Contact hypersensitivity in experimental animals.

Publisher: S. Karger in Basel, New York

Written in English
Published: Pages: 182 Downloads: 650
Share This


  • Contact dermatitis.

Edition Notes

StatementEditors: Darien Parker and J. L. Turk.
SeriesMonographs in allergy,, v. 8, Monographs in allergy ;, vol. 8.
ContributionsParker, Darien, ed., Turk, J. L., ed., Frey, Johann R.
LC ClassificationsQR188 .C66
The Physical Object
Paginationxiv, 182 p.
Number of Pages182
ID Numbers
Open LibraryOL5107887M
LC Control Number74180282

Allergies to nickel (Ni(2+)) are the most frequent cause of contact hypersensitivity (CHS) in industrialized countries. The efficient development of CHS requires both a T lymphocyte-specific. (). Animal Models of Complement-Mediated Hypersensitivity Reactions to Liposomes and Other Lipid-Based Nanoparticles. Journal of Liposome Research: Vol. 17, No. 2, pp.   The corpus contains approximately 5,2 million of books published between and , about billions of words ( billion in English); this corresponds to over 4% of all books edited in this period, sufficient to show significant cultural trends. Most books were drawn from over 40 university libraries around the world. Contact hypersensitivity: It occurs when the body comes in contact with chemicals (like Nickel, Formaldehyde), drugs (sulphonamides & neomycin), plant materials (poison ivy and poison oak), Some cosmetic soaps, etc. These act as haptens and combine with proteins to form complete Antigen which initiates the hypersensitive reaction.

The author of this paper nowhere defines what hemeans by "hypersensitivity" to tuberculin, but it. can be inferred from his use of the term in various. contexts that it is synonymous with "sensitivity and" "marked sensitivity". The term "allergy" is. used only in a quotation from CLARKE in which the degree of allergy produced by BCG vaccination is contrasted with hypersensitivity.   Type IV hypersensitivity is involved in the pathogenesis of many autoimmune and infectious diseases (tuberculosis, leprosy, blastomycosis, histoplasmosis, toxoplasmosis, leishmaniasis, etc.) and granulomas due to infections and foreign antigens. Another form of delayed hypersensitivity is contact dermatitis (poison ivy (figure 6), chemicals, heavy metals, etc.) in which the lesions are more. -Induction of dentin hypersensitivity In order to expose dentin tubules and induce hypersensitivity, the teeth of the animals were eroded using a va- lidated model (13). In brief, animals ingested. METHODOLOGY/PRINCIPAL FINDINGS: In this study, we examined the aggravation effect of long-term dermal exposure to DBP in a T-helper type 2 (Th2) model of contact hypersensitivity (CHS) in mice, and sought the potential molecular mechanisms. Experimental tests were conducted after day dermal exposure to saline or three concentrations of DBP.

"3. Sera from experimental animals animals Subject Category: Organism Names see more details exhibiting delayed hypersensitivity or sera containing precipitating antibody did not sensitize normal cells to antigen. "4. The inhibition still occurs when heat-inactivated sera are used. "5. Hypersensitive definition, excessively sensitive: to be hypersensitive to criticism. See more.   Common disease of type IV hypersensitivity 1) Infectious delayed type hypersensitivity OT(OldTuberculin) test 2) Contact dermatitis: Paint, drug red rash, papula, water blister, dermatitis 3) Acute rejection of allogenic transplantation and immune response in local tumor mass Same disease (SLE), multiple immune injury,hypersensitivity. @article{osti_, title = {Oral administration of drugs with hypersensitivity potential induces germinal center hyperplasia in secondary lymphoid organ/tissue in Brown Norway rats, and this histological lesion is a promising candidate as a predictive biomarker for drug hypersensitivity occurrence in humans}, author = {Tamura, Akitoshi and Miyawaki, Izuru and Yamada, Toru and .

Contact hypersensitivity in experimental animals. Download PDF EPUB FB2

Genre/Form: Congress: Additional Physical Format: Online version: Contact hypersensitivity in experimental animals. Basel, New York, S. Karger,   REFERENCES Andersen K. () Testing for contact allergy in experimental animals.

Pharmacology and Toxicol Basketter D. A., Selbie E., Scholes E. W., Lees D., Kimber I. and Botham P. () Results with OECD recommended positive control sensitizers in the maximization, Buehler and local lymph node by: 2.

Abstract. Contact hypersensitivity has been studied extensively in man and experimental animals. It represents one particular type of delayed-type hypersensitivity and was thought to provide a simple model of this type of : G.

Stingl, W. Aberer. Contact hypersensitivity J Exp Med () G.B. Toews, P.R. Bergstresser, J.W. Streilein, S. Sullivan, Epidermal Langerhaus cell density determines whether contact hypersensitivity or unresponsiveness follows painting with DNFB J Immunol () Cited by:   Allergic contact dermatitis is a rare hypersensitivity disorder in the dog.

Clinical diagnosis is not easy. Primary lesions are transient. Secondary lesions caused by chronic inflammation and self. Experimental studies from the last 10 years have demonstrated that, in normal contact hypersensitivity responses to strong haptens, CD8(+) type 1 T-cells are effector cells of contact.

This study indicates that clonidine-TTS suppressed the elicitation of contact hypersensitivity reactions. The observed Contact hypersensitivity in experimental animals. book effect of clonidine may account for the relatively weak hypersensitivity reactions to this drug in experimental animal studies.

Induction of experimental contact hypersensitivity in mouse ear. For the induction of contact hypersensitivity (CHS), mice were divided into 3 groups with 5 mice per each treatment group; normal healthy control treated with PBS alone without CHS induction, treatment groups treated either with vacant gel or gel containing placenta extract.

Contact hypersensitivity response to TNCB in BALB/c mice. BALB/c mice on a HFD and a ND for 4 weeks were sensitized with 1% TNCB (25 μL in acetone) on their shaved abdomen. Seven days later, mice were challenged with 10 μL of % (A) and % (B) of TNCB solution in acetone to both sides of the ear pinnae to induce a contact hypersensitivity.

Introduction. Allergic contact dermatitis is a common skin disease that is caused by type IV delayed type hypersensitivity responses to antigens that come in contact with the skin ic contact dermatitis is a major cause of occupational skin disease, and accounts for approximately 20% of all work-related health complaints.

Contact hypersensitivity (CHS) responses require the participation of T cells, along with a variety of cytokines and adhesion molecules. In the classical CHS, antigen-specific T cells are recruited to a site of antigenic challenge, where they react with antigen, release cytokines, and attract other inflammatory cells.

Definitions. Hypersensitivity reaction: a condition in which the normally protective immune system has a harmful effect on the body; Allergy: an abnormal immunological response to an otherwise harmless environmental stimulus (e.g., food, pollen, animal dander); Autoimmune disease: an abnormal immunological response directed against an antigen that is actually part of the body itself.

Many forms of delayed-onset, lymphocyte-mediated hypersensitivity reactions in animals and man are characterized by an extensive infiltration of basophilic leukocytes [1–6]. We have designated such reactions by the descriptive term “cutaneous basophil hypersensitivity” (CBH) to distinguish them from classic delayed hypersensitivity (DH).

Cutaneous basophil hypersensitivity, an immune inflammatory reaction characterized by infiltrates of basophils and a delayed time-course, was studied in guinea pigs contact sensitized with oxazolone. Routine histological techniques, employing ordinary paraffin sections, were modified to.

Allergic contact dermatitis (ACD) caused by reactive haptens and metal ions, a form of delayed type hypersensitivity, is one of the most common skin diseases (1, 2).Contact hypersensitivity (CHS), the recognized mouse model for studying human ACD, involves painting a small area of abdominal skin with the allergen (sensitization), e.g., 2,4,6-trinitrochlorobenzene (TNCB), followed by an.

Contact hypersensitivity is part of the adaptive immune response and a form of delayed-type hypersensitivity (DTH) or cell-mediated immune reaction that is expressed in the epidermis.

It is the most frequent form of DTH reaction and the most prominent clinical manifestation of a. Contact hypersensitivity testing is typically performed either in mice or in guinea pigs and is directly derived from classical models used for the detection of contact sensitizing chemicals.

Whatever the selected model, it is comprised of a sensitizing phase where the animals are applied a strong contact sensitizer topically, then a rest phase. experimental hypersensitivity in the rabbit: e ffect of i nhibition of a ntibody f ormation by x-r adiation and n itrogen m ustards on the h istologic and s erologic s equences, and on the b ehavior of s erum c omplement, f ollowing s ingle l arge i njections of f oreign p roteins.

Search the world's most comprehensive index of full-text books. My library. An analysis of allergic contact dermatitis - a common occupational health problem affecting between % of the workforce. This book considers the condition from the perspective of the toxicologist rather than the dermatologist.

Allergic contact dermatitis (ACD) is one of the most prevalent skin diseases consisting of sensitization and elicitation phases 1,ed studies of hapten-induced contact hypersensitivity (CHS) as a murine model of ACD have expanded our understanding of the mechanism of allergic reactions occurring in the skin, especially the specific roles of a variety of immune cells.

Experimental animals A total of 72 female Balb/c mice (6–8 weeks; 17± g) were purchased from the Guangdong Medical Laboratory Animal Center (Guangdong, China).

The animals were housed at 24°C with 40–60% humidity on a h dark/light cycle, and provided with food and water ad libitum. Examples of this T H 1-mediated hypersensitivity are observed in tuberculin the Mantoux skin test and contact dermatitis, such as occurs in latex allergy reactions.

In the second type IV subcategory, CD4 T H 2-mediated reactions result in chronic asthma or chronic allergic rhinitis.

Feline allergic skin disease presents a unique set of challenges to the veterinary practitioner. Although there is some similarity to what is seen in the allergic canine patient, cutaneous hypersensitivity dermatoses in cats can manifest with strikingly different clinical signs, treatment options and outcomes, and secondary complications/disease entities.

Recruitment of polymorphonuclear leukocytes (PMNs) into sites of inflammation plays a central role in the pathogenesis of rheumatoid arthritis, Crohn's disease, inflammatory bowel disease, or psoriasis, whereas PMNs are virtually absent during other T cell–mediated diseases such as experimental allergic encephalomyelitis (EAE) or autoimmune pancreatitis 1,2,3,4,5,6,7,8,9,10, Murine contact hypersensitivity (CHS) is widely used as a model for allergic contact dermatitis (ACD).

One of the most common diseases caused by repeated skin exposure to contact allergens, ACD is classified as a type IV or a delayed type hypersensitivity reaction. After the inoculation of the Enders strain of mumps virus into the anterior chamber of the eye of guineapigs, and also intranasally, the animals developed corneal opacity, miosis and exophthalmos; the changes attained a maximum after hours and passed off after days.

Inhibiting antibody appeared after 72 hours and attained a titre of after 3 weeks. Hypersensitivity responses are commonly categorized in four groups (Type I, Type II, Type III, and Type IV) later the proposal of Gell and Coombs in Discover the world's research 17+ million.

meters in animals under experimental conditions. Restraint Restraint is described as immobilization of an animal by keeping it or parts of it, in a comfortable but safe hold by hand or by means of a physical device. Physical restraint is performed on conscious animals undergo-ing manipulations, which do not require sedation or.

Using the fluorescent antibody technique we here demonstrate that fibrin deposition is a prominent and consistent feature of both allergic contact dermatitis and classic delayed hypersensitivity skin reactions in man.

Fib was detected in 55 of 58 delayed reactions studied at the peak of their intensity. Examples of this T H 1-mediated hypersensitivity are observed in tuberculin the Mantoux skin test and contact dermatitis, such as occurs in latex allergy reactions. In the second type IV subcategory, CD4 T H 2-mediated reactions result in chronic asthma or chronic allergic rhinitis.

In these cases, the soluble antigen is first inhaled.The cellular mechanism of tolerance and desensitization in contact hypersensitivity to DNCB in guinea pigs. In Contact Hypersensitivity in Experimental Animals (eds. J. L. Turk and D. Parker). Monogr. Allergy, vol. 8, p.Buy this book on publisher's site; Personalised recommendations.In previous reports Salvin [this Bulletin,v.

28, ;v. 30, ] showed that mice experimentally infected by intraperitoneal injection of sub-lethal doses of living yeast phase cells of Histoplasma capsulatum became partially resistant to a challenging lethal injection of the same organism administered 14 days later. However, many of the mice died during the first 48 hours.