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T Terui

Publications and source records attributed to T Terui.

At least 37 records · Page 2Linked to original sources
PubMed2001

Production and pharmacologic modulation of the granulocyte-associated allergic responses to ovalbumin in murine skin models induced by injecting ovalbumin-specific Th1 or Th2 cells.

Because interferon-gamma, interleukin-4, and interleukin-5 have been identified at the mRNA and protein levels in the lesional skin of patients with atopic dermatitis, we investigated the roles played by granulocytes as effector cells in allergic inflammation by using two unique murine skin models. In vitro generated Th1 and Th2 cells from naïve splenocytes of antiovalbumin T cell receptor transgenic BALB/C mice were adoptively transferred with ovalbumin into the ear pinnae or air-pouches produced in the back skin of naïve, nontransgenic BALB/C mice. The injection of Th1 cells with ovalbumin induced delayed type ear swelling that peaked at 48 h, whereas that of Th2 resulted in ear swelling that peaked at a much earlier time, 24 h. Histologic study of the swollen ear skin and granulocytes recruited into the air-pouch demonstrated that, although the Th1-induced inflammation caused a neutrophil-predominant infiltrate with few eosinophils, larger numbers of eosinophils accumulated in the Th2-induced inflammation. Using these murine models, we further evaluated the effects of drugs used for the treatment of atopic diseases. The results showed that FK506 administration could effectively reduce skin inflammation induced by either Th cells. Interestingly, the neutrophil elastase inhibitor ONO-6818 efficiently inhibited Th1-induced inflammation. In contrast, a leukotriene receptor antagonist, ONO-1078, specifically suppressed Th2-induced inflammation. We also found that each ONO drug exerted direct influence on specified granulocytes, as neither affected in vitro production of relevant Th cytokines. Thus, we succeeded in developing animal skin inflammation models in which we can evaluate the contribution of protein antigen-specific Th1 or Th2 cells through the action of granulocytic effector cells.

Animals↗
PubMed2001

Pleuropericarditis and disseminated intravascular coagulation in ulcerative colitis.

We report a 30-year-old woman with pleuropericarditis, cardiac tamponade, and disseminated intravascular coagulation complicating active ulcerative colitis (UC). Other autoimmune diseases were not present. She responded to pulsed steroid therapy and anticoagulant with resolution of the complication and UC. We reviewed the literature and found 27 cases of pleuropericarditis associated with idiopathic inflammatory bowel disease (IBD). It has been reported that pleuropericarditis associated with IBD responds well to nonsteroidal antiinflammatory drugs, as well as steroids. The causes of cardiac involvement in IBD remain unclear, but the pleuropericarditis must be recognized as a potential extraintestinal manifestation of IBD.

Adult↗
PubMed2001

Molecular events occurring behind ultraviolet-induced skin inflammation.

We reviewed a recent advance in the studies of the molecular mechanisms for 'ultraviolet responses', paying special attention to two transcription factors, nuclear factor kappa B and p53, and to a balance noted between an anti-apoptotic phosphatidylinositol 3-kinase-Akt pathway and its inhibitory ceramide-caveolin-1 pathway. These studies were mostly carried out using in vitro or animal models. On the basis of these results, we determined that phase by phase molecular events clarified in these studies correspond well with the three phases of ultraviolet-induced inflammation observed, i.e. the early vasodilatory phase, the second inflammatory phase in which many inflammatory cells such as neutrophils and T cells accumulate in the skin, and the last regressive phase based on several anti-inflammatory events.

Humans↗
PubMed2000

Thermal remediation of PCDD/Fs contaminated soil by zone combustion process.

A new thermal process has been proposed for remediating soils contaminated by chlorinated organic compounds, e.g., PCDD/Fs and PCBs. This is to apply the "zone combustion process" which utilizes stable combustion of coke particles in the packed bed to soils with air flow across the bed. The usefulness and validity were obtained the results showing that more than 98.9% of PCDD/Fs in the soil was successfully removed in a laboratory-scale experiment. Some pretreatment of the soil sample, such as drying, pre-granulation and addition of limestone was found to make the removal efficiency better. Although, some fundamentals on the behavior of PCDD/Fs, e.g., decomposition/vaporization ratios and formation of other compounds cannot be certainly identified yet, the present results clearly show a way to remediate the contaminated soils and solid wastes.

Benzofurans↗
PubMed2000

Mediators of inflammation involved in UVB erythema.

In this review, we discuss the mediators and inflammatory cells involved in UVB-induced inflammatory changes phase by phase. We especially stress the importance of IFNgamma secreted by activated CD4(+) T cells in the development of UVB erythema. We also speculate on the mechanism underlying regression of UVB erythema.

Animals↗
PubMed2000

Role of neutrophils in induction of acute inflammation in T-cell-mediated immune dermatosis, psoriasis: a neutrophil-associated inflammation-boosting loop.

A growing body of evidence has indicated that T-cell-mediated immunity plays an important role in triggering and maintenance of psoriatic lesions. In this review we present our own experimental results as well as those from the literature related to the pathomechanism of the development of inflammatory changes in psoriatic lesions. First of all it is important to acknowledge the fact that psoriatic lesions are not uniform as assumed by many authors but that they are actually rather heterogeneous both clinically and histologically even within the same plaques. Lymphokines produced by activated T cells in psoriatic lesions have a strong influence on the proliferation of the epidermis, whose stimulated kertinocytes released several cytokines, which in turn enhance the activation state of T cells. Thus, they form a vicious cycle, a T-cell-mediated inflammation-sustaining loop. Although the interaction between T-cell-mediated immunity and epidermal keratinocytes may well explain the maintenance of background "chronic" inflammatory changes diffusely observed throughout psoriatic lesions, it is not enough to explain the island-like, "acute" inflammatory changes observed within and at the border of the plaque lesions. Characteristic neutrophil accumulation under the stratum corneum can be observed in the highly inflamed and therapeutically recalcitrant areas of psoriatic lesions. They are chemotactically attracted and activated there by synergistic action of chemokines, IL-8 and Gro-a released by the stimulated keratinocytes, and particularly C5a/C5a des arg produced via the alternative complement pathway activation possibly on the surface of corneocytes. In this review, we emphasize that the accumulation of neurophils is not simply a passive event. We think that those stimulated neutrophils are able to influence not only the growth and differentiation of epidermal keratinocytes but also the activation-state of T cells by aberrant expression of HLA-DR on their surfaces as well as by their effects. These T cells in turn influence the transepidermal neutrophil migration through the effect of their lymphokines on the keratinocyte production of pro-inflammatory mediators including C3. Therefore, we propose a neutrophil-associated inflammation-boosting loop that may well explain the localized "acute" inflammatory changes scattered over the "chronic" psoriatic plaques as well as in the acutely inflamed lesions of pustular psoriasis.

Acute Disease↗
PubMed2000

Ultraviolet B radiation exerts enhancing effects on the production of a complement component, C3, by interferon-gamma-stimulated cultured human epidermal keratinocytes, in contrast to photochemotherapy and ultraviolet A radiation that show suppressive effects.

The present study was designed to investigate by using enzyme-linked immunosorbent assay and reverse transcriptase-polymerase chain reaction methods whether photochemotherapy (PUVA) or ultraviolet (UV) B treatment affects C3 production by interferon (IFN)-gamma-stimulated keratinocytes cultured in serum-free medium. The results showed that PUVA and UVA reduced C3 production by IFN-gamma-stimulated epidermal keratinocytes dose-dependently, although the effect of PUVA was stronger than that of UVA alone. Interestingly, UVB induced an enhancement of C3 production at doses ranging from 10 to 50 mJ cm-2. This phenomenon was found at both the protein and mRNA levels. In every experiment, changes in C3 mRNA levels preceded those in its protein levels. Reduced C3 production at higher doses of 75 and 100 mJ cm-2 were probably due to cytotoxic effects of UVB. In our experimental system, PUVA, UVA or UVB treatment did not affect C3 production without IFN-gamma stimulation. Our results suggest that a reduction in C3 production by PUVA treatment may in part explain the efficacy of PUVA in the treatment of inflammatory dermatoses such as psoriasis, while the results of the UVB experiments may partially explain the proinflammatory nature of UVB.

Cells, Cultured↗
PubMed2000

Dermatofibroma with diffuse eosinophilic infiltrate.

Dermatofibroma, a common form of benign fibrous histiocytoma, is characterized by the presence of different cell types consisting of fibroblastic, histiocytic, and even multinucleated cells. Dermatofibromas are always accompanied by an inflammatory lymphoid cell reaction, including B cells and T cells at their border. To our knowledge, however, there is no report of an infiltration of eosinophils within this tumor. We describe a dermatofibroma on the pretibial region of an 8-year-old boy. Microscopic examination revealed a diffuse eosinophilic infiltration within the dermatofibroma, which was typically composed of histiocytic cells and mature collagen. The diagnosis of dermatofibroma was confirmed by demonstrating the immunoreactivity of tumor cells to an anti-factor XIIIa antibody.

Child↗
PubMed2000

Inflammatory and immune reactions associated with stratum corneum and neutrophils in sterile pustular dermatoses.

In this review we present our own experimental findings as well as those from the literature related to the pathomechanisms for the inflammatory changes in psoriasis and its related diseases. A growing body of evidence has indicated that T cell-mediated immunity plays an important role in triggering and maintenance of psoriatic lesions. It has been revealed that lymphokines produced by activated T cells in psoriatic lesions have a strong influence on the proliferation of the epidermis. Characteristic neutrophil accumulation under the stratum corneum can be observed in the highly inflamed areas of psoriatic lesions. These neutrophils are chemotactically attracted and activated there by synergistic action of chemokines, IL-8 and Gro-alpha released by stimulated keratinocytes, and particularly by C5a/C5a des arg produced via the alternative complement pathway activation. We demonstrated that the infiltrating neutrophils adhere to iC3b-opsonized corneocytes to produce active oxygen and probably lysosomal enzymes. From a close relationship observed between neutrophil accumulation and high mitotic ratio of the lesional epidermis, we think that these stimulated neutrophils influence the growth and differentiation of epidermal keratinocytes. Aberrant expression of HLA-DR on neutrophils suggests their activation of infiltrating T cells in the presence of bacterial superantigen. These T cells in turn influence the transepidermal neutrophil migration through the effect of their cytokines on the keratinocyte production of proinflammatory mediators including IL-8 and C3. In this review we discuss the pivotal roles played by stratum corneum and neutrophils in several skin diseases, where neutrophils accumulate beneath the stratum corneum in a sterile condition.

Dermatitis↗
PubMed2000

[Learning from fungus allergy in atopic dermatitis patients].

It has been recognized that there are considerable variations in their skin reactivity to environmental allergens as well as in immunoreactivities, even in AD patients with similar signs and symptoms. Some AD patients have high serum IgE antibody levels, while others show low levels. There are also differences in the kinds of triggering factors that are related to the development and maintenance of AD, e.g., allergic or non-allergic. Even among AD patients with high titers of serum IgE antibodies, the kinds and number of allergens involved in the exacerbation of AD are different and can change with time. The types of the underlying allergic reactions vary as well, i.e., some show immediate reactions, while others show delayed type hypersensitivity responses to environmental allergens. Thus, even AD patients diagnosed by the established criteria may have remarkably different backgrounds. When we looked over our published data, we noticed that there were differences in levels of IgE RAST and skin reactions between AD with atopic respiratory diseases (ARD) and pure AD without ARD. Levels of IgE RAST against airborne allergens, which come into the body mainly through the respiratory tract, were higher in AD with ARD, while those against allergens such as Candida albicans and Malassezia furfur, which can colonize on the skin, were higher in pure AD. In addition to these Th2-mediated immunological abnormalities, Th1-mediated DTH reaction and lymphocyte proliferation indices against airborne allergens were remarkably low in AD with ARD, whereas those against Candida albicans and Malassezia furfur were relatively preserved, although they were lower than those found in normal subjects. We understand from these findings that routes of allergen entry are important for the outcome of the resultant allergic reactions. This point of view is important answering questions such as how AD develops and how it can be prevented from the insults of each allergen.

Antibodies, Fungal↗
PubMed1999

[Cutaneous immune and inflammatory reactions to Malassezia furfur].

Initiation and aggravation of several inflammatory skin diseases are associated with Malassezia furfur. These are divided into at least two groups. In one group including tinea versicolor and Malassezia folliculitis, the growth of Malassezia furfur directly triggers the development of the cutaneous lesions. In another group including atopic dermatitis, seborrheic dermatitis, and psoriasis, cutaneous lesions already developed by other mechanisms are aggravated by the growth of Malassezia furfur. Recent progress of molecular biology techniques revealed that Malassezia furfur is divided into at least seven species. Since their clinical and histological findings are quite diverse, their differences cannot be explained solely by the difference in antigenicity of each Malassezia. Instead, the cutaneous defense mechanisms against Malassezia furfur must be considered. In this article, we reviewed the mechanisms at three levels: 1) barrier functions of the uppermost layer of the skin, the stratum corneum, 2) cytokine production by epidermal keratinocytes, and 3) immune and inflammatory responses by infiltrating neutrophils and T cells.

Dermatomycoses↗
PubMed1998

Solitary subcutaneous mucinosis surrounded by bizarre-shaped, factor XIIIa-positive cells with intranuclear vacuoles.

We describe a subcutaneous mucinosis developing in the right cheek of a 38-year-old man. Histologic examination revealed bipolar fibroblast-like cells embedded in a well demarcated mucinous stroma in the subcutis without a manifest reticulin network. In addition, bizarre, sometimes multinucleate, cells with intranuclear vacuoles were found at the periphery of the mucinous stroma. Immunohistologically, both the bipolar fibroblastic cells and bizarre-shaped cells were positive for vimentin, but were negative for smooth muscle A-actin, desmin, CD34, S100, trypsin, or chymotrypsin. However, the latter reacted to anti-factor XIIIa antibody, suggesting that they are derived from dermal dendritic cells. We think that this solitary subcutaneous mucinosis is a unique variant of cutaneous focal mucinosis, because neither a reticulin network nor reactivity to anti-smooth muscle A-actin antibody were demonstrable.

Adult↗
PubMed1998

Release of monocyte chemoattractants by polymorphonuclear leukocytes stimulated by their adhesion to stratum corneum opsonized via complement activation, measured with a human acute monocytic leukemic cell line, THP-1.

Stratum corneum (SC) exposed to living tissues, induces inflammation characterized by the formation of mixed cell granulomas consisting of infiltrative polymorphonuclear leukocytes (PMNs) and monocytes/macrophages. In this study, to clarify the mechanism for the later monocyte accumulation in SC-induced granulomas, we evaluated monocyte chemotactic activity induced by PMNs treated with serum-opsonized SC by using a human acute monocytic leukemic cell line, THP-1. When the supernatant was obtained from a PMN suspension cultured with opsonized plantar SC, higher THP-1 chemotactic activity was detected as compared with that cultured with non-opsonized SC. Although some concentrations of the chemokines, MIP-1alpha and MIP-1beta, were detected in supernatants obtained from the PMN suspensions cultured with plantar SC than in the control suspensions of PMN alone, their production by PMN was not influenced by the opsonization procedure. In contrast, MCP-1 was found to be secreted from PMN suspensions constitutively, showing no correlation to this THP-1 chemotactic activity. Moreover, HPLC analysis of PMN suspensions indicated that factors with far higher molecular weight values than these chemokines are involved in the chemotaxis of THP-1 cells.

Cell Adhesion↗
PubMed1998

An increased ratio of interleukin-1 receptor antagonist to interleukin-1alpha in inflammatory skin diseases.

IL-1 receptor antagonist (IL-1ra) is a cytokine that competitively binds the IL-1 receptor to antagonize IL-1 activity without any agonist function. Previous experiments indicated that the ratio of IL-1ra to IL-1alpha in the normal stratum corneum (SC) was much higher in the sun-exposed face than in the sun-protected area, upper arms. It was also reported by another laboratory that IL-1ra is increased in the lesional skin of psoriatic patients. This study was designed to measure the contents of IL-1alpha and IL-1ra in non-lesional and pathological SC obtained from inflammatory skin diseases including psoriasis and non-psoriatic dermatoses such as atopic dermatitis. The SC materials were obtained with a non-invasive tape-stripping method. Their soluble fractions were prepared and assayed for IL-1alpha and IL-1ra by enzyme-linked immunosorbent assays. As a result we confirmed the previous findings that the ratio of IL-1ra to IL-1alpha in the normal SC was much higher in the face than in the sun-protected sites, the trunk as well as extremities. Next, we found that IL-1alpha contents were significantly reduced in the SC samples obtained from inflammatory skin regardless of whether their IL-1ra contents increased or unchanged. Moreover, we noted that an increased ratio of IL-1ra to IL-1alpha in the SC was not specific to psoriasis, but was also found in other inflammatory skin diseases including atopic dermatitis. This ratio was found to become lower after successful treatment of these skin lesions with topical glucocorticoids. We conclude from these observations that the increased ratio of IL-1ra to IL-1alpha in the SC is a non-specific phenomenon that can occur in any inflammatory skin diseases regardless of the inflammatory pattern, probably reflecting a skin regulation process against various kinds of inflammation.

Dermatitis↗
PubMed1998

Annular elastolytic sarcoidosis of the face.

We report a case of facial annular lesions in a non-diabetic, Japanese woman aged 78, the histopathological study of which showed noncaseating, epithelioid cell granuloma with multinucleated giant cells. Together with the aberrant laboratory data, these clinical and histopathological findings were considered to be compatible with those of sarcoidosis, but elastic tissue stain disclosed the existence of elastolytic changes which were clinically and histopathologically similar to those found in actinic granuloma or annular elastolytic giant cell granuloma. Based on a review of the literature, we believe that several annular elastolytic granulomatous diseases of the face form a disease spectrum, some of which are identified with intermediate features of these three diseases.

Aged↗
PubMed1997

Dehydroepiandrosterone may be one of the regulators of cytokine production in atopic dermatitis.

Previous studies in mice have shown that dehydroepiandrosterone (DHEA) increases the production of Th1-associated lymphokines, and of interleukin-2 (IL-2) and interferon-gamma (IFN-gamma), by lymphocytes. However, there are no reports concerning the effect of DHEA on the production of Th2-associated lymphokines, IL-4 and IL-5, by lymphocytes in humans. We examined serum DHEA levels in patients with atopic dermatitis (AD), which is thought to be associated with a higher activity of Th2 cells than of Th1 cells. We also studied the effects of DHEA on the production of IL-4 and IL-5 by human lymphocytes. Serum DHEA concentrations in 47 adult male patients with AD aged 19-30 years were significantly lower than those of 53 age-matched healthy male controls. Preincubation of peripheral blood mononuclear cells (PBMCs) with DHEA reduced the IL-4 production by concanavalin A-stimulated PBMCs. Their IL-5 production also showed a tendency to decrease. These results suggest that DHEA may be one of the regulators of IgE synthesis and eosinophil proliferation in patients with AD and it may act by controlling IL-4, IL-5 and IL-2 production by lymphocytes.

Adult↗