensitivity responses were measured as an increase in skin thickness following intradermal injection. In young calves, skin test responses were maximal at 24 h and were found to correlate with IgG1 and IgG2 responses (P less than 0.01), with IgA (P less than 0.05) but not with IgM or LTT. Histological examination of skin swellings found a sequence of cellular events, with polymorphonuclear cells dominating until 48 h after intradermal injection, when mononuclear cells became involved. However, in older calves, skin test responses correlated not only with IgG1 and IgA responses but also with lymphocyte transformation (P less than 0.05). These findings suggest that, while immune responses to KLH may be a useful indicator of immune competence in calves, interpretation should be made with caution particularly in young calves.

Animals↗
PubMed2000

Lymphocyte subset proliferative responses of Mycobacterium bovis-infected cattle to purified protein derivative.

Despite highly successful eradication efforts in several countries, Mycobacterium bovis infection of cattle remains a significant health concern worldwide. Immune mechanisms of resistance to and/or clearance of M. bovis infection of cattle, however, are unclear. Recent studies have provided evidence supporting a role for CD4(+), CD8(+), and gammadelta TCR(+) T cells in the response of cattle to M. bovis. In the present study, we utilized a flow cytometric-based proliferation assay to determine the relative contribution of individual lymphocyte subsets in the response to M. bovis infection and/or sensitization with mycobacterial purified protein derivative (PPD). Peripheral blood mononuclear cells (PBMC) from M. bovis-infected cattle proliferated in response to in vitro stimulation with M. bovis PPD. CD4(+) T cells and gammadelta TCR(+) cells were the predominate subsets of lymphocytes responding to PPD. gammadelta TCR(+) cells also proliferated in non-stimulated cultures; however, the gammadelta TCR(+) cell proliferative response of infected cattle was significantly (p<0.05) greater in PPD-stimulated cultures as compared to non-stimulated cultures. Intradermal injection of PPD for comparative cervical testing (CCT) induced a boost in the in vitro proliferative response of CD4(+) but not gammadelta TCR(+) cells of infected cattle. Administration of PPD for CCT also boosted interferon-gamma (IFN-gamma) production by PBMC of infected cattle following in vitro stimulation with M. bovis PPD. Injection of PPD for CCT did not, however, elicit a proliferative or IFN-gamma response in cells isolated from non-infected cattle. These data indicate that CD4(+) and gammadelta TCR(+) cells of M. bovis-infected cattle proliferate in a recall response to M. bovis PPD and that the CD4(+) cell response is boosted by intradermal injection with PPD for CCT.

Animals↗
PubMed1988

A case study on the induction of clinical tolerance in cold urticaria.

The mechanism(s) by which repeated cold challenge in a patient with idiopathic acquired cold urticaria resulted in the induction of clinical tolerance to cold stimuli was studied. Plasma histamine levels, mast cell ultrastructure, and the cutaneous response to intradermal injections of morphine, histamine, and substance P were examined before and after the induction of tolerance. Plasma histamine levels draining cold-challenged, clinically tolerant skin were markedly diminished compared to histamine levels obtained during cold-induced angioedema. Furthermore, electronmicroscopy of skin samples taken from tolerant skin after cold challenge revealed intact, largely normal appearing mast cells. Intradermal injection of mast cell secretagogues and vasoactive agonists into normal and tolerant skin sites resulted in similar whealing responses. Thus, these studies suggest that the state of clinical tolerance to cold stimuli is due neither to mast cell-mediator depletion or tachyphylaxis of the cutaneous vasculature to vasoactive agonists. It appears likely that tolerance may be due to the induction of a specific state of unresponsiveness of mast cells to cold stimuli or possibly to depletion of a cold-induced cutaneous antigen capable of triggering mast cell degranulation.

Adaptation, Physiological↗
PubMed2001

Optimization of cottontail rabbit papilloma virus challenge technique.

Disease induced by Cottontail Rabbit Papilloma Virus (CRPV) scarification in domestic rabbits shares many attributes with disease induced by human papilloma virus (HPV). CRPV induces squamous papillomas in domestic rabbits, of which approximately 70% transform into invasive carcinomas. In advanced tumors, virus is often undetectable, and occasionally, some rabbits undergo spontaneous regression of papillomas. Techniques utilized to scarify rabbit skin are diverse, often labor intensive and time consuming with the possibility for significant variability. Using four unique infection techniques, resultant papilloma incidence, time to onset, and total papilloma volumes were compared to determine an optimal challenge method. Five rabbits were each infected with CRPV via a tattoo gun with and without ink, an intradermal injection, manual use of a tattoo needle, or a sterile blade followed by manual use of a tattoo needle. Papilloma formation was monitored weekly after inoculation for 6 weeks. CRPV papillomas began as pinpoint foci at 3 weeks post challenge and grew exponentially throughout the course of measurement. Individual foci coalesced rapidly to form larger papilloma aggregates. Although intradermal injection was well tolerated and easily performed, it was the worst method of papilloma production (2.2 mm(3) at 6 weeks). The best method, a sterile blade followed by manual use of a tattoo needle, produced significantly larger papillomas over all time periods (>1100 mm(3) at 6 weeks, P<0.01). Inoculation of CRPV using this method produces highly repeatable papillomas beginning 3 weeks post-infection.

Animals↗
PubMed1987

Evidence for histamine in the urticating hairs of Hylesia moths.

An urticarial dermatosis after contact with the urticating hairs of the adult female Hylesia moth may occur by several mechanisms including the intradermal injection of inflammatory mediators through the urticating hairs. Extracts were prepared from whole moths, urticating hairs, and other moth parts. Each of these extracts was subjected to a radioenzyme assay for histamine. Histamine was present in extracts made from whole moths and from urticating hairs. Extracts made from other moth parts contained no histamine. Cutaneous wheals occurred after intradermal injections of histamine and various concentrations of Hylesia extract (HE) into the backs of cynomolgus monkeys. This whealing response was suppressed by pretreatment of the animals with diphenhydramine hydrochloride, but not by pretreatment with indomethacin. Histologic examinations showed a perivascular lymphocytic infiltrate around dilated capillaries without evidence of mast cell degranulation in HE-injected sites but not in controls. These findings provide evidence that histamine may be the mediator responsible for the urticarial lesions seen after contact with Hylesia moths.

Animals↗
PubMed2006

Role of substance P on histamine H(3) antagonist-induced scratching behavior in mice.

The purpose of the present study was to investigate the involvement of chemical mediators, other than histamine, in the scratching behavior induced by H(3) antagonists. Scratching behavior was induced by the histamine H(3) antagonists iodophenpropit and clobenpropit (10 nmol/site) when they were injected intradermally into the rostral part of the back of mast-cell-deficient (WBB6F1 W/W(v)) and wild-type (WBB6F1 +/+) mice. Subsequently, the effect of spantide, a tachykinin NK(1) antagonist, was measured for 60 min. The effects of the H(3) antagonists on in vitro histamine release from rat peritoneal mast cells were also investigated. When spantide was injected intradermally at a dose of 0.5 nmol/site, it significantly inhibited the response. Furthermore, iodophenpropit and clobenpropit (10(-6)-10(-8) M) did not induce histamine release in isolated rat peritoneal mast cells. Our results indicate that substance P is involved in the skin responses elicited by the histamine H(3) antagonists. Moreover, the fact that these histamine H(3) antagonists did not induce significant increases in the histamine release from rat peritoneal mast cells suggests that the histamine H(3) receptor may not be present in the peripheral cells considered in this study.

Amphetamines↗
PubMed1992

The effects of a non-competitive NMDA receptor antagonist, MK-801, on behavioral hyperalgesia and dorsal horn neuronal activity in rats with unilateral inflammation.

The involvement of NMDA receptors in rats with peripheral inflammation and hyperalgesia was evaluated by administration of the non-competitive NMDA receptor antagonist, MK-801. Inflammation and hyperalgesia was induced by intradermal injection of complete Freund's adjuvant (CFA) or carrageenan into the left hind paw. The latency of paw withdrawal from a thermal stimulus was used as a measure of hyperalgesia in awake rats. MK-801 (1.6 mg/kg, i.p., or 31.5 micrograms, intrathecal) significantly attenuated thermal hyperalgesia and reduced its duration in comparison to saline-injected rats (P less than 0.05). The receptive field size of nociceptive-specific and wide-dynamic-range neurons in the superficial and deep spinal dorsal horn recorded 24 h after injection of CFA was significantly reduced to 73 +/- 6% (P less than 0.05, n = 8) and 74 +/- 4% (P less than 0.05, n = 8) of control values, respectively, by a cumulative dose of 3 mg/kg of MK-801 (i.v.). MK-801 (2 mg/kg) prevented the expansion of the receptive fields of dorsal horn neurons recorded 5 +/- 0.4 h (n = 5) after intradermal injection of CFA as compared to saline-injected rats (P less than 0.05). MK-801 had no significant effect on receptive field size of dorsal horn neurons in rats without CFA-induced inflammation but blocked a transient expansion of the receptive fields induced by 1 Hz, C-fiber intensity electrical stimulation of the sciatic nerve. The background activity and noxious heat-evoked response of dorsal horn neurons in rats with CFA-induced inflammation were primarily inhibited and noxious pinch-evoked activity was both facilitated and inhibited by the administration of MK-801. These results support the hypothesis that NMDA receptors are involved in the dorsal horn neuronal plasticity and behavioral hyperalgesia that follows peripheral tissue inflammation.

Animals↗
PubMed2001

[Diagnosis of normal and abnormal delayed hypersensitivity to Candida albicans. Importance of evaluating lymphocyte activation by flow cytometry].

Delayed type hypersensitivity (DTH) to Candida albicans is commonly observed in human. Abnormal DTH has already been described but its diagnosis is difficult to ascertain. We present now a clinical and biological study in 60 patients with a clear distinction between these two kind of Candida albicans DTH. Clinical abnormal Candida albicans DTH was characterized by a syndromic reaction 24 to 48 hours after intradermal injection. This reaction was characterized by an exacerbation of clinical symptoms. In vitro, activation of whole blood with Candida albicans antigen was detected by using flow cytometry after staining for activating markers. CD 25 positive T cells were detected in a 7 days culture in all patients. Percentage of CD 25 positive T cells was correlated to the intensity of the local cutaneous DTH reaction. CD 69 positive T cells were detected after a one day culture only in patient who presented a syndromic reaction to intradermal injection.

Adolescent↗
PubMed1991

Delayed activation of nociceptors: correlation with delayed pain sensations induced by sustained stimuli.

1. In this study we used psychophysical experiments in humans and behavioral and electrophysiological studies in rats to evaluate nociceptive and C-fiber mechanoheat nociceptor (C-MH) responses to sustained mechanical stimuli that are initially nonpainful or nonnoxious. 2. In normal rat skin, sustained subthreshold mechanical stimuli activate C-MHs (n = 36) with a delayed onset that parallels the delayed pain sensation recorded in human psychophysical tests. 3. The subthreshold stimuli did not induce a decrease in mechanical threshold (n = 11), and the effect of the subthreshold stimulus on latency to firing of C-MHs (n = 6) persists for a very short time after the stimulus is removed (less than 10 s). 4. Intradermal injection of prostaglandin E2 (PGE2; 100 ng), which induced a significant decrease in the mechanical threshold of C-MHs (n = 7), had no effect on the latency of the delayed activation of C-MHs. Also, indomethacin, which inhibits the synthesis of prostaglandins, had no effect on the latency of the delayed paw-withdrawal response in the behavioral test. 5. Intradermal injection of the calcium ionophore A23187 significantly reduced the latency of the delayed activation of C-MHs (n = 6) the calcium chelator Quin 2 (n = 6) significantly increased the latency. A23187 and Quin 2 had similar effects on the latencies to paw withdrawal in behavioral tests. The sensitization of C-MHs (n = 9) by PGE2 was not, however, affected by Quin 2.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminoquinolines↗
PubMed2001

The pan-chemokine inhibitor NR58-3.14.3 abolishes tumour necrosis factor-alpha accumulation and leucocyte recruitment induced by lipopolysaccharide in vivo.

Chemokines participate in the regulation of leucocyte recruitment in a wide variety of inflammatory processes, including host defence and diseases such as asthma, atherosclerosis and autoimmune disorders. We have previously described the properties of Peptide 3, the first broad-specificity chemokine inhibitor in vitro. Here, we report the properties of NR58-3.14.3, a retroinverso analogue of Peptide 3. NR58-3.14.3 inhibited leucocyte migration induced by a range of chemokines, including monocyte chemoattractant protein-1 (MCP-1) (2.5 nM), macrophage inflammatory protein-1alpha (MIP-1alpha) (5 nM), regulated on activation, normal T-cell expressed and presumably secreted (RANTES) (20 nM), stromal cell-derived factor-1alpha (SDF-1alpha) (25 nM) and interleukin-8 (IL-8) (30 nM), but did not affect migration induced by N-formyl-methionyl-leucyl-phenylalanine (FMLP) or complement C5a (> 100 microM). NR58-3.14.3 is therefore approximately 1000-fold more potent than Peptide 3 but retains the broad-spectrum chemokine inhibitory activity of the parent peptide. In vivo, pretreatment with a systemic dose of 10 mg of NR58-3.14.3, but not the inactive derivative NR58-3.14.4, abolished leucocyte recruitment in response to intradermal injection of 500 ng of MCP-1 into rat skin. This suggests that NR58-3.14.3 is a functional chemokine inhibitor in vivo as well as in vitro. We utilized NR58-3.14.3 as a tool to investigate the role of chemokine activity during leucocyte recruitment in response to lipopolysaccharide (LPS) in vivo. NR58-3.14.3, but not NR58-3.14.4, abolished leucocyte recruitment in response to intradermal injection of 50 ng of LPS into rat skin. Furthermore, NR58-3.14.3 completely inhibited LPS-induced accumulation of tumour necrosis factor-alpha (TNF-alpha). This data is consistent with a model in which multiple chemokines act in parallel upstream of TNF-alpha. NR58-3.14.3 is therefore a powerful anti-inflammatory agent in vivo, suppressing proinflammatory cytokine production and leucocyte recruitment in response to endotoxin stimulus in rat skin.

Animals↗
PubMed2003

Normal and gene-corrected dystrophic epidermolysis bullosa fibroblasts alone can produce type VII collagen at the basement membrane zone.

Type VII collagen is synthesized and secreted by both human keratinocytes and fibroblasts. Although both cell types can secrete type VII collagen, it is thought that keratinocytes account for type VII collagen at the dermal-epidermal junction (DEJ). In this study, we examined if type VII collagen secreted solely by dermal fibroblasts could be transported to the DEJ. We established organotypic, skin-equivalent cultures composed of keratinocytes from patients with recessive dystrophic epidermolysis bullosa (RDEB) and normal dermal fibroblasts. Immuno-labeling of skin equivalent sections with the anti-type VII collagen antibody revealed tight linear staining at the DEJ. RDEB fibroblasts, were gene-corrected to make type VII collagen and used to regenerate human skin on immune-deficient mice. The human skin generated by gene-corrected RDEB fibroblasts or normal human fibroblasts combined with RDEB keratinocytes restored type VII collagen expression at the DEJ in vivo. Further, intradermal injection of normal human or gene-corrected RDEB fibroblasts into mouse skin resulted in the stable expression of human type VII collagen at the mouse DEJ. These data demonstrate that human dermal fibroblasts alone are capable of producing type VII collagen at the DEJ, and it is possible to restore type VII collagen gene expression in RDEB skin in vivo by direct intradermal injection of fibroblasts.

Animals↗
PubMed1989

Involvement of the mu-opiate receptor in peripheral analgesia.

The intradermal injection of mu (morphine, Tyr-D-Ala-Gly-NMe-Phe-Gly-ol and morphiceptin), kappa (trans-3,4-dichloro-N-methyl-N[2-(1-pyrrolidinyl) cyclohexyl]benzeneactemide) and delta ([D-Pen2.5]-enkephalin and [D-Ser2]-[Leu]enkephalin-Thr) selective opioid-agonists, by themselves, did not significantly affect the mechanical nociceptive threshold in the hindpaw of the rat. Intradermal injection of mu, but not delta or kappa opioid-agonists, however, produced dose-dependent inhibition of prostaglandin E2-induced hyperalgesia. The analgesic effect of the mu-agonist morphine was dose-dependently antagonized by naloxone and prevented by co-injection of pertussis toxin. Morphine did not, however, alter the hyperalgesia induced by 8-bromo cyclic adenosine monophosphate. We conclude that the analgesic action of opioids on the peripheral terminals of primary afferents is via a binding site with characteristics of the mu-opioid receptor and that this action is mediated by inhibition of the cyclic adenosine monophosphate second messenger system.

Analgesia↗
PubMed2001

Non-noxious A fiber afferent input enhances capsaicin-induced mechanical hyperalgesia in the rat.

Intradermal injection of capsaicin induces primary hyperalgesia at the injection site and secondary hyperalgesia in the surrounding undamaged skin. The secondary hyperalgesia is thought to be due to central sensitization of the dorsal horn neurons while primary hyperalgesia is caused by sensitization of nociceptors in the damaged skin. In this study, we asked if additional non-noxious afferent input from the undamaged skin influences the already developed secondary hyperalgesia, which follows an intradermal injection of capsaicin. Capsaicin dissolved in olive oil was injected into the middle of the hind paw of male Sprague-Dawley rats (250-300 g) under gaseous anesthesia. This produced a decrease in the mechanical threshold at the base of the toes for hind limb withdrawals lasting for 1-2h, thus showing a short-lasting (hours) secondary hyperalgesia. When the capsaicin injection was immediately followed by repeated non-noxious mechanical stimuli or weak electrical stimuli (A fiber strength) applied to the area of secondary hyperalgesia (toes) for 30 min, the reduction of the mechanical threshold lasted longer than 24h. These results suggest that non-noxious A fiber afferent input can powerfully modulate central sensitization in the spinal dorsal horn, causing the duration of the secondary hyperalgesia to be greatly extended.

Animals↗
PubMed1999

Experimental models of skin inflammation.

The skin is the most accessible organ of the body in which to view the inflammatory process and its pharmacological modulation. However, there are relatively few studies in which the response of the dermal vasculature to inflammatory stimuli has been assessed quantitatively or the chemical mediators of the response measured directly. The mechanisms underlying these responses remain unclear despite the fact that altered microvascular function plays an important part in a number of clinical conditions. This paper describes recent studies in which an experimental model of inflammation in the skin has been used to investigate the pharmacological mechanisms underlying microvascular responses. As allergen-induced cutaneous weal and flare responses are mediated mainly by histamine, we first set out to characterize the vascular responses using the intradermal injection of histamine as a first step, experimental model of allergic skin disease. To quantify the inflammatory responses and to explore the mediator mechanisms underlying them we have combined the techniques of scanning laser Doppler imaging of blood flux and dermal microdialysis to make simultaneous measurements of changes in skin blood flow and the release of mediators within the weal and flare response to intradermal injection of histamine in human skin, in vivo.

Animals↗