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Biomedical subjects

I Katayama

Publications and source records attributed to I Katayama.

At least 55 records · Page 3Linked to original sources
PubMed1999

Animal model of sclerotic skin. I: Local injections of bleomycin induce sclerotic skin mimicking scleroderma.

We have established a mouse model for scleroderma induced by repeated local injections of bleomycin (BLM). Daily injection of BLM at a dose of >10 microg per ml for 4 wk induced histologic changes of dermal sclerosis, but not fibrosis, with thickened and homogenous collagen bundles and cellular infiltrates in BALB/C mice, whereas clinical signs of scleroderma were not apparent. In addition, lung fibrosis was also induced preceding the cutaneous changes. Sclerotic changes were not found in other sites of the skin distant from the injection site. Dermal sclerosis could also be induced by injecting BLM only every other day. The sclerotic changes of the dermis were sustained after ceasing BLM applications for at least 6 wk. Mast cells gradually increased in number as the sclerotic changes developed. Marked degranulation of mast cells was observed with elevated histamine release. The amount of hydroxyproline in skin was significantly increased at 4 wk of BLM treatment as compared with that in untreated or phosphate-buffered saline-treated mice. Anti-nuclear antibody was detected in serum of BLM-treated mice. Transforming growth factor-beta1 mRNA was detected at an early phase, while transforming growth factor-beta2 mRNA was strongly expressed at 4 wk when the sclerotic features were prominent. These results suggest that dermal sclerosis induced by BLM closely resembles systemic sclerosis both histologically and biochemically. Our mouse model can provide a powerful tool of inducing dermal sclerosis to examine the pathogenesis and the therapeutic approach of scleroderma.

Animals↗
PubMed1999

IL-4 inhibits the migration of human Langerhans cells through the downregulation of TNF receptor II expression.

The migration of Langerhans cells is an initial event in the sensitization phase of contact sensitivity. Langerhans cells travel from the epidermis to the regional lymph node, and can be variously modulated in the skin where many cytokines are released from epidermal cells, dermal cells, T helper (Th) cells, and other inflammatory cells during the sensitization and elicitation phase of contact dermatitis, and thus induce an altered inflammatory skin reaction. The modulatory effect of the cytokines released in the skin, such as IL-1beta, GM-CSF, and TNF-alpha as epidermal cytokines, IL-2, IL-12, and IFN-gamma as Th1 type cytokines, and IL-4 and IL-10 as Th2 type cytokines, was analyzed using the chemotactic chamber method in this study. Both GM-CSF and TNF-alpha induced the migration of human Langerhans cells in vitro, whereas IL-1beta, IL-2, IL-10, IL-12, and IFN-gamma had no effect on Langerhans cell migration. In contrast, IL-4 inhibited Langerhans cell migration in a dose dependent manner. The inhibitory activity of IL-4 was reversed by both anti-human IL-4 monoclonal antibody and anti-human IL-4 receptor monoclonal antibody. IL-4 inhibited the Langerhans cell migration induced by both TNF-alpha and GM-CSF. Furthermore, anti-TNF-RII monoclonal antibody inhibited both random migration and the migration induced by TNF-alpha, but not that induced by GM-CSF. A reverse-transcriptase-polymerase chain reaction and fluorescence-activated cell sorter analysis revealed that TNF-alpha up-regulated and IL-4 downregulated the TNF receptor II (TNF-RII) expression of Langerhans cells at both the mRNA and the protein levels. The pretreatment of Langerhans cells with TNF-alpha enhanced the migration of Langerhans cells and the expression of TNF-RII. After pretreating Langerhans cells with TNF-alpha, IL-4 inhibited both the migration of Langerhans cells and the expression of TNF-RII in a time dependent manner. These results indicate that IL-4 inhibits the migratory activity of Langerhans cells by downregulating the expression of TNF-RII in human Langerhans cells and thereby modulates the immune response in the skin.

Antibodies, Monoclonal↗
PubMed1999

Effect of superoxide dismutase on bleomycin-induced dermal sclerosis: implications for the treatment of systemic sclerosis.

Bleomycin has a chemical toxicity capable of inducing superoxide radicals, which are suggested to play an important part in bleomycin-induced pulmonary fibrosis. We have recently established a mouse model for scleroderma induced by repeated local injections of bleomycin. In this study, we examined the inhibitory effect of superoxide dismutase on the development of dermal sclerosis induced by bleomycin using this mouse model. PC-superoxide dismutase, which is a lecithinized superoxide dismutase with high tissue accumulation and long half-life in blood, was administered (3000 U per kg; dissolved in 5% mannitol) 3 h before the injection of bleomycin in C3H mice for 3 wk. Systemic PC-superoxide dismutase markedly inhibited the development of dermal sclerosis, which was also accompanied by a decrease in the number of infiltrating mast cells and eosinophils. Furthermore, the hydroxyproline content in the skin was significantly reduced, as compared with mice treated with bleomycin only or bleomycin and 5% mannitol. In a separate experiment, after the development of dermal sclerosis following treatment with bleomycin for 3 wk, PC-superoxide dismutase was administered for 2 wk. Histologic examination again revealed a reduction of dermal sclerosis, followed by a significant associate in the number of both mast cells and eosinophils. The hydroxyproline content in the skin was not significantly decreased, however, even after injections of high amounts of PC-superoxide dismutase (30,000 U per kg). These results support the involvement of oxygen free radicals in bleomycin-induced dermal sclerosis, and also indicate that administration of superoxide dismutase may be effective in the therapeutic approach in systemic sclerosis.

Animals↗
PubMed1999

Cutaneous angiosarcoma with thrombocytopenia.

Thrombocytopenia was observed in 3 patients with cutaneous angiosarcoma of the scalp and face. A sudden decrease in the platelet count occurred in association with rapid enlargement of primary or metastatic lesions. Neither antiplatelet antibody nor platelet-associated IgG was detected. Increased serum levels of beta-thromboglobulin and platelet factor 4 indicated that platelets were destroyed and consumed within the vascular bed of the tumor. Prominent PECAM-1 expression on tumor cells may be involved in intratumoral platelet aggregation and consumption. We suggest that the sudden development of profund thrombocytopenia in patients with angiosarcoma may suggest either rapid growth of the primary tumor or herald the development of metastatic disease.

Aged↗
PubMed1999

Pseudolymphomatous folliculitis: a clinicopathologic study of 15 cases of cutaneous pseudolymphoma with follicular invasion.

We report the clinical, histopathologic, and immunohistologic features of 15 cases of pseudolymphomatous folliculitis (PLF). The patients comprised seven males and eight females (mean age, 38.6 years; age range, 2-67 years). All patients had dome-shaped or flat-elevated nodules suggestive of cutaneous lymphoid hyperplasias (CLHs). The lesions were solitary in all 15 cases, except in one case with duplex lesions. All lesions were located on the face and measured less than 1.5 cm. In 14 cases with one lesion each, five lesions showed rapid regression after incisional biopsy, whereas the remaining nine underwent excisional biopsy. In the case with duplex lesions, one regressed spontaneously after excisional biopsy of the other. Histopathologically, all PLFs showed dense lymphocytic infiltrates from the dermis to the subcutis simulating cutaneous lymphomas. The walls of hair follicles in all cases were enlarged and irregularly deformed with their epithelium blurred by lymphocytic infiltrates; we called this change "activation" of hair follicles. In nine cases, many atypical lymphocytes were intermingled; three of these cases had been misdiagnosed as cutaneous T-cell lymphoma at other institutions. Immunohistologically, 10 and 5 cases showed predominantly B cells and predominantly T cells, respectively. Remarkably, all lesions showed increased numbers of perifollicular histiocytes expressing anti-S-100 protein and CD1a, and seven lesions showed histiocytes in aggregates. We conclude that PLF is a subset of CLH with characteristic clinical and pathologic features showing perifollicular clustering of T-cell-associated dendritic cells with activation of pilosebaceous units. PLF is an entity to be differentiated from malignant lymphomas and other cutaneous pseudolymphomas.

Adolescent↗
PubMed1999

Cataract and retinal detachment in patients with severe atopic dermatitis who were withdrawn from the use of topical corticosteroid.

Many patients with severe atopic dermatitis (AD) in Japan are afflicted with persistent erythema of the face (atopic red face) that is not only resistant to topical corticosteroid, but often becomes worse with its use. During a three-year period (1991-1993), we treated 79 inpatients with severe AD by a combination of careful daily skin care, use of emollients, and exclusion of exacerbating factors. Occular complications before and after treatment were examined in these cases. After withdrawal of topical corticosteroid, almost all of the patients showed a temporary worsening of their skin condition. Immediately thereafter, their occular symptoms did not change. Cataract was found in 20 cases (25.3%), and retinal detachment in 9 (11.4%). After 2 months, 11 cases of cataract and 5 cases of retinal detachment in the peripheral retina were observed. However, these incidences were similar to the numbers reported in Japan during conventional treatment with topical corticosteroid. The development of cataract or retinal detachment had no relationship to serum IgE levels, personal history of respiratory atopy, the duration of topical corticosteroid use on the face, or treatment with systemic corticosteroid. Our observations suggest that patients who habitually tap or rub their faces strongly tend to develop cataract or retinal detachment at a statistically significant higher frequency. Patients with AD should have ophthalmologic examinations every one to two months for at least one year after a facial oozing attack or withdrawal of corticosteroid.

Administration, Topical↗
PubMed1999

A Japanese case of dengue fever with lymphocytic vasculitis: diagnosis by polymerase chain reaction.

A 37-year-old Japanese male was admitted to Nagasaki University Hospital with abrupt onset of biphasic fever, general malaise and myalgia 9 days after coming back to Japan from Manila. He developed a rubella like erythematous rash 3 days after admission and purpuric eruption one week after admission. A biopsied specimen from the purpura revealed lymphocytic vasculitis with T cell dominance and without immunoglobulin or complement deposition around the blood vessels. RT-PCR analysis on peripheral blood mononuclear cells using dengue virus specific primers confirmed the diagnosis of type 3 dengue fever. PCR analysis using virus specific primers is a rapid and valuable method for making a correct diagnosis of dengue fever.

Adult↗
PubMed1999

Treatment of reticular erythematous mucinosis with a large dose of ultraviolet B radiation and steroid impregnated tape.

To date, there are no successful treatments for reticular erythematous mucinosis (REM) other than antimalarial drugs such as chloroquine; these have many adverse side effects and are prohibited for use in Japan. We report a case of REM improved by a large dose of ultraviolet B (UVB) radiation and a steroid impregnated tape. The large dose of UVB radiation improved the erythema after 5 weeks. Application of steroid impregnated tape to a lesion where a large dose of UVB had been given produced an additive clinical effect. UVB radiation and steroid impregnated tape are considered to be effective treatments for REM.

Combined Modality Therapy↗
PubMed1999

Solar urticaria: A consideration of the mechanism of inhibition spectra.

BACKGROUND: Solar urticaria is a rare disorder characterized by pruritus, erythema and wheal upon sunlight exposure. Inhibition spectra (IS), which prevent wheal formation, have been found mainly in Japanese patients and lie mostly in longer wavelengths than the action spectrum (AS). The exact mechanism of AS and IS has not been clarified. PATIENTS AND METHODS: To elucidate the mechanism of AS and IS, we conducted photobiological studies including in vitro irradiated serum injection tests and measurements of plasma histamine levels in 3 patients with IS. RESULTS: All patients had AS ranging between 400 and 490 nm and IS ranging between 520 and 610 nm. A wheal reaction appeared soon after the termination of IS irradiation. The patients developed no wheal or erythema upon intradermal injection of preirradiated serum. Plasma histamine levels were not elevated during irradiation with slide projector light, but marked elevation of histamine was observed when wheals developed after the termination of inhibitory irradiation. CONCLUSION: These results suggest that the IS in our cases might inactivate photoallergens produced by AS and, additionally, stabilize mast cell degranulation.

Adolescent↗
PubMed1999

Polymorphous light eruption. A case report and consideration of the hardening mechanism.

BACKGROUND: Polymorphous light eruption (PLE) is a common form of photodermatosis. The pathogenesis of the disease and the mechanism of the hardening phenomenon, however, have not been clarified. OBSERVATION: We report a 62-year-old Japanese woman with PLE. Provocation and hardening induction testing revealed that hardening was induced at the sites irradiated by a sufficient dose of UV for reproduction of the lesion. Topical steroid could prevent a positive reaction but not the hardening induction. The expression of adhesion molecules and CD1a was decreased at the hardening site. CONCLUSION: From these results, the hardening phenomenon in our case might be due to immunosuppression by UV exposure supported by the down-regulation of cell adhesion molecule expression and partially due to the depletion of endogenous antigens which cause a delayed-type hypersensitivity reaction.

Antigens, CD1↗
PubMed1999

Fibroblast proliferation by bleomycin stimulated peripheral blood mononuclear cell factors.

OBJECTIVE: To evaluate the role of bleomycin for cutaneous fibrosis, we investigated the effects of bleomycin stimulated peripheral blood mononuclear cell (PBMC) factors on in vitro proliferation of mouse 3T3 fibroblasts. METHODS: PBMC were incubated with 10(-4) to 10 microg/ml of bleomycin, and the supernatants (conditioned media) were collected after 48 h. 3H-TdR incorporation was assayed to examine the effects of conditioned medium on 3T3 fibroblast proliferation, which was also compared between 8 patients with systemic sclerosis (SSc) and 8 control subjects. RESULTS: Conditioned medium stimulated 3T3 fibroblasts to proliferate in a dose dependent manner, while culture supernatant without stimulation of bleomycin showed no growth stimulatory activity. Conditioned medium derived from PBMC of patients with SSc exhibited a significantly higher growth activity than that from controls (p < 0.05). Among PBMC subpopulations, macrophages showed the most increased growth effect on 3T3 fibroblasts, although T lymphocyte populations also showed growth activity. The growth activity was inhibited up to 35% by anti-platelet derived growth factor (PDGF) antibody. In addition, growth activity was also partially blocked by antibodies against basic fibroblast growth factor (bFGF) (20%), interleukin 1beta (IL-1beta) (15%), tumor necrosis factor-alpha(TNF-alpha) (7.9%), and transforming growth factor-beta (TGF-beta)(9.5%). The cellular release of IL-1beta, TNF-alpha, and IL-6 was elevated in response to bleomycin exposure in both controls and patients with SSc. Reverse transcriptase-polymerase chain reaction revealed that conditioned medium derived from both patients with SSc and controls induced mRNA expression of several fibrogenic cytokines such as IL-6, TNF-alpha, TGF-beta, and PDGF. IL-1alpha was induced only by conditioned medium derived from patients with SSc. CONCLUSION: These results suggest that bleomycin induced cutaneous fibrosis as well as pulmonary fibrosis may be induced by inflammatory cells through several fibrogenic cytokines.

3T3 Cells↗
PubMed1999

[Antidiuretic hormone in severe cases of atopic dermatitis].

32 out of 83 in patients with atopic dermatitis showed a decrease of urine excretion during acute exacerbation and elevated levels of antidiuretic hormone (ADH 23 of 29 cases), renin (18 of 32 cases), angiotensin (22 of 29 cases) and aldosterone (16 of 37 cases). Six cases with high ADH showed severe pitting edema of lower legs with hypoalbuminemia. ADH, volume of urine and edema were improved when their skin symptoms subsided. There was no statistically significant relationship between the dose of steroid ointment and ADH. Also there was no correlation between low 17-OHCS or 17-KS and high ADH or renin.

Adult↗
PubMed1999

[Site specific difference of PCB concentration in the skin derived sebum and collection of excreted sebum with commercial sebum-remover sheet].

The PCB concentrations in the sebum of Yusho patients showed a site specific difference. It was higher in the sebum derived from the chest (1128.0 +/- 374.1 ng/g), the upper arm (1460.0 +/- 350.7 ng/g) and the femur (1456.0 +/- 488.5 ng/g) than from the forehead (758.0 +/- 233.7 ng/g) and the upper back skin (638.0 +/- 165.3 ng/g). To remove PCB in the sebum, a sebum-remover sheet was applied on the femur of two patients. During the four times of application, the mean amounts of removed sebun was 10.5 mg and 28.3 mg respectively. These results are unsatisfactory for practical treatment of Yusho patient. However, this approach seems to be safe and convenient and modification to collect large scale of sebum from the skin is required.

Aged↗
PubMed1999

Confluent ecchymoses on the lower extremities of a malnourished patient.

Nutritional deficiencies result in many distinctive cutaneous manifestations. Vitamin C deficiency, or scurvy, produces follicular hyperkeratosis, perifollicular hemorrhages, gingival hypertrophy, and bleeding (1). We report here a case of malnutrition who suddenly developed extensive eccymoses on the lower extremities sharing morphological similarities with purpura fulminans. Although the patient did not have the characteristic dermatological features of scurvy, serum levels of vitamins C, K, B12, and E were decreased.

Aged↗
PubMed1999

Animal model of sclerotic skin. II. Bleomycin induced scleroderma in genetically mast cell deficient WBB6F1-W/W(V) mice.

OBJECTIVE: Previously, we established a mouse model of scleroderma induced by repeated subcutaneous bleomycin injections. In this model, increased numbers of mast cells were observed in the lesional skin of dermal sclerosis, and degranulation of mast cells was prominent prior to the increase of mast cell numbers. Mast cells have been suggested to play an important role in tissue fibrosis. In this study, we investigated whether dermal sclerosis is also induced by bleomycin administration in genetically mast cell deficient WBB6F1-W/W(V) mice. METHODS: Bleomycin was subcutaneously injected every day in WBB6F1-W/W(V) and their normal littermate WBB6F1-+/+ mice for 4 weeks, and mice were analyzed for histological sclerosis, mast cell number, plasma histamine level, and hydroxyproline content. RESULTS: Four weeks' injections of bleomycin effected histological dermal sclerosis in both mast cell deficient and control strains; however, at 1 week, dermal sclerosis was induced only in WBB6F1-+/+ mice. Mast cells gradually increased in number around or on the edge of sclerotic lesions in WBB6F1-+/+ mice, as the dermal sclerosis developed. Hydroxyproline content of the skin of WBB6F1-+/+ mice was higher than that of WBB6F1-W/Wv mice at 1 week, but was not statistically significant. After 2 weeks' treatment with bleomycin, the hydroxyproline content of the skin was similar in both strains. The number of infiltrating macrophages and CD4+ T cells also gradually increased in both strains; however, the difference did not reach significance during the course of bleomycin treatment. CONCLUSION: These results show that mast cell is not necessary for inducing dermal sclerosis by bleomycin, and other types of inflammatory cells such as infiltrating macrophages or T lymphocytes may play a role in triggering induction of dermal sclerosis via fibrogenic cytokines. However, mast cell releasing mediators or cytokines may play a role in accelerating formation of dermal sclerosis, in particular, at an early phase of the sclerotic process, and not merely as a result of sclerosis.

Animals↗