ovalbumin and Dermatitis

A set of histopathological elements with death of epidermal basal cell layer keratinocytes along with inflammatory cell infiltration distinguishes lichenoid tissue reaction (LTR)/interface dermatitis (IFD) from other inflammatory mucocutaneous diseases. The LTR/IFD can be seen in skin disorders like as lichen planus, acute graft-versus-host disease, lupus erythematosus, dermatomyositis, and toxic epidermal necrolysis/Stevesn-Johnson syndrome. Clinical and basic researches suggested that cytotoxic CD8 T cells producing interferon-γ and FasL are final effector cells to cause apoptosis of keratinocyte. Some murine models of LTR/IFD have been established, for example, LTR/IFD reactions of keratinocyte-specific ovalbumin (OVA)-transgenic mice after OVA-specific T-cell-receptor(+)CD8 T cells. By analysis of the murine model, a new class of immunosuppressant, a JAK inhibitor, has been suggested as a new candidate for treatment of LTR/IFD.

Topics: Adoptive Transfer; Animals; Apoptosis; CD8-Positive T-Lymphocytes; Dermatitis; Disease Models, Animal; Fas Ligand Protein; Humans; Interferon-gamma; Keratinocytes; Lichenoid Eruptions; Ovalbumin

Topics: Animals; Apoptosis; CD8-Positive T-Lymphocytes; Dermatitis; Graft vs Host Disease; Keratinocytes; Mice; Mice, Inbred C57BL; Ovalbumin; Protein Precursors

Perinatal exposures are associated with altered risks of childhood allergy. Human studies and our previous work suggest that restricted growth in utero (IUGR) is protective against allergic disease. The mechanisms are not clearly defined, but reduced fetal abundance and altered metabolism of methyl donors are hypothesized as possible underlying mechanisms. Therefore, we examined whether late-gestation maternal dietary methyl donor and cofactor supplementation of the placentally restricted (PR) sheep pregnancy would reverse allergic protection in progeny. Allergic outcomes were compared between progeny from control pregnancies (CON; n = 49), from PR pregnancies without intervention (PR; n = 28), and from PR pregnancies where the dam was fed a methyl donor plus cofactor supplement from day 120 of pregnancy until delivery (PR + Methyl; n = 25). Both PR and PR + Methyl progeny were smaller than CON; supplementation did not alter birth size. PR was protective against cutaneous hypersensitivity responses to ovalbumin (OVA; P < 0.01 in singletons). Cutaneous hypersensitivity responses to OVA in PR + Methyl progeny were intermediate to and not different from the responses of CON and PR sheep. Cutaneous hypersensitivity responses to house dust mites did not differ between treatments. In singleton progeny, upper dermal mast cell density was greater in PR + Methyl than in PR or CON (each P < 0.05). The differences in the cutaneous allergic response were not explained by treatment effects on circulating immune cells or antibodies. Our results suggest that mechanisms underlying in utero programming of allergic susceptibility by IUGR and methyl donor availability may differ and imply that late-gestation methyl donor supplementation may increase allergy risk.

Topics: Animals; Cobalt; Dermatitis; Dietary Supplements; Disease Models, Animal; DNA Methylation; Female; Fetal Growth Retardation; Folic Acid; Gestational Age; Hypersensitivity; Immunoglobulin E; Mast Cells; Methionine; Ovalbumin; Placenta; Pregnancy; Prenatal Exposure Delayed Effects; Pyroglyphidae; Sheep, Domestic; Skin; Sulfur

Allergen sources such as mites, insects, fungi, and pollen contain proteases. Airway exposure to proteases induces allergic airway inflammation and IgE/IgG1 responses via IL-33-dependent mechanisms in mice. We examined the epicutaneous sensitization of mice to a model protease allergen, papain; the effects of tape stripping, which induces epidermal barrier dysfunction; and the atopic march upon a subsequent airway challenge. Papain painting on ear skin and tape stripping cooperatively promoted dermatitis, the skin gene expression of proinflammatory cytokines and growth factors, up-regulation of serum total IgE, and papain-specific IgE/IgG1 induction. Epicutaneous sensitization induced T helper (Th) 2 cells and Th17 differentiation in draining lymph nodes. Ovalbumin and protease inhibitor-treated papain induced no or weak responses, whereas the co-administration of ovalbumin and papain promoted ovalbumin-specific IgE/IgG1 induction. Wild-type and IL-33-deficient mice showed similar responses in the epicutaneous sensitization phase. The subsequent airway papain challenge induced airway eosinophilia and maintained high papain-specific IgE levels in an IL-33-dependent manner. These results suggest that allergen source-derived protease activity and mechanical barrier damage such as that caused by scratching cooperatively promote epicutaneous sensitization and skin inflammation and that IL-33 is dispensable for epicutaneous sensitization but is crucial in the atopic march upon a subsequent airway low-dose encounter with protease allergens.

Topics: Allergens; Animals; Cell Differentiation; Cytokines; Dermatitis; Enzyme-Linked Immunosorbent Assay; Female; Hypersensitivity; Immunoglobulin E; Immunoglobulin G; Inflammation; Interleukin-33; Mice; Mice, Inbred C57BL; Ovalbumin; Papain; Protease Inhibitors; Real-Time Polymerase Chain Reaction; Skin; Stress, Mechanical; Th17 Cells; Th2 Cells; Wounds and Injuries

Allergic asthma is a chronic inflammatory disorder that affects ∼20% of the population worldwide. Microarray analyses of nasal epithelial cells from acute asthmatic patients detected a 50% decrease in expression of Stard7, an intracellular phosphatidylcholine transport protein. To determine whether loss of Stard7 expression promotes allergic responses, mice were generated in which one allele of the Stard7 locus was globally disrupted (Stard7 (+/-) mice). OVA sensitization and challenge of Stard7(+/-) mice resulted in a significant increase in pulmonary inflammation, mucous cell metaplasia, airway hyperresponsiveness, and OVA-specific IgE compared with OVA-sensitized/challenged wild-type (WT) mice. This exacerbation was largely Th2-mediated with a significant increase in CD4(+)IL-13(+) T cells and IL-4, IL-5, and IL-13 cytokines. The loss of Stard7 was also associated with increased lung epithelial permeability and activation of proinflammatory dendritic cells in sensitized and/or challenged Stard7 (+/-) mice. Notably, OVA-pulsed dendritic cells from Stard7(+/-) mice were sufficient to confer an exaggerated allergic response in OVA-challenged WT mice, although airway hyperresponsiveness was greater in Stard7(+/-) recipients compared with WT recipients. Enhanced allergic responses in the lung were accompanied by age-dependent development of spontaneous atopic dermatitis. Overall, these data suggest that Stard7 is an important component of a novel protective pathway in tissues exposed to the extracellular environment.

Topics: Adoptive Transfer; Animals; Carrier Proteins; Cytokines; Dendritic Cells; Dermatitis; Disease Models, Animal; Disease Progression; Female; Gene Deletion; Haploinsufficiency; Hypersensitivity; Lung; Male; Mice; Mice, Knockout; Models, Biological; Ovalbumin; Permeability; Respiratory Mucosa; Skin; Th2 Cells

We have previously shown that T helper type 2 (Th2)-polarized airway inflammation can facilitate priming to new antigens in the lungs, which we called "collateral priming". To investigate whether allergic skin inflammation can also facilitate priming toward new antigens, we developed an allergic skin inflammation model based on an allergic lung inflammation model. Mice were sensitized intraperitoneally toward the primary antigen, ovalbumin. Challenge was subsequently performed intranasally or epicutaneously with ovalbumin and a secondary antigen, keyhole limpet hemocyanin (KLH). Re-challenge consisted of local application of either antigen alone. Analysis of KLH-specific antibody responses, KLH-specific cytokines, and local inflammation demonstrated tolerance induction toward the secondary antigen in the skin, whereas in the lung priming had occurred. Flow-cytometric analysis revealed increased numbers of regulatory T cells (Tregs), increased cytotoxic T lymphocyte antigen-4 (CTLA-4) expression, and an enhanced suppressive capacity of Tregs from skin-draining lymph nodes when compared with Tregs from the lung-draining lymph nodes. Furthermore, depletion of Tregs resulted in restoration of collateral priming in the skin. These results demonstrate crucial local differences between the Treg function in the skin and lung to repetitive antigen exposure, which can decisively influence the immune response toward new antigens.

Topics: Analysis of Variance; Animals; Bronchial Hyperreactivity; Cytokines; Dermatitis; Disease Models, Animal; Enzyme-Linked Immunosorbent Assay; Female; Humans; Immune Tolerance; Immunization; Lung; Lymphocyte Activation; Mice; Mice, Inbred BALB C; Ovalbumin; Random Allocation; Skin; T-Lymphocytes, Regulatory; Th2 Cells

Oral administration of specific food ingredients can modify mucosal and systemic inflammatory processes. Such food components are fatty acids or carbohydrates. Nevertheless, little is known about the impact of oral administration of polyunsaturated fatty acids (PUFA) and non-digestible oligosaccharides on allergen-induced dermatitis.. In this pilot study, skin inflammation was induced by serial epicutaneous OVA applications in OVA-sensitized mice. In parallel, mice were fed with solid food containing arachidonic acid/docosahexaenoic acid (AA/DHA), galactooligosaccharide/polydextrose (GOS/PDX) or their combination. Skin lesions were assessed by clinical skin score, but also skin barrier parameters, immunohistochemical analyses, and local cytokine expression profile.. Both dietary AA/DHA and GOS/PDX significantly ameliorated the severity of allergen-induced dermatitis. The clinical improvement upon oral AA/DHA and GOS/PDX supplementation was associated with a reduction in transepidermal water loss and reduced KI-67 expression in the skin. Lesional CD8+ and mast cells were reduced in all treatment groups, but appeared to be most pronounced in combined AA/DHA/GOS/PDX-treated mice. Moreover, in GOS/PDX-treated mice, IFNγ and TGFβ expression was increased in skin lesions.. Dietary supplementation with DHA/AA and GOS/PDX ameliorates symptoms of allergen-induced dermatitis and may thus be beneficial in the dietary management of human atopic eczema.

Topics: Allergens; Animals; Ascorbic Acid; CD8-Positive T-Lymphocytes; Cytokines; Dermatitis; Diet; Disease Progression; Docosahexaenoic Acids; Fatty Acids, Unsaturated; Feeding Behavior; Female; Glucans; Humans; Mast Cells; Mice; Mice, Inbred BALB C; Ovalbumin; Pilot Projects; Skin

Nuclear receptor-mediated signaling via RARs and PPARδ is involved in the regulation of skin homeostasis. Moreover, activation of both RAR and PPARδ was shown to alter skin inflammation. Endogenous all-trans retinoic acid (ATRA) can activate both receptors depending on specific transport proteins: Fabp5 initiates PPARδ signaling whereas Crabp2 promotes RAR signaling. Repetitive topical applications of ovalbumin (OVA) in combination with intraperitoneal injections of OVA or only intraperitoneal OVA applications were used to induce allergic dermatitis. In our mouse model, expression of IL-4, and Hbegf increased whereas expression of involucrin, Abca12 and Spink5 decreased in inflamed skin, demonstrating altered immune response and epidermal barrier homeostasis. Comprehensive gene expression analysis showed alterations of the cutaneous retinoid metabolism and retinoid-mediated signaling in allergic skin immune response. Notably, ATRA synthesis was increased as indicated by the elevated expression of retinaldehyde dehydrogenases and increased levels of ATRA. Consequently, the expression pattern of genes downstream to RAR was altered. Furthermore, the increased ratio of Fabp5 vs. Crabp2 may indicate an up-regulation of the PPARδ pathway in allergen-induced dermatitis in addition to the altered RAR signaling. Thus, our findings suggest that ATRA levels, RAR-mediated signaling and signaling involved in PPARδ pathways are mainly increased in allergen-induced dermatitis and may contribute to the development and/or maintenance of allergic skin diseases.

Topics: Allergens; Animals; ATP-Binding Cassette Transporters; Dermatitis; Fatty Acid-Binding Proteins; Female; Gene Expression Regulation; Heparin-binding EGF-like Growth Factor; Intercellular Signaling Peptides and Proteins; Interleukin-4; Mice; Mice, Inbred BALB C; Neoplasm Proteins; Ovalbumin; PPAR delta; Protein Precursors; Receptors, Retinoic Acid; Retinoic Acid Receptor alpha; Serine Peptidase Inhibitor Kazal-Type 5; Serpins; Signal Transduction; Tretinoin

To investigate the role of cannabinoid receptor-2 (CB2) in allergic inflammation in CB2 knockout (CB2-KO) mice.. The swelling reaction of the pinna to various stimuli was compared between CB2-KO and wild-type (WT) mice in terms of edema and acanthosis.. Ear swelling induced by repeated application of 2,4-dinitrofluorobenzene in CB2-KO mice was significantly decreased compared with that in WT mice. In an ovalbumin model, pinna edema was significantly suppressed in CB2-KO mice in comparison with that in WT mice. The contribution of CB2 to edema was investigated in a more extreme dermatitis model using oxazolone. Delayed-type hypersensitivity reactions in this model were also suppressed in CB2-KO mice. In each of these three different allergic dermatitis models, there was a significant decrease in edema and acanthosis in CB2-KO mice compared with WT mice.. These results clearly demonstrate that CB2 and its endogenous ligands participate not only in the acute, edematous phase of allergic dermatitis, but also in the chronic irreversible acanthosis reaction.

Topics: Animals; Dermatitis; Disease Models, Animal; Edema; Hypersensitivity, Delayed; Inflammation; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Ovalbumin; Oxazolone; Receptor, Cannabinoid, CB2

Thymic stromal lymphopoietin (TSLP) is a cytokine expressed by epithelial cells, including keratinocytes, and is important in allergic inflammation. Allergic skin inflammation elicited by epicutaneous immunization of mice with ovalbumin (OVA), a potential model of atopic dermatitis, was severely impaired in TSLPR(-/-) mice, as evidenced by decreased infiltration of eosinophils and decreased local expression of T helper 2 (Th2) cytokines. However, secretion of Th2 cytokines by splenocytes from epicutaneous sensitized TSLPR(-/-) mice in response to OVA was normal. Skin dendritic cells from TSLPR(-/-) mice were normal in their ability to migrate to draining lymph nodes, express activation markers, and induce proliferation and Th2 cytokine production by naïve T cells. CD4(+) T cells from TSLPR(-/-) mice expressed the skin homing receptor E-selectin ligand normally, and homed to the skin normally, but failed to transfer allergic skin inflammation to WT recipients. TSLP enhanced Th2 cytokine secretion in vitro by targeting TSLPR on antigen specific T cells. Intradermal injection of anti-TSLP blocked the development of allergic skin inflammation after cutaneous antigen challenge of OVA immunized WT mice. These findings suggest that TSLP is essential for antigen driven Th2 cytokine secretion by skin infiltrating effector T cells and could be a therapeutic target in allergic skin inflammation.

Topics: Animals; Cell Movement; Cell Proliferation; Cells, Cultured; Cytokines; Dendritic Cells; Dermatitis; Female; Hypersensitivity; Immunity, Innate; Immunoglobulins; Lymph Nodes; Mice; Mice, Knockout; Ovalbumin; Receptors, Cytokine; Spleen; T-Lymphocytes; Thymic Stromal Lymphopoietin

2-Hydroxyethylmethacrylate (HEMA), a common constituent in dental materials, is known to cause hypersensitivity reactions. While the means by which this small molecule causes adverse responses has not been ascertained, we have previously demonstrated that it binds to protein and in mice induces the production of autoantibodies to HEMA-conjugated self-protein. The present study explores the inflammatory and adjuvant properties of HEMA in response to the subcutaneous injection of HEMA and a protein. Ovalbumin (OVA) was used as a 'reporter antigen', and mouse serum albumin (MSA), conjugated in vitro with HEMA (MSA(H)) to a low degree (0.5 molecules of HEMA per molecule of MSA on average), was used to mimic a possible in vivo situation. Inflammatory responses at injection sites were scored by using an ordinal scale, and immunoglobulin (Ig)G1, IgG2a, and IgE activities to OVA or MSA were assessed by enzyme-linked immunosorbent assay (ELISA). Injections of 20 micromol HEMA induced overt inflammatory skin responses, the severity of which was influenced by the co-administered substances. A significantly higher IgG1 and IgE response to OVA was induced by the presence of HEMA. Interestingly, injections with low conjugated MSA(H) only induced the production of autoantibodies if free HEMA was included at the time of immunization. These findings suggest that HEMA is an inflammatogenic substance with adjuvant properties.

Topics: Adjuvants, Immunologic; Animals; Antibodies; Autoantibodies; Cells, Cultured; Dental Materials; Dermatitis; Female; Immunization; Immunoglobulin E; Immunoglobulin G; Inflammation Mediators; Injections, Subcutaneous; Methacrylates; Mice; Mice, Inbred BALB C; Ovalbumin; Protein Binding; Serum Albumin; Spleen

We investigated the effects of 1-4% ointments of metronidazole and tinidazole (derivatives of nitroimidazole) on models of inflammatory dermatitis evoked by antigen, hapten and monoclonal anti-dinitrophenol (DNP) IgE antibody in mice. Metronidazole and tinidazole ointments (1) suppressed the late-phase reaction (LPR) of biphasic ear edema in mice sensitized with ovalbumin (OA), (2) suppressed trinitrochlorobenzene-induced inflammatory dermatitis, (3) suppressed the immediate phase reactions and LPR in mice passively sensitized with anti-DNP IgE mAb, and (4) enhanced vascular permeability and the number of scratching reactions, presumably due to itching, in passively sensitized mice. These results strongly indicate that metronidazole and tinidazole 1-4% ointments possess antiinflammatory, immunosuppressive and anti-itching effects, and have the potential for clinical use in the treatment of human inflammatory skin diseases including atopic dermatitis in addition to rosacea and acne vulgaris.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Antigens; Antipruritics; Capillary Permeability; Dermatitis; Dermatologic Agents; Disease Models, Animal; Edema; Humans; Immunosuppressive Agents; Male; Metronidazole; Mice; Ointments; Ovalbumin; Picryl Chloride; Pruritus; Tacrolimus; Tinidazole

Advances in the treatment of allergic disorders require elucidation of the autoregulatory immune systems induced in averting detrimental inflammatory responses against invading foreign Ags. We previously reported that excessive Ags intruding through the airway mucosa induce a subset of regulatory CD4+ T cells secreting TGF-beta in the regional mediastinal lymph nodes (MLNs), which inhibits Th2 cells and subsequent eosinophilic inflammation in the trachea. In the present experiments we examined whether and in what mechanisms TGF-beta-secreting CD4+ T cells in the MLNs regulate Th cell-mediated skin inflammation using a previously established murine model. Th1 or Th2 cells injected s.c. into ear lobes of naive mice induced swelling, whereas the concomitant local injection of MLN cells suppressed the inflammation. The suppressor activities of MLN cells were markedly neutralized by anti-TGF-beta mAb and were mimicked by rTGF-beta. The MLN cell- and rTGF-beta-induced inhibition was reversed by anti-IL-10 mAb significantly in Th1-induced inflammation and only partially in Th2-induced inflammation. rIL-10 reduced Th-induced ear swelling, although higher doses of rIL-10 were required in Th2-induced one. Thus, allergen-specific TGF-beta-producing CD4+ T cells induced in the respiratory tract controlled cutaneous inflammatory responses by Th1 or Th2 cells either directly by TGF-beta or indirectly through IL-10 induction. From a clinical standpoint, these observations might explain the mechanism of spontaneous regression in some patients with atopic dermatitis, which exhibits both Th1- and Th2-mediated skin inflammation in response to airborne protein Ags.

Topics: Animals; CD4-Positive T-Lymphocytes; Cells, Cultured; Dermatitis; Dermatitis, Atopic; Immune Tolerance; Interleukin-10; Lymph Nodes; Male; Mediastinum; Mice; Mice, Inbred BALB C; Ovalbumin; Th1 Cells; Th2 Cells; Trachea; Transforming Growth Factor beta

In this study, we investigated the involvement of the adhesion molecules intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), very late activation antigen-4 (VLA-4), lymphocyte function-associated antigen 1 (LFA-1) and macrophage antigen-1 (Mac-1) on eosinophil infiltration in the cutaneous late phase response (LPR) in OVA-sensitized Balb/c mice by two approaches, immunostaining and inhibition assays with each monoclonal antibody. The eosinophil infiltration into the skin reached a peak at 12 hr after an intradermal challenge with OVA. Infiltrated eosinophils and mononuclear cells in the skin expressed Mac-1 (eosinophils: 38.9 +/- 1.55%, mononuclear cells: 51.2 +/- 2.15%), LFA-1 (eosinophils: 33.3 +/- 0.95%, mononuclear cells: 23.1 +/- 1.07%) and VLA-4 (eosinophils: 14.3 +/- 1.6%, mononuclear cells: 17.2 +/- 1.38%) at 12 h. Intraperitoneal administration of anti-mouse ICAM-1, VCAM-1, and VLA-4 monoclonal antibodies (mAb) before the challenge decreased the eosinophil infiltration by 66.2%, 61.0%, and 54.0%, respectively. On the other hand, pretreatment with anti-mouse LFA-1 mAb or Mac-1 mAb did not significantly decrease the infiltration. These results suggest that VCAM-1/VLA-4 interaction and ICAM-1 play important roles in eosinophil infiltration in cutaneous LPR.

Topics: Animals; Antibodies, Monoclonal; Cell Adhesion Molecules; Coloring Agents; Dermatitis; Eosinophils; Female; Immunization; Immunohistochemistry; Injections, Intradermal; Integrin alpha4beta1; Integrins; Intercellular Adhesion Molecule-1; Leukocytes, Mononuclear; Lymphocyte Function-Associated Antigen-1; Macrophage-1 Antigen; Mice; Mice, Inbred BALB C; Ovalbumin; Receptors, Lymphocyte Homing; Receptors, Very Late Antigen; Serine Proteinase Inhibitors; Skin; Vascular Cell Adhesion Molecule-1

ACE-inhibitors have for some time been used in the treatment of hypertension. Apart from inhibiting the conversion of angiotensin I to II, the drugs also affect the metabolism of some inflammatory agents, like bradykinin and substance P. Egg albumin (EA)-sensitized guinea pigs were pretreated with the ACE-inhibitors. Measurement of flare and wheal areas induced by an intradermal injection of EA, showed that enalaprilat significantly increased, whereas cilazaprilat slightly decreased, the reaction area. Enalaprilat also showed an enhancement in histamine and substance P (SP) contents in the skin. In vitro incubation of guinea pig biopsies with enalaprilat potentiated EA- but not SP-induced histamine release. The EA-induced effect was abolished if the animals were pretreated with capsaicin. The conclusion is that cilazaprilat, in contrast to enalaprilat, does not potentiate inflammatory reactions in the guinea pig.

Topics: Angiotensin-Converting Enzyme Inhibitors; Animals; Antigens; Cilazapril; Dermatitis; Enalaprilat; Female; Guinea Pigs; Histamine Release; Hypersensitivity; Ovalbumin; Pyridazines

Two non-sulfur containing ACE-inhibitors were tested concerning their local effect on experimental dermatitis in ovalbumin-sensitized guinea pigs. Enalaprilat but not cilazaprilat potentiated the ovalbumin-evoked inflammatory response. Furthermore, enalaprilat clearly enhanced the erythema evoked by substance P, whereas cilazaprilat did not. Concerning, the bradykinin-evoked erythema, enalaprilat significantly potentiated the response, whereas cilazaprilat only caused a slight increase. Our results suggest that different affinities for peptidases involved in degradation of inflammatory peptides can explain differences between the pro-inflammatory properties of enalaprilat and cilazaprilat.

Topics: Angiotensin-Converting Enzyme Inhibitors; Animals; Bradykinin; Cilazapril; Dermatitis; Drug Synergism; Enalaprilat; Erythema; Female; Guinea Pigs; Inflammation; Ovalbumin; Pyridazines; Substance P

The effects of the antihypertensive drugs clonidine, prazosin, and MK 422 (the active parent diacid of enalapril) were studied on the cutaneous blood flow and allergen evoked inflammatory skin reactions in ovalbumin sensitized guinea pigs. The hypotensive effect of the drugs did not significantly change the basal cutaneous blood flow at the time of allergen challenge. MK 422 (0.02 mg/kg) markedly enhanced the wheal and flare reaction following allergen challenge, whereas clonidine (0.005 and 0.05 mg/kg) inhibited the inflammatory response. Prazosin (0.03 mg/kg) did not significantly influence the wheal and flare reaction. Our results indicate that some antihypertensive drugs (clonidine) could be beneficial to antihypertensive patients with inflammatory diseases, while others (ACE-inhibitors) may enhance their inflammatory disorders.

Topics: Allergens; Angiotensin-Converting Enzyme Inhibitors; Animals; Antihypertensive Agents; Clonidine; Dermatitis; Enalapril; Enalaprilat; Female; Guinea Pigs; Ovalbumin; Prazosin; Regional Blood Flow; Skin

Megestrol acetate was found to have no influence on immunological skin and corneal reactivity nor on antibody responses in guinea pigs. Its curative effect in feline miliary eczema is probably not, therefore, the result of interference with the immune response.

Topics: Animals; Antibody Formation; Cat Diseases; Cats; Cornea; Dermatitis; Drug Evaluation, Preclinical; Female; Freund's Adjuvant; Guinea Pigs; Hypersensitivity, Delayed; Immunity, Cellular; Male; Megestrol; Megestrol Acetate; Mycobacterium tuberculosis; Ovalbumin; Skin