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At least 19 recordsLinked to original sources
PubMed1984

Pharmacological comparison of the immune and non-immune inflammations induced by picryl chloride and oxazolone in mice.

Picryl chloride applied to the ears of Swiss mice induced a clearcut primary irritation inflammation (maximal after 3 to 6 hr) and after contact sensitization performed 7 days before a delayed hypersensitivity reaction. Oxazolone produced only a weak primary irritation reaction. After contact sensitization in the same conditions as above, oxazolone induced an immune response that was already substantial 3 to 6 hr after the challenge and generally reached a maximum after 24 hr. We tried to alter these four types of inflammation (the primary irritation and delayed hypersensitivity to picryl chloride, and the 6-hr and 24-hr phases of hypersensitivity to oxazolone) by various types of compounds administered cutaneously or sytemically. Mepyramine, methysergide, cimetidine, disodium cromoglycate, phenylbutazone, and acetylsalicylic acid reduced to varying degrees after cutaneous application the primary irritation and the delayed hypersensitivity inflammation induced by picryl chloride. Methysergide was the only one of these drugs that on topical application clearly reduced the immune response to oxazolone (decrease in the 6-hr phase). After systemic administration, these same drugs had no effect on the four types of reaction. Both the corticosteroids tested (hydrocortisone acetate and desonide) reduced all the inflammations to various degrees and were always more active (particularly desonide) when applied topically than when administered systemically. On the other hand indomethacin, which inhibited all types of inflammation, was more active when administered systemically. Study of the kinetics and trials of pharmacological modulation of the various reactions induced by picryl chloride and oxazolone in Swiss mice provided evidence of differences in behavior between the two agents.

Adrenal Cortex Hormones↗
PubMed1979

Suppression of antibody responses by cells from mice painted with picryl chloride.

T cells from mice painted with picryl chloride inhibit secondary IgG anti-TNP antibody responses of normal mice to the sensitizer. Like other suppressor T cells produced after painting which inhibit DNA synthesis and the generation of cytotoxic T cells, these cells could be produced in adult thymectomized mice but not by mice treated with high doses of cyclophosphamide (250 mg/kg). The cells had to be injected within 48 h of a primary painting to inhibit the response to challenge 2-3 weeks later. This associated with their ability to inhibit DNA synthesis in draining lymph nodes after a primary painting. Double transfer experiments using spleen and lymph node cells failed to show any further activation or induction of suppressor function after challenge with antigen. As judged by the ability of anti-theta treated cells from suppressed mice to function as anti TNP primed B cells in adoptive responses to TNP-KLH no defect in B-cell memory was found. When, however, the ability of painting with picryl chloride to prime for challenge with TNP-KLH was used as a measure of B-cell function in situ it was found that the cells could inhibit responses. Responses to primary and secondary injections of TNP-KLH were not inhibited.

Administration, Topical↗
PubMed1982

Modulation by various locally applied anti-inflammatory and anti-allergic compounds of the immune and non-immune inflammation induced by picryl chloride in mice.

The authors studied the primary irritation and contact delayed hypersensitivity inflammation induced by picryl chloride in mice. The primary irritation reaction was induced by the application of various concentrations of the phlogogenic agent on an ear. Seven days after contact sensitization of the animals on their shaved abdomen, the immune inflammation was also induced on an ear by various doses of picryl chloride. Clear 24 hour-delayed hypersensitivity reactions were induced only by picryl chloride doses that induced a primary oedematous irritation 3 to 6 hours after application. After selection of the 3%-concentration of picryl chloride for challenge on ear, attempts were made to modulate these two types of reaction pharmacologically with various anti-allergic or anti-inflammatory compounds mixed with the inflammation-inducing agent. The inhibition of the non-immune reaction by mepyramine, methysergide, and the two anti-allergic compounds F 1865 and disodium cromoglycate demonstrated the participation of histamine and serotonin in this inflammation. Vasoactive amines seemed also to be involved in the immune reaction, but to a lesser extent. Hydrocortisone reduced the two types of inflammation by the same amount, while desonide had more effect on the delayed hypersensitivity reaction. In addition, both indomethacin and acetylsalicylic acid affected the two reactions equally, whereas phenylbutazone had a greater effect on the primary irritation inflammation.

Administration, Topical↗
PubMed1966

Concomitant anaphylactic sensitization and contact unresponsiveness following the infusion or feeding of picryl chloride to guinea pigs.

Guinea pigs receiving one large dose of picryl chloride by the intravenous or oral routes commonly develop circulating antibody demonstrable by passive cutaneous anaphylaxis or by active anaphylaxis. They often concommittantly become unresponsive to the induction of delayed contact hypersensitivity by intracutaneous injections. Erythrocytes obtained from guinea pigs after infusion or feeding of picryl chloride may be used to sensitize other animals when injected with adjuvant. It is concluded that guinea pigs may be anaphylactically sensitized to simple chemicals by the intravenous and oral routes if a sufficient dose is administered.

Anaphylaxis↗
PubMed1976

DNA synthesis in vitro by cells from mice immunized with picryl chloride: effect of injection of immune cells.

Mice were immunized with picryl chloride and the regional nodes taken at various times afterwards. These cells spontanesouly synthesized DNA in vitro as measured by thymidine incorporation over an 18-hour period and the peak incorporation occurred when the cells were takin on day 3. When the mice were injected with cells taken 5 days after immunization with picryl chloride and then immunized, there was a depression of the spontaneous DNA synthesis in vitro. This was absent on day 2, most marked on day 3 and still present on day 4. Cells from donors immunized with 4-ethoxymethylene-2-phenyloxazolone had a smaller but definite effect. Attempts to reproduce the phenomenon by in vitro mixtures of cells taken at various times after immunization in vivo were unsuccessful.

Animals↗
PubMed1985

Immunotoxicity screening of drugs and chemicals: value of contact hypersensitivity to picryl chloride in the mouse.

Contact hypersensitivity to picryl chloride in the mouse is proposed as a valuable tool for the in vivo immunotoxicological testing of new compounds. Reproducibility was found to be excellent. Results obtained in the present work with chlorpromazine, cyclophosphamide, diazepam, haloperidol, hydrocortisone, promethazine and lead acetate, nickel chloride and selenium were similar to those previously reported regarding the effects of these compounds on cell-mediated immunity.

Animals↗
PubMed1978

Split unresponsiveness to trinitrophenyl (TNP) determinant. Suppression of anti-TNP antibody responses by sensitization with picryl chloride.

Contact sensitization by epicutaneous application of picryl chloride causes in mice a significant reduction of the antibody responses to immunogenic TNP-conjugates. This split unresponsiveness is along-lasting. It was found that hapten applied on the skin became attached to the serum proteins and the transfer of such a serum into normal recipients, while not influencing the ability of these animals to become contact-sensitized to PCl, rendered them unable to mount the anti-TNP antibody response. Possible mechanisms of split unresponsiveness to the TNP determinant induced by PCl treatment are suggested.

Animals↗
PubMed1980

T suppressor cells and suppressor factor which act at the efferent stage of the contact sensitivity skin reaction: their production by mice injected with water-soluble, chemically reactive derivatives of oxazolone and picryl chloride.

The water soluble, chemically reactive thioglycollic acid thioether derivatives of oxazolone and picryl chloride were synthesized and tested for their ability to prevent the development of contact sensitivity. Mice given two injections of these agents showed partial or complete unresponsiveness when subsequently sensitized and challenged with oxazolone and picryl chloride, respectively. This unresponsiveness was associated with T suppressor cells, Ts-eff(cs), which blocked the efferent stage of the contact sensitivity reaction, i.e. the passive transfer of contact sensitivity. These Ts-eff(cs) were entirely specific when tested with the corresponding antigen. However, the suppression which they caused had a non-specific final common pathway. Cell from mice injected with the oxazolone and picryl thioethers and painted with the corresponding contact sensitizer produced a suppressor factor in vitro. This factor specifically blocked passive transfer by immune cells incubated in it. It also armed macrophages which then caused suppression. These macrophages were most effective when injected intraperitoneally. The suppressor factor had a molecular weight between 30,000 and 100,000 and the alpha-oxazolone factor was absorbed by oxazolone-albumin Sepharose and could be eluted with oxazolone-epsilon-aminocaproic acid. It was also absorbed by concanavalin-A-sepharose and could be eluted with alpha-methylmannoside. It is proposed that the ability of water soluble, chemically reactive haptenes to evoke a Ts-eff(cs) population may be relevent to the rarity of severe drug reactions following the injection of chemically reactive drugs.

Absorption↗
PubMed1983

The cellular infiltrate of the contact sensitivity reaction to picryl chloride in the mouse.

Contact sensitivity to picryl chloride was studied in the mouse ear. The skin hypersensitivity, as a factor of ear swelling, and the intensity of the cellular infiltrate in the skin were evaluated together during the elicitation of the contact sensitivity reaction. It was found that the ear swelling is a mainly vascular reaction preceding the appearance of inflammatory cells. The infiltrating cells in this model of skin sensitivity were differentiated in Giemsa-stained plastic-embedded sections and recorded in a semi-quantitative way. When the cellular reaction was most intense at 48 and 72 hours after challenge, the most numerous inflammatory cells were lymphocytes and eosinophils.

Animals↗
PubMed1997

One-shot delayed-type hypersensitivity reaction in the mouse liver causes a sustained liver injury to picryl chloride.

The developmental characteristics of liver injury induced by a delayed-type hypersensitivity (DTH) mechanism against picryl chloride were examined for 9 consecutive weeks in 3 mouse strains, BALB/c, Kunming and ICR mice. The changes of most biochemical parameters were similar in these three strains, namely, the activities of serum transaminases, lactic dehydrogenase, and prolidase were elevated significantly on day 1, during the first several weeks, and almost throughout the duration, respectively, of liver injury. The content of liver hydroxyproline was also increased after 1-9 weeks of liver injury. In addition, a significant decrease of liver weight, serum alkaline phosphatase and albumin level was observed in BALB/c and Kunming mice. Similar changes in liver histology were also found in the three strains. The hepatocellular necrosis and inflammatory infiltration into the portal area were the predominant features on day 1 and were still distinct during the subsequent several weeks. The mild or moderate hepatocellular degeneration, regeneration and connective tissue hyperplasia were observed after 1 or 3 weeks. A bridging necrosis between portal and portal was observed in several BALB/c and ICR mice, reflecting the possibility of exacerbation of liver injury. These results suggest that the liver injury could be caused and sustained by a one-shot DTH reaction to picryl chloride. The chronicity of the biochemical and histopathological characteristics may be helpful in elucidating the mechanisms of chronic development of liver injury.

Animals↗
PubMed1969

Studies on the sensitization of animals with simple chemical compounds. XI. The fate of labeled picryl chloride and dinitrochlorobenzene after sensitizing injections.

The fate of (14)C-labeled allergens injected intradermally into guinea pigs, namely picryl chloride (PCl*) and 2:4 dinitrochlorobenzene (DNCB*), was followed during the induction period of delayed hypersensitivity. Both chemicals were applied in a single injection into one ear in amounts that approached their minimal sensitizing doses (PCl, 0.25 microg; DNCB, 5.0 microg). Radioactivity in the various tissues was determined by liquid scintillation counting after combustion of tissues to CO(2) and H(2)O. The injected allergens seemed to leave the injection site in three phases. A large proportion of allergen escaped rapidly from the ear, about 50% within 3 hr in the case of PCl, within 15 min for DNCB, the difference probably reflecting their unequal reaction constants. Initially there was a "half-life" escape in 2.5 hr with injected dosage of 0.25 microg PCl and in 18 hr for 5.0 microg DNCB. This escape occurred via the regional veins and not via the lymphatics. Radioactive decomposition products of the allergens were already present in the urine within 3-4 hr. After 6-8 hr, the half-life time of escape lengthened to approximately 28 hr for both allergens used in their respective initial dosages, holding up to 2 days after which there occurred still further slowing; between 2 and 4 days the time was about 43 hr for PCl, much longer (72-88 hr?) for DNCB, apparently reflecting different physicochemical properties of this second fraction. Sensitization seemed to be connected with the portion that was present between 12 hr and 4 days of the induction period. It is not known how far the escape of radioactivity during this period may represent gradual hydrolysis of attached picryl and dinitrophenyl groupings, respectively, to form picric acid and dinitrophenol. Gradual accumulation of the second fraction in the regional lymph nodes could definitely be excluded. It was noted that no hypersensitivity arose and essentially no depot of radioactivity existed between 12 hr and 4 days when DNCB was injected in a dose of 0.25 microg, owing to its ready escape from the ear; but 20 times as much DNCB caused sensitization and provided about the same fixed depot as 0.25 microg of picryl chloride. After delayed hypersensitivity had been established, traces of radioactivity were still measurable at the site. This third fraction, probably representing a different coupling product, escaped at a very low rate and was traceable up through several weeks. No demonstrable radioactivity could be detected in thymus, spleen, and mesenteric nodes when examined at short intervals between (1/2) min and 17 days. In analogy with findings on transplantation "immunity" and with studies reported in the following paper, the induction of delayed hypersensitivity can be explained by encounters between lymphoid cells and the hapten complex which is found present in the local site for 4 days, in agreement with Medawar's concept of peripheral sensitization.

Allergens↗
PubMed1985

Infection of mice with Newcastle disease virus inhibits the T suppressor afferent cell circuit which regulates contact sensitivity to picryl chloride.

The interaction between Newcastle disease virus (NDV) and the suppressor cell circuit which regulates the induction phase of contact sensitivity reaction to picryl chloride (Pcl) was investigated. NDV infection impairs the activity of the T suppressor afferent cells (Ts-aff) which inhibit DNA synthesis in the draining lymph nodes of mice specifically sensitized with Pcl and the development of contact sensitivity. The inhibitory effect of NDV was evident when the virus was administered up to 2 days before or at the same time as the injection of picrylsulfonic acid; this effect required infectious virus, as NDV inactivated by ultraviolet irradiation failed to inhibit Ts-aff activity. Taken together with the previous finding that the T suppressor efferent cell is unaffected by NDV, the present results support the view that contact sensitivity reaction to picryl chloride is regulated by two distinct T-suppressor-cell circuits.

Animals↗
PubMed1983

Suppression of contact sensitivity to picryl chloride. Interaction between T suppressor auxiliary cells, suppressor factors and macrophages.

Immunization with picryl chloride generates cyclophosphamide resistant T immune cells (TDH) as well as cyclophosphamide sensitive T suppressor auxiliary cells (Ts-aux). T suppressor efferent cells do not inhibit effector phase of contact sensitivity in the absence of Ts-aux. These cells as well as macrophages adsorb TNP--T suppressor factor (TNP-TSF) and on these "armed" cells suppression may be transferred into recipients. Interactions between T-suppressor cells, their factors, Ts-auxiliary cells and macrophages are discussed.

Animals↗
PubMed1979

The cellular infiltrate in contact hypersensitivity to picryl chloride in the mouse.

In the present work, the contact hypersensitivity skin test reaction to picryl chloride in CBA mice was examined. The test was performed by applying the contact allergen to the ear skin and making a series of histological analyses up to 24 hours after challenge. An increment in ear thickness, measured with an engineer's micrometer 24 hours after challenge, was obvious in a group of sensitized mice when compared with a nonsensitized control group, and the difference was found to be highly significant. One hour after challenge, mononuclear cells appeared in the dermis, increasing in numbers during the following 12 hours. At this time, neutrophil granulocytes were the dominant cells in the infiltrate and remained so up to 24 hours after challenge. On the basis of the experiments performed here we conclude that measuring of the ear swelling with a micrometer 24 hours after challenge is a useful and reliable test of contact sensitivity in the mouse.

Allergens↗
PubMed1977

The I-J subregion codes for determinats on suppressor factor(s) which limit the contact sensitivity response to picryl chloride.

The cell-mediated immune reactivity (CMI) of mice to contact chemicals such as picryl chloride (PCI) is influenced by thymus-derived suppressor T lymphocytes (1,2). The development of these suppressor T lymphocytes is stimulated by the intravenous administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS). Zembala and Asherson have further demonstrated that a specific suppressor factor(s) can be detected in the supernates of cultured suppressor T cells. This factor suppresses the transfer of contact sensitivity (CS) to PCl (1,2). In experiments reported elsewhere (3), we have shown that the PCl suppressor supernates of Zembala and Asherson can also suppress the development of contact sensitivity to PCl. The immunochemical analysis of suppressor factor (SF) operative in the CS response to PCl has revealed many similar properties (3) to other suppressive moieties functioning to limit the plaque-forming cell (PFC) response to dinitrophenylated-keyhole limpet hemocyanin (DNP-KLH) as well as the strict antigen specificity of each respective suppressive factor, suggested that there might be a common origin of these substances. Indeed, in each case these respective factors were found to bear determinants controlled by the H-2 gene complex (4,5). Recently, in selected systems, the I-J subregion has been found to code for the Ia determinants present on suppressor cells (6) and suppressor factors (4,5). In accord with these findings, we report that antigen-specific SF which limit the CS response to PCl bear I-J determinants, implying that analogous suppressive regulatory mechanisms in CMI as well as antibody responses may be determined by genes of one subregion of the H-2 complex.

Animals↗
PubMed1999

Effects of several drugs on the liver injury induced by delayed-type hypersensitivity to picryl chloride by regulating suppressor or helper T cells.

The effects of histamine, cimetidine, and diphenhydramine on picryl chloride (PCl)-induced ear contact sensitivity, as well as liver injury, were examined in mice. Histamine was found to produce less response in mice to PCl. In contrast, cimetidine, a selective antagonist of histamine type 2 receptor, significantly enhanced the response, while diphenhydramine, a selective antagonist of histamine type 1 receptor showed no effect. The pre-treatment of 2,4, 6-trinitrobenzene sulphonic acid (TNBS) significantly caused a tolerance to the formation of the liver injury induced by delayed-type hypersensitivity (DTH) to PCl. Against the tolerance, the single intravenous administration of 150 mg kg-1 cyclophosphamide (Cy) at 3 days before the TNBS-treatment recovered the response and induced a remarkable elevation of serum transaminases. On the other hand, cyclosporin A protected the liver injury. These observations revealed that the development of acute PCl-DTH liver injury was regulated by the functional state of suppressor and helper T cells.

Animals↗
PubMed1980

Antigen-specific mast cell degranulation in contact sensitivity to picryl chloride. An early event.

Mast cells from the peritoneum of mice painted with the contact sensitizing agent picryl chloride degranulate when exposed to antigen (TNP) in vitro. Degranulation was consistently demonstrated 4 days after painting which associated with the ability of mice to produce contact sensitivity reactions as measured by ear swelling and radiometric assays. Serum reagin or reagin-producing cells could not be detected until 6 days after painting but TNP-phage neutralizing activity was detected after 2 days. Mast cell degranulation could be elicited by TNP or DNP derivatives indicating the involvement of antibody.

Animals↗
PubMed1976

Occurrence of suppressor cells in lymph nodes and spleen at later times after immunization with contact-sensitizing agent picryl chloride.

The lymph node and spleen cells of mice painted on the skin with the contact sensitizing agent, picryl chloride, transfer contact sensitivity. Their ability to transfer reaches a peak 4 days after immunization and is absent by day 6 providing the recipient mice are challenged shortly after transfer (Chase type transfer). In contrast, when challenge of the recipients is delayed for 6 days (adoptive transfer), lymph node and spleen cells show the greatest ability to transfer 8-12 days after immunization. When cells taken 4 days after immunization (which transfer contact sensitivity) are mixed with cells taken at 6-11 days (which fail to transfer), the mixture shows little ability to transfer. This provides evidence for the occurrence of suppressor cells. Lymph node and spleen, and thymus cells show suppressor activity. The suppression is specific and cells from donors immunized with the contact-sensitizing agent oxazolone will not suppress passive transfer of contuse of the loss of ability of lymph node and spleen cells in transfer later than day 6 after immunization. Experiments on the loss of radioactivity from lymph nodes labelled with 125I-iododeoxyuridine (IUDR) suggest that loss of cells from the lymph nodes may be a contributory factor.

Animals↗