bromochloroacetic-acid and Dermatitis--Allergic-Contact

bromochloroacetic-acid has been researched along with Dermatitis--Allergic-Contact* in 8 studies

Other Studies

8 other study(ies) available for bromochloroacetic-acid and Dermatitis--Allergic-Contact

ArticleYear
Induction of allergic contact dermatitis and pervasive face edema due to Brazilian keratin treatment.
    Journal of cosmetic dermatology, 2021, Volume: 20, Issue:3

    Brazilian keratin treatment (BKT) is a prevalent hair straightening method widely used by women in the world. The degree of concentration of formaldehyde safe for sensitive patients is still obscure. Report claims that these products contain intolerably high levels of formaldehyde. Yet, hair straightening products may lead to severe allergic contact dermatitis, by means of the responsible allergens such as formaldehyde and its releasers. This case report presents the case of a 37-year-old female patient developing extensive edema of the face and acute inflammatory changes in the scalp from chemical-induced irritation, on the day following the application of BKT to straighten her hair.

    Topics: Adult; Brazil; Dermatitis, Allergic Contact; Female; Formaldehyde; Hair Preparations; Humans; Keratins; Patch Tests

2021
Modification and expulsion of keratins by human epidermal keratinocytes upon hapten exposure in vitro.
    Chemical research in toxicology, 2011, May-16, Volume: 24, Issue:5

    Allergic contact dermatitis is the most prevalent form of human immunotoxicity. It is caused by reactive low molecular weight chemicals, that is, haptens, coming in contact with the skin where hapten-peptide complexes are formed, activating the immune system. By using sensitizing fluorescent thiol-reactive haptens, that is, bromobimanes, we show how keratinocytes respond to hapten exposure in vitro and reveal, for the first time in a living system, an exact site of haptenation. Rapid internalization and reaction of haptens with keratin filaments were visualized. Subsequently, keratinocytes respond in vitro to hapten exposure by release of membrane blebs, which contain haptenated keratins 5 and 14. Particularly, cysteine 54 of K5 was found to be a specific target. A mechanism is proposed where neoepitopes, otherwise hidden from the immune system, are released after hapten exposure via keratinocyte blebbing. The observed expulsion of modified keratins by keratinocytes in vitro might play a role during hapten sensitization in vivo and should be subject to further investigations.

    Topics: Bridged Bicyclo Compounds; Cell Line; Dermatitis, Allergic Contact; Epidermal Cells; Haptens; Humans; Keratinocytes; Keratins

2011
Exacerbated and prolonged allergic and non-allergic inflammatory cutaneous reaction in mice with targeted interleukin-18 expression in the skin.
    The Journal of investigative dermatology, 2003, Volume: 121, Issue:3

    Interleukin 18 induces both T helper 1 and T helper 2 cytokines, proinflammatory cytokines, chemokines, and IgE and IgG1 production. A role of interleukin 18 in inflammatory cutaneous reactions is still unclear, however. Here we generated keratin 5/interleukin 18 transgenic mice overexpressing mature murine interleukin 18 in the skin using a human keratin 5 promoter. In the contact hypersensitivity model, trinitrochlorobenzene elicited a stronger ear swelling in keratin 5/interleukin 18 transgenic mice compared with control littermate wild-type or immunoglobulin/interleukin 18 transgenic mice in which mature interleukin 18 was expressed by B and T cells under the control of the immunoglobulin promoter. Application of an irritant, croton oil, induced stronger and more sustained ear swelling in keratin 5/interleukin 18 transgenic mice than in immunoglobulin/interleukin 18 transgenic or wild-type mice. Repetitive topical application (weekly for six consecutive weeks) of trinitrochlorobenzene to their ears also elicited a stronger cutaneous inflammation in keratin 5/interleukin 18 transgenic mice than seen in immunoglobulin/interleukin 18 transgenic or wild-type mice. After these six trinitrochlorobenzene applications, the expression of interferon-gamma, interleukin-4, and CCL20 mRNA in the ear tissue was increased and dermal changes, such as acanthosis and eosinophilic, neutrophilic, and mast cell infiltration, were greater in keratin 5/interleukin 18 transgenic mice than in wild-type mice. Furthermore, the repetitive application elicited a significant increase in serum IgE levels and the number of B cells in the draining lymph node in keratin 5/interleukin 18 transgenic mice. These results suggest that overexpression of interleukin 18 in the skin aggravates allergic and nonallergic cutaneous inflammation, which is accompanied by high expression of T helper 1 and T helper 2 cytokines and chemokines in the skin.

    Topics: Animals; Cell Lineage; Chemokines; Croton Oil; Cytokines; Dermatitis, Allergic Contact; Ear, External; Female; Gene Expression; Interleukin-18; Irritants; Keratin-15; Keratin-5; Keratinocytes; Keratins; Lymph Nodes; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Picryl Chloride; Promoter Regions, Genetic; RNA, Messenger; Skin

2003
The selective triggering of CD40 on keratinocytes in vivo enhances cell-mediated immunity.
    European journal of immunology, 2002, Volume: 32, Issue:3

    CD40 is expressed on a wide array of hematopoietic and non-hematopoietic cells, including keratinocytes. The pivotal in vivo function of CD40 on hematopoietic cells in the regulation of both humoral and cell-mediated immunity is well established. However, whether CD40 expression on non-hematopoietic cells influences immunity has until now not been addressed. Therefore, we transgenically expressed human CD40 (hCD40) under the control of the keratin 14 promoter to drive expression of hCD40 in basal keratinocytes of mice. When we selectively engaged hCD40 in vivo on the keratinocytes of these mice, the keratinocytes secreted TNF-alpha, resulting in dendritic cell migration to draining lymph nodes and enhanced in vitro T cell priming to an epicutaneously applied chemical sensitizer. Exclusive CD40 engagement on keratinocytes during a contact hypersensitivity response displayed exacerbated and prolonged cutaneous immune reactions relative to control mice. Thus, CD40 engagement on non-hematopoietic cells, such as keratinocytes, can amplify cutaneous and regional T cell responses in vivo.

    Topics: Animals; Antibodies, Monoclonal; CD40 Antigens; Chemotaxis; Dendritic Cells; Dermatitis, Allergic Contact; Ear, External; Epidermis; Female; Humans; Immunity, Cellular; Keratinocytes; Keratins; Lymph Nodes; Mice; Mice, Transgenic; Organ Specificity; Oxazolone; Promoter Regions, Genetic; Recombinant Fusion Proteins; RNA, Messenger; T-Lymphocytes; Tumor Necrosis Factor-alpha

2002
Hydrolyzed protein shampoo additives are not a common contact allergen.
    Contact dermatitis, 2000, Volume: 43, Issue:4

    Topics: Allergens; Collagen; Dermatitis, Allergic Contact; Elastin; Hair Preparations; Humans; Hydrolysis; Keratins; Patch Tests

2000
Expression of fetal cytokeratins in epidermal cells and colloid bodies in lichen planus.
    Journal of cutaneous pathology, 1998, Volume: 25, Issue:1

    Clusters of immunoglobulin (Ig)-coated colloid bodies (CBs) in the dermo-epidermal zone are a typical immunohistochemical feature in lichen planus (LP)-lesions. They are considered to represent dyskeratotic basal keratinocytes, yet their composition has not been completely elucidated. In the present study, skin biopsies of 10 LP-lesions, 3 other dermatoses, and 10 biopsies of normal skin were studied immunohistochemically using monoclonal antibodies (MAbs) against fetal and differentiated epidermal antigens. CBs were identified by FITC-anti-Ig. Binding of MAb was visualized by double staining technique. Cytokeratin (CK) 10/11, a marker of epidermal differentiation, was consistently detected in suprabasal keratinocytes and also in up to 95% of Ig-positive CBs in LP. CK10/11 was additionally detected in basal keratinocytes in 9 LP-lesions, but not in normal skin. The basal cell-specific MAb BL7 stained basal layer keratinocytes in all biopsies. In contrast to normal skin, in LP scattered suprabasal keratinocytes and CBs were also positive for BL7 in 10 and 7 cases, respectively. While fetal cytokeratins (CK13 and CK8/18) were completely absent in control skin specimens, both cytokeratins were detected in various numbers of keratinocytes and CBs in all LP-lesions. Our results support the hypothesis of an epidermal origin of CBs. The cytokeratin profile seems to be severely disturbed in LP. This includes both accelerated differentiation by the expression of suprabasal CK10/11 in basal keratinocytes and dedifferentiation by the expression of fetal epidermal antigens (CK13 and CK8/18). It is tempting to speculate that the observed alterations may trigger T-cell activation and inflammatory onset in LP.

    Topics: Adolescent; Adult; Aged; Antibodies, Monoclonal; Cell Count; Dermatitis, Allergic Contact; Drug Eruptions; Female; Fluorescent Antibody Technique, Direct; Humans; Immunohistochemistry; Inclusion Bodies; Keratinocytes; Keratins; Lichen Planus; Lupus Erythematosus, Discoid; Male; Middle Aged; Skin

1998
Changes in epidermal proliferation and differentiation in allergic and irritant contact dermatitis reactions.
    The British journal of dermatology, 1995, Volume: 133, Issue:2

    Allergic and irritant contact dermatitis are similar clinically, histologically and on immunohistochemistry. In the present investigation, we assessed whether study of the recruitment of cycling epidermal cells, and the expression of keratin 16 and involucrin, are of use in differentiating between the response to contact allergens and the response to the irritant detergent sodium lauryl sulphate. Both allergic and irritant challenges induced epidermal proliferation, and the expression of keratin 16 and involucrin, but the dynamics were different. Two and 3 days after challenge, a highly significant difference between the allergic and irritant reactions was observed with respect to involucrin expression assessed by MON-150 staining.

    Topics: Adult; Aged; Cell Differentiation; Cell Division; Dermatitis, Allergic Contact; Dermatitis, Irritant; Epidermis; Female; Humans; Immunohistochemistry; Keratins; Male; Middle Aged; Protein Precursors; Time Factors

1995
STUDIES ON THE BINDING OF PROTEIN BY NICKEL. WITH SPECIAL REFERENCE TO ITS ROLE IN NICKEL SENSITIVITY.
    The British journal of dermatology, 1964, Volume: 76

    Topics: Animals; Antigen-Antibody Reactions; Caseins; Cattle; Cyanides; Dermatitis; Dermatitis, Allergic Contact; Dermatitis, Atopic; Erythema; gamma-Globulins; Gelatin; Hydrogen-Ion Concentration; Keratins; Nickel; Proteins; Research; Serum Albumin; Serum Albumin, Bovine; Sulfides; Toxicology

1964