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At least 19 recordsLinked to original sources
PubMed1996

Dinitrochlorobenzene is genotoxic by sister chromatid exchange in human skin fibroblasts.

Dinitrochlorobenzene (DNCB) is clinically efficacious in the therapy of alopecia areata, but its use was limited when it was found to be mutagenic in the Ames test. However, there has been renewed interest in the immunomodulatory benefits of topically applied dinitrochlorobenzene in patients with human immunodeficiency virus and systemic lupus erythematosus. The current study examines the genotoxicity of dinitrochlorobenzene in human skin fibroblasts using sister chromatid exchange. Dinitrochlorobenzene caused a significant increase in sister chromatid exchange at concentrations ranging from 2.5 to 10 microM. Thus, dinitrochlorobenzene is genotoxic in human skin fibroblasts at concentrations well below those used clinically. The potential for long-term toxicity from dinitrochlorobenzene will have to be weighed against the severity and prognosis of the diseases for which it is used.

Dinitrochlorobenzene↗
PubMed2003

p38 Mitogen-activated protein kinase and extracellular signal-regulated kinases play distinct roles in the activation of dendritic cells by two representative haptens, NiCl2 and 2,4-dinitrochlorobenzene.

Previous studies have demonstrated that haptens induce several phenotypic and functional changes of dendritic cells in vivo as well as in vitro. Although recently, the crucial role of p38 mitogen-activated protein kinase has been reported in the activation of dendritic cells by haptens, the signal transduction elements involved in each phenotypic and functional changes that occur in the activation of dendritic cells by haptens remain unknown. Therefore, we examined the role of mitogen-activated protein kinases and nuclear factor-kappaB in the signal transduction of dendritic cells stimulated with two representative haptens, i.e., NiCl2 and 2,4-dinitrochlorobenzene. Human monocyte-derived dendritic cells stimulated with 2,4-dinitrochlorobenzene induced the phosphorylation of p38 and stress-activated protein kinase/c-jun N-terminal kinases, whereas NiCl2 induced that of p44/42 extracellular signal-regulated kinases, p38, and stress-activated protein kinase/c-jun N-terminal kinases. In addition, NiCl2 phosphorylated inhibitor kappaB and activated nuclear factor-kappaB. In contrast, primary irritants, e.g., benzalkonium chloride, or sodium lauryl sulfate, did not activate these signal transduction pathways. By using specific inhibitors for extracellular signal-regulated kinases and p38 pathways, PD98059 and SB203580, respectively, we demonstrated that the augmentation of CD86, HLA-DR, and CD83, and the production of interleukin-8 along with its increased mRNA expression by monocyte-derived dendritic cells stimulated with 2,4-dinitrochlorobenzene, and the augmentation of CD83 and the interleukin-12 p40 production by monocyte-derived dendritic cells stimulated with NiCl2, were suppressed by SB203580, whereas PD98059 suppressed the production of interleukin-1beta and tumor necrosis factor-alpha, together with their increased mRNA expression by monocyte-derived dendritic cells treated with NiCl2. On the other hand, in spite of the activation of nuclear factor-kappaB by monocyte-derived dendritic cells stimulated with NiCl2, nuclear factor-kappaB inhibitor did not significantly affect the phenotypic and functional changes in the activation of monocyte-derived dendritic cells. These data indicate that NiCl2 and 2,4-dinitrochlorobenzene stimulate different signal transduction pathways in monocyte-derived dendritic cells, and subsequently induce different phenotypic and functional changes in them.

Antigens, CD↗
PubMed1979

Dinitrochlorobenzene responsivity: difference between patients with severe pulmonary coccidioidomycosis and patients with disseminated coccidioidomycosis.

Immunologic responses in 15 patients with severe pulmonary coccidioidomycosis and in 50 patients with disseminated coccidioidomycosis were measured by determination of complement-fixing (CF) antibody titers to coccidioidin in serum, coccidioidin (1:100) skin tests, and sensitization to dinitrochlorobenzene. Among the patients with desseminated coccidioidomycosis, the nine with CF antibody titers of less than or equal to 1:8 had normal responses to dinitrochlorobenzene, but the 41 with titers of greater than or equal to 1:16 had responses that were significantly lower than those of controls (P less than 0.001). In contrast, all patients with severe pulmonary coccidioidomycosis had CF antibody titers of greater than or equal to 1:16 and had responses to dinitrochlorobenzene that were greater (but not significantly greater) than those of controls. Among subjected with antibody titers of greater than or equal to 1:16, responsiveness to coccidioidin was found in 27% of those with severe pulmonary disease and in 39% of those with disseminated disease. Thus impaired responsivity to dinitrochlorobenzene in coccidioidomycosis is restricted to patients who have disseminated illness and high titers of CF antibody and is separable from lack of responsiveness to coccidioidin.

Antibodies, Fungal↗
PubMed1981

Dinitrochlorobenzene-induced colitis in the guinea-pig: studies of colonic lamina propria lymphocytes.

Dinitrochlorobenzene-induced colitis in guinea-pigs may be immunologically mediated: animals must be presensitised to dinitrochlorobenzene to develop colitis, sensitivity can be passively transferred by lymphocytes and the injury can be mitigated by immunosuppression. In this study, we examined lamina propria lymphocytes isolated from colons of animals with dinitrochlorobenzene-induced colitis, and appropriate controls. Lamina propria lymphocytes from colitis animals have a greater percentage of rabbit erythrocyte-rosetting cells (T cells) (20.1 +/- 3.0 vs 2.3 +/- 0.8, p less than .01) and a greater capacity to mediate mitogen-induced cellular cytotoxicity with phytohaemagglutinin than lamina propria lymphocytes from normal colon (% specific cytoxicity = 29.4 +/- 8.7 vs 5.0 +/- 4.5, P less than .005). There was no difference in the percentage of rosetting cells or cytotoxicity index of spleen or mesenteric lymph node lymphocytes between the colitis animals and controls. These data suggest that there are changes in the distribution and functional characteristics of lamina propria lymphocytes which correlate with mucosal cell injury in the dinitrochlorobenzene-colitis model.

Animals↗
PubMed1983

The predictive value of 2,-4, dinitrochlorobenzene skin testing in patients with bilharzial bladder cancer.

A group of 40 patients with bilharzial bladder cancer underwent quantitative skin testing with dinitrochlorobenzene and purified protein derivative of tuberculin before radical surgery. Correlations were made between various clinical parameters, patient outcome, skin test results and pathologic changes in the resected bladder and draining lymph nodes. Striking associations between dinitrochlorobenzene responses and tumor stage, tumor recurrence and several specific parameters of lymph node stimulation were found, while no correlations were made with the pathologic grade, size or type of tumor, degree of schistosomal infestation or tumor bed inflammation. Purified protein derivative responses showed no correlation with any parameter examined. Patient outcome also showed a good correlation with tumor stage and draining lymph node reaction. These findings indicate that dinitrochlorobenzene skin testing as a presumptive test of cell-mediated immunity may represent a good predictor of clinical outcome in patients with bilharzial bladder cancer, and correlates well with draining lymph node stimulation.

Dinitrochlorobenzene↗
PubMed2000

Treatment of severe atopic dermatitis by topical immune modulation using dinitrochlorobenzene.

We present the results of a small uncontrolled pilot trial which suggest that contact sensitization to dinitrochlorobenzene and repeated weekly applications significantly improve the clinical status of severe atopic dermatitis in adults. Although no changes were noted in circulating levels of either lymphocyte subset populations or the serum cytokines assayed in this trial, our observations may be due to topical immune modulation by dinitrochlorobenzene. Larger controlled studies of dinitrochlorobenzene treatment in atopic dermatitis are warranted.

Administration, Topical↗
PubMed1999

[Determination of 2,4-dinitrochlorobenzene in environmental water by primary-secondary wavelengths new spectrophotometry].

In basic solution, dinitrochlorobenzene may react on pyridine to form a purplish red compound. In this paper with the absorption property of a suspended liquid against light a new analytical method as primary-secondary wavelengths spectrophotometry was studied to determine trace dinitrochlorobenzene in environmental water. In 0-50 microg dinitrochlorobenzene/25 mL, the calculation curve is very stable and hardly affected by environment conditions. Experiments for practical waters have shown that the detection limit was 0.7 microg/25 mL dinitrochlorobenzene and RSD < or = 2.7% and the recovery rate was 99.2%-101.0%.

Dinitrochlorobenzene↗
PubMed2001

Phenotypic characterization of human CD4+ regulatory T cells obtained from cutaneous dinitrochlorobenzene-induced delayed type hypersensitivity reactions.

In this study, we describe the generation and characterization of cloned human CD4+ T lymphocyte populations that have infiltrated into cutaneous, 2,4-dinitrochlorobenzene-induced delayed type hypersensitivity reactions in healthy human subjects. It is shown that, in addition to T helper type 1 clones, elevated numbers of regulatory T clones, producing high levels of interleukin-10 and interleukin-5, but no measurable interleukin-4, were isolated from delayed type hypersensitivity reactions in four of six donors. A subsequent challenge with 2,4-dinitrochlorobenzene of two donors from whom only few interleukin-10-producing T cell clones had been generated after primary challenge, resulted in a decrease in the frequency of T helper type 1 clones and a strong increase in the number of interleukin-10-producing T helper type 2 and regulatory T clones. Culture supernatants from the latter cells, activated with anti-CD3 and anti-CD28 monoclonal antibody, inhibited alloantigen-mediated T cell proliferation which was, partly dependent on interleukin-10, and independent of transforming growth factor-beta. In addition, dendritic cells generated in vitro in the presence of these culture supernatants were impaired in their ability to induce alloantigen-induced proliferative responses. Differential expression of transcripts for the T1/ST2 molecule enabled a phenotypic distinction between resting regulatory T cells and T helper type 2 cells, but not between regulatory T cells and T helper type 1 cells. This experimental model provides a useful tool to isolate human inflammatory and anti-inflammatory T cell subpopulations and, furthermore, enables the study of the kinetics of their appearance into delayed type hypersensitivity reactions.

CD4-Positive T-Lymphocytes↗
PubMed1989

Dinitrochlorobenzene contact hypersensitivity as a marker trait for selection to improve disease resistance in calves.

Measurements of double skin fold thickness (mm) were used to assess the feasibility of use of cutaneous delayed-type hypersensitivity response as a marker trait to select for genetically improved disease resistance. Data were from a sample of 149 7-wk-old Holstein calves, from 15 sires, that previously had been sensitized to the contact allergen dinitrochlorobenzene. Response was monitored 24 and 48 h postchallenge. Analysis was by least squares according to a model that included fixed managerial effects, disease prevalence, and severity categories and sire of calf. Double skin fold thickness increased about 50% by 24 h, followed by a 4% decrease between 24 and 48 h. Season of birth was the only consistently significant fixed effect. Calves born in fall showed larger skin changes at each stage of response than calves born in spring. Restricted maximum likelihood estimates of paternal half-sib heritability were moderate to high for all stages of response, and phenotypic and genetic correlations between stages were significant and positive. Although the prevalence and severity of naturally occurring pneumonia and diarrhea did not significantly affect quantity of response, there is need to study further this relationship for intracellular pathogens. Delayed-type hypersensitivity response to dinitrochlorobenzene can meet requirements for a successful marker on which to base sire selection for disease resistance, if it is related to economically important, intracellularly characterized, pathogenic bovine diseases.

Analysis of Variance↗
PubMed1990

Contact sensitivity to dinitrochlorobenzene is impaired in atopic subjects. Controversy revisited.

If there is a primary dysfunction of the immune system in atopic eczema it might be reflected in altered capacity to generate delayed-type hypersensitivity. Therefore, the dose-response relationships for contact sensitization were determined for 22 patients (10 men) with minimal atopic eczema and compared with those from 27 nonatopic, healthy control subjects (12 men). Sensitization was induced with 30 micrograms of dinitrochlorobenzene applied to the thigh. Four weeks later the subjects were challenged with three doses of dinitrochlorobenzene (8.8, 12.5, and 17.7 micrograms), and responses were quantified with calipers as change in skinfold thickness at 48 hours. Atopic patients were significantly less responsive with smaller reactions at all challenge doses and a flatter challenge dose-response curve than that for control subjects. Thus, proper quantitative comparisons have shown that subjects with minimal atopic eczema do not mount a normal contact hypersensitivity response. However, it is not clear whether this is a consequence of the atopic state per se or is related to the presence of even a minor degree of eczema.

Adolescent↗
PubMed1978

[Reproduction of amyloidosis in mice by contact sensitization with dinitrochlorobenzene].

Induction of murine amyloidosis by contact sensitization with hapten--dinitrochlorobenzene is described. Three to five applications of 15--25% dinitrochlorobenzene solution in acetone during two weeks are necessary for this. Within 3 weeks after the 1st application amyloidosis develops involving consecutively the spleen, liver, kidney and heart. Such consequence of the organ involvement and tinctorial pecularities are typical of murine amyloidosis.

Amyloidosis↗
PubMed1977

Bacillus Calmette-Guérin and dinitrochlorobenzene immunotherapy of chemically induced bladder tumors.

Immunologic incompetence is correlated with increased susceptibility to malignacy. Immunostimulation with such agents as Bacillus Calmette-Guérin (BCG) and dinitrochlorobenzene (DNCB) have resulted in regression of cutaneous maligancies. An evaluation of the effect of BCG and dinitrochlorobenzene sensitization and bladder irrigation in Fischer rats revealed no decrease in the incidence of bladder tumors induced by 2-formylamino-4-(5-nitro-2-furyl) thiazole (FANFT). However, direct intralesional injection of BCG into early bladder tumors was effective in preventing the progression of such tumors in seven of ten BCG-sensitized rats (P less than 0.005). No effect was seen when BCG was injected intralesionally in unsensitized rats or when control solutions were injected.

Animals↗
PubMed1982

Dinitrochlorobenzene treatment of alopecia areata.

Forty-two patients with alopecia areata were treated with local applications of dinitrochlorobenzene (DNCB); We used DNCB in two forms, an acetone solution applied weekly or a cream used every day, employing a wide range of DNCB concentrations. The concentration used was varied at the time of each application to produce a contact dermatitis. Seven patients experienced complete and lasting hair regrowth, 17 had poor results, and in 18 patients the treatment was a failure. Acquired tolerance to DNCB was observed in six patients; in five it was abolished by the administration of cimetidine. Certain factors such as the delay in appearance and the intensity of the sensitization reaction influence the hair regrowth. Poor prognostic criteria for treatment effect included a history of previous systemic corticosteroid therapy, atopy, and the presence of alopecia areata in close relatives.

Administration, Topical↗