Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0152030 (skin irritation)
 2,146 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

All LMW respiratory allergens known to date can also induce skin allergy in test animals. The question here was if in turn skin allergens can induce allergy in the respiratory tract. Respiratory allergy was tested in Th2-prone Brown Norway (BN) rats by dermal sensitization with the contact allergen dinitrochlorobenzene (DNCB; 1%, day 0; 0.5%, day 7) and a head/nose-only inhalation challenge of 27mg/m3 of DNCB (15 min, day 21), using a protocol that successfully identified chemical respiratory allergens. Skin allergy to DNCB was examined in BN rats and Th1-prone Wistar rats in a local lymph node assay followed by a topical patch challenge of 0.1% DNCB. Sensitization of BN rats via the skin induced DNCB-specific IgG in serum, but not in all animals, and an increased number of CD4+ cells in the lung parenchyma. Subsequent inhalation challenge with DNCB did not provoke apneas or allergic inflammation (signs of respiratory allergy) in the BN rats. However, microarray analysis of mRNA isolated from the lung revealed upregulation of the genes for Ccl2 (MCP-1), Ccl4 (MIP-1beta), Ccl7 and Ccl17. Skin challenge induced considerably less skin irritation and allergic dermatitis in the BN rat than in the Wistar rat. In conclusion, the Th2-prone BN rat appeared less sensitive to DNCB than the Wistar rat; nevertheless, DNCB induced allergic inflammation in the skin of BN rats but even a relatively high challenge concentration did not induce allergy in the respiratory tract, although genes associated with allergy were upregulated in lung tissue.
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PMID:The contact allergen dinitrochlorobenzene (DNCB) and respiratory allergy in the Th2-prone Brown Norway rat. 1831 51

It is often difficult to discriminate between chemically induced skin irritation and sensitization due to their similar clinical, pathological, and immunological responses. More information than that currently available from local lymph node assays (LLNAs), such as data from gene expression and pathway analysis, can provide more insightful data than the assay itself for distinguishing skin sensitization from skin irritation. This study investigated the gene expression profiles and pathways in ear skins of mice topically exposed daily for three consecutive days to the known strong contact sensitizer 1-chloro-2,4-dinitrobenzene, the skin contact sensitizer 2-phenyl-4-ethoxymethylene-5-oxazolone, the skin or respiratory sensitizer toluene 2,4-diisocyanate, or to the non-sensitizing irritant croton oil. All the sensitizers induced histological changes in ear tissues similar to those induced by the croton oil. In gene expression microarrays, sensitizers up-regulated 193 genes and down-regulated 61 genes in ear skin following chemical exposure. 13 genes whose expression was affected by more than two-fold by all three of the sensitizers, but not by the irritant, were selected by microarray analysis. Microarray and real-time RT-PCR analyses revealed that, of these genes, the allergic inflammation-related genes Oasl2 and Zbp1 were up-regulated in skin inflammation by the sensitizers. In gene expression pathway analysis of all the sensitizers and the croton oil, the top functions of the 48 genes were related to cytokine and cytokine receptors interactions, and only two genes (Cxcl9 and Cxcl10) were specific to skin sensitizer-induced skin inflammation. Thus, although contact sensitizer-induced skin inflammation is similar to irritant-induced responses in terms of histological changes and gene expression profiles, the regulation of allergic inflammation-related gene transcripts, such as those of Oasl2 and Zbp1 or Cxcl9 and Cxcl10, could help to discriminate skin sensitization from chemically induced skin inflammation.
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PMID:Gene expression profiles and pathways in skin inflammation induced by three different sensitizers and an irritant. 1964 56

In the present investigation, the safety of novel combinational silver sulfadiazine-bFGF-loaded hydrogel was assured by performing acute skin irritation, sensitization, acute dermal toxicity, and eye irritation in compliance with the Organization for Economic Co-operation and Development guidelines. In the skin irritation study, placebo, test, and positive control (0.8% w/v aqueous solution of formaldehyde) were applied on New Zealand rabbits and monitored for abnormal skin responses including erythema and edema. The placebo and test formulation did not induce any adverse reactions and were classified as nonirritating materials. In the skin sensitization test, guinea pigs were sensitized by positive control (0.1% w/v 1-chloro-2,4-dinitrobenzene in 10% of propylene glycol as a standard skin sensitizing agent), placebo, and test formulations. Weak sensitization was observed in the placebo and test formulation treated groups. Additionally, acute dermal toxicity test was performed in Wistar rats, where no signs of toxicity were observed in biochemical, hematological, and histopathological studies. Moreover, the acute eye irritation test was carried out in rabbits and no abnormal clinical signs were evident in the cornea or iris. As a whole, these findings suggest that the hydrogel formulation does not cause any skin irritation, skin sensitizationand dermal toxic effects, and eye irritation following dermal and ocular applications, respectively. Therefore, all the findings obtained from this preclinical study indicated that this hydrogel formulation is nontoxic and safe for use in animal models.
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PMID:Safety profile of silver sulfadiazine-bFGF-loaded hydrogel for partial thickness burn wounds. 2948 78