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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↗
PubMed1996

Liver injury model in mice induced by a cellular immunologic mechanism--delayed-type hypersensitivity-induced liver injury to picryl chloride and phenotype of effector cell.

Liver injury was induced in BALB/c mice by local delayed-type hypersensitivity (DTH) to picryl chloride (PC1). Distinct changes of biochemical parameters were observed including the elevation of serum alanine and aspartate aminotransferases, increase of liver lipid peroxides, as well as decrease of serum alkaline phosphatase. Damage was confirmed by histopathological findings such as hepatocellular necrosis, granulocyte infiltration, and fatty degeneration. The liver injury was passively transferred into naive syngeneic mice by infusing spleen cells from immune mice. The capacity of the splenocytes to induce liver injury in recipient mice was almost completely abolished by pretreatment of the cells with anti-Thy 1.2 or anti-CD4, but not anti-CD8 antibody. These findings suggest that the production of liver injury by a local DTH mechanism is possible and the subpopulation of T cells, Thy-1.2+, L3T4+, and Lyt-2- cells, is at least one of the effector cells that mediate the injury.

Animals↗
PubMed2000

Protective involvement of nitric oxide in the liver injury induced by delayed-type hypersensitivity to picryl chloride.

OBJECTIVE AND DESIGN: To investigate the role of nitric oxide (NO) in the liver injury induced by delayed-type hypersensitivity to picryl chloride (PCl-DTH). MATERIALS AND METHODS: Liver injury was induced in mice by PCl-DTH. NO production was examined using the Griess reagent. Isolated hepatocytes (HC) and nonparenchymal cells (NPC) were used. RESULTS: NO production in both serum and liver tissue reached a peak at 36 h after the elicitation of liver injury. The in vitro NO production was only observed by NPC or HC isolated at 24 h after the injury. Co-stimulation of IFN-gamma and TNF-alpha significantly triggered the HC and NPC isolated at 0 h to produce NO. As NO synthase inhibitors, Nomega-Nitro-L-Arginine exacerbated the liver injury in mice and NG-Monomethyl-L-Arginine enhanced the hepatotoxicity of IFN-gamma and TNF-alpha in vitro. In contrast, NO producer, S-nitroso-N-acetylpenicillamine dose-dependently inhibited the hepatotoxicity of NPC. CONCLUSIONS: NO may be produced by HC and NPC under the co-stimulation of IFN-gamma and TNF-alpha, and may play an important role for alleviating the liver injury.

Animals↗
PubMed1999

Role of Th1 and Th2 cytokines in regulating the liver injury induced by delayed-type hypersensitivity to picryl chloride.

AIMS/BACKGROUND: We have previously reported that a new model of liver injury induced in mice by delayed-type hypersensitivity (DTH) to picryl chloride (PCl) mimicks the pathogenesis of human hepatitis. This liver injury is mediated by CD4+ T cells. The interaction between lymphocyte function associated antigen 1 (LFA-1) and intercellular adhesion molecule 1 (ICAM-1) is an essential process for hepatocyte (HC) damage. The present study was undertaken to reveal the role of Th1 and Th2-like cytokines in regulating the liver injury. METHODS: The kinetics of cytokine production were examined by ELISA and RT-PCR after the elicitation of liver injury for both serum protein and liver mRNA expression, respectively. A co-culture assay between liver nonparenchymal cells (NPC) and HC was conducted to evaluate the cytokine regulation on the cell-cell interaction. Expression of LFA-1 on NPC and ICAM-1 on HC were examined by FACScan and ELISA, respectively. RESULTS: Serum IL-2 and IFN-gamma showed a peak production at 6 and 12 h, while IL-5 and IL-4 reached their maximum levels at 18 and 24 h after induction of liver injury, respectively. Liver mRNA expression of IFN-gamma and IL-4 had a similar time course to their corresponding products. Both recombinant murine IFN-gamma and IL-2 triggered the hepatotoxicity of NPC or spleen cells at 0 h. In this case, an increased expression of both LFA-1 on NPC and ICAM-1 on HC was also observed. In contrast, IL-4 and IL-5 completely abolished the hepatotoxicity of NPC at 12 h without influencing the adhesion molecules. CONCLUSION: Th1 and Th2 may be involved in regulating liver injury. Th1/Th2 balance may critically contribute to the production of the liver injury or recovery from it.

Animals↗
PubMed1998

Role of CD4+ and CD8+ T cells in regulating the chronic development of liver injury induced by delayed-type hypersensitivity to picryl chloride.

In this study we first investigated the cellular immune responses in mice with chronic liver injury induced by delayed-type hypersensitivity to picryl chloride (PCl). A continuous reduction, after week 3 of liver injury, was observed in the level of PCl-induced contact sensitivity but not in sheep red blood cell-induced footpad reaction, suggesting the presence of PCl-specific suppression. When spleen cells from mice whose liver had been injured for 1 week were systemically transferred into syngeneic recipients with the liver injury, the elevation in serum lactic dehydrogenase and the decrease in alkaline phosphatase and albumin levels in recipient mice were significantly exacerbated. However, when the liver damage in the donor mouse was allowed to proceed for 3, 5 or 7 weeks, biochemical changes in recipients were reduced to near normal levels. A flow-cytometric assay demonstrated that the number of CD4+ T cells in both spleen cells and liver nonparenchymal cells decreased dramatically during the late phase of liver injury, while CD8+ counts did not. These findings suggest that CD4+ and CD8+ T lymphocytes may contribute to the positive and negative regulation, respectively, of the early and late phases in the chronic development of liver injury.

Animals↗
PubMed1985

Use of dose-response data to compare the skin sensitizing abilities of dicyclohexylmethane-4,4'-diisocyanate and picryl chloride in two animal species.

Groups of English smooth-haired guinea pigs and BALB/cBy mice were exposed to dicyclohexylmethane-4,4'-diisocyanate (HMDI) and picryl chloride (PiCl) by topical exposure. Guinea pigs were challenged 7 days later by patch testing and responses graded at 24 hr. Application of high doses of each chemical resulted in extensive erythema and a large proportion of animals became sensitized. Lower doses produced less sensitivity. In mice, sensitivity was assessed by extent of ear swelling upon challenge 5 days following the sensitization exposure. In mice, as well as in guinea pigs, a dose-response relationship was apparent between the sensitizing dose and both severity of response and number of animals responding. For mice, comparison of the dose of chemical required to sensitize 50% of the animals (SD50) yielded 0.40 mg/kg for PiCl and approximately 0.20 mg/kg for HMDI. Use of the SD50 should provide a method for assessing the ability of various chemicals to cause contact sensitivity.

Abdomen↗
PubMed1988

Role of macrophages in bypassing the inhibitory activity of Newcastle disease virus on the T-suppressor-cell circuit which regulates contact sensitivity to picryl chloride.

The interaction between the paramyxovirus of Newcastle disease virus (NDV) and the T-suppressor-cell circuit which regulates the expression phase of contact sensitivity reaction to picryl chloride was investigated. NDV infection impairs the T-acceptor-cell (Tacc) activity, as demonstrated by the failure of Tacc from mice infected with NDV both on Day 0 and on Day 3 to release the nonspecific inhibitor of the passive transfer of contact sensitivity. Tacc from NDV-infected mice fail to bind appreciable amounts of exogenous T suppressor factor, so indicating that the virus eliminates this T-cell population. However, macrophages from mice infected with NDV are able to release a nonspecific inhibitor of the passive transfer of contact sensitivity, indicating that the inhibition of Tacc activity in mice infected with NDV is bypassed by macrophages, so that the T-suppressor circuit is functionally active in NDV-infected mice. The mechanism of the selective inhibition of the Tacc activity by NDV is discussed.

Animals↗
PubMedDate not supplied

Production of T suppressor factor specific for the hapten picryl chloride requires both T suppressor cells and an antigen-specific, genetically restricted second signal.

We investigated the requirement for activation of T suppressor cells specific for the hapten picryl chloride and the release of hapten-specific T suppressor factor. Using an in vivo experimental system, we report that activation of T suppressor cells and the consequent release of T suppressor factor required two signals: one was provided by primed T suppressor cells, i.e. spleen cells from mice injected with the tolerogen picrylsulphonic acid, and the other was provided by the specific antigen in the context of H-2 gene products. Mechanisms by which the interaction between these two signals led to activation of T suppressor cells and the production of T suppressor factor, as well as a comparison with other antigen-specific suppressor systems, are discussed.

Animals↗
PubMed1986

Immune serum from mice contact-sensitized with picryl chloride contains an antigen-specific T cell factor that transfers immediate cutaneous reactivity.

This report describes an activity in serum from mice that were contact-sensitized with picryl chloride (PCl) 1 to 4 days earlier. Immune serum, when given i.v., transfers the ability to elicit an immediate hypersensitivity-like ear swelling reaction in naive recipients following local challenge with PCl. This serum activity is due to an antigen-binding T cell factor that shares some properties with IgE antibody. The activity is antigen specific, and due to an antigen-binding moiety that is heat labile (56 degrees C, 4 h). However, unlike IgE antibody the serum activity is resistant to reduction and alkylation, and is retained by columns of Sepharose beads coupled with polyclonal or monoclonal antibodies that react with antigen-specific T cell factors from other systems. These columns did not retain IgE antibody activity in our experiments. Importantly, the serum activity was not retained by columns linked with antibodies directed to mouse immunoglobulins, which do retain IgE activity. We conclude from these data that the activity in PCl immune serum is not caused by IgE antibody, and is due to the presence of the previously described antigen-specific T cell factor (PCl-factor), that can activate serotonin-containing cells, such as mast cells, to release the vasoactive amine serotonin. PCl-factor transfers the ability to elicit an immediate hypersensitivity-like reaction that is an early component of delayed-type hypersensitivity. The presence of this T cell factor in the serum of actively sensitized mice provides a means to sensitize tissues throughout the body for this required, initial, serotonin-dependent component of delayed-type hypersensitivity reactions.

Alkylation↗
PubMed1986

T suppressor afferent cells which regulate contact sensitivity to picryl chloride act across genetic barrier.

This paper investigates the requirement for genetic restriction in the action of T suppressor afferent cells (Ts-aff) which regulate the induction phase of contact sensitivity to picryl chloride. The results here reported show that Ts-aff which inhibit both the induction of contact sensitivity and DNA synthesis in the draining lymph nodes of sensitized mice, act across both H-2 and Igh genetic barrier and constitute new evidence which discriminates between two T suppressor cell populations in contact sensitivity.

Animals↗
PubMed1997

A new strategy for regulating the immunological liver injury--effectiveness of DTH-inhibiting agents on DTH-induced liver injury to picryl chloride.

Aqueous extracts from various crude drugs showing a selective inhibition on the induction or effector phase of delayed-type hypersensitivity (DTH) reaction were applied to the new model of liver injury induced in mice by picryl chloride(PCl)-induced DTH. The inhibiting drugs to the induction phase of DTH, Fructus Triburi (FT) and Er-Miao-San (EMS), showed a remarkable improvement against the elevation in serum transaminase levels as well as in histopathological changes when given during this phase. The administration in the effector phase by Rhizoma Smilacis Glabrae (RSG) and Cortex Dictamni (CD), selectively inhibiting the phase of DTH, also significantly improved the liver damage. In addition, RSG and CD showed an almost complete recovery of serum alkaline phosphatase from a persistent decrease in the sustaining process of liver injury when given consecutively for 4 weeks after the elicitation of liver injury. Cyclophosphamide, an immunosuppressive agent, significantly inhibited the enzymatic elevation given in either phase, while it did not affect the ability to sustain liver injury. When the above extracts were given in a combined manner to the same mouse during these two phases, respectively, FT with RSG and EMS with CD showed a distinct synergism against the liver injury. RSG or CD also enhanced the activity of prednisolone in suppressing PCl-induced ear contact sensitivity. These findings suggest that this immunological liver injury may be regulated by a set of selective suppressants to DTH reaction and the suitable application of such agents may pave the way for a new strategy in treating liver damage.

Animals↗
PubMed1998

LEA-1/ICAM-1 interaction is essentially involved in the pathogenesis of delayed-type hypersensitivity-induced liver injury to picryl chloride.

The kinetics of lymphocyte function associated antigen 1 (LFA-1) expression on spleen cells (SPC) and liver non-parenchymal cells (NPC), and intercellular adhesion molecule 1 (ICAM-1) expression on hepatocytes (HC) was examined in acute liver injury mice induced by a DTH reaction to picryl chloride (PCl). The peak expression of LFA-1 on SPC was seen at 6 hr after eliciting liver injury, and then that of LFA-1 on NPC and ICAM-1 on HC appeared at 12 hr. Thereafter, the serum ALT elevation reached to a peak at 18 hr. A splenectomy before the PCl elicitation significantly reduced the ALT elevation. Both SPC and NPC from liver injury mice induced a remarkable release of ALT from HC in vitro, in parallel with their LFA-1 expression. The pre-treatment of NPC or SPC with anti-LFA-1 mAb, irrespective of the presence of complement, completely blocked the ALT release. Also, when HC was prebound with anti-ICAM-1 mAb, neither NPC nor SPC showed a cytotoxicity against the HC. Furthermore, the treatment of NPC with either anti-Thy1.2 or anti-CD4 mAb in the presence but not absence of complement, showed a complete abolishment of ALT release. Anti-CD8 mAb plus complement also tended to inhibit ALT release. The twofold increase in CD4+ LFA-1+ and mild increase in CD8+ LFA-1+ populations were also confirmed in NPC at 12 hr. These results suggest that PCl elicitation in liver may trigger an increased expression of LFA-1 on SPC and NPC and ICAM-1 on HC. LFA-1/ICAM-1 interaction between liver-infiltrating NPC, mainly including CD4+ and CD8+ T cells, and HC may be an essential step for the hepatocyte damage in PCl-DTH liver injury.

Alanine Transaminase↗
PubMed2003

Ultrastructural features of mast cells in picryl chloride (PCL)-induced contact dermatitis in IQI/Jic mice.

Mast cells are one of the major effector cells in the pathogenesis of allergic diseases such as contact dermatitis. In the present study, ultrastructural features of mast cells in contact dermatitis were examined. Namely, the ear of IQI/Jic mice was topically applied with picryl chloride (PCL) at 4 (1st), 11 (2nd), 18 (3rd) and 25 days (4th) after the sensitization with PCL to the abdominal skin. The changes in the ear swelling responses, total serum IgE levels and histology including mast cell numbers were similar to those of previous reports by our research group (Ikeda et al. 2000; Jung et al. 2001). Ultrastructurally, after the 1st application, a close spacial relationship between mast cells and neutrophils and phagocytosis of mast cell granules by neutrophils were observed. Mast cells generally contained non-fused swollen granules filled with altered contents with low electron density and showed an extrusion of membrane-free granules through membrane pores. In addition, interestingly, a few mast cells secreted membrane-bound granules into the dermis without leaving cell membrane damage. After the 4th application when the number of mast cells prominently increased and the total serum IgE level was greatly elevated, in addition to mast cells showing typical anaphylactic degranulation, many mast cells probably in the recovery process from degranulation and several immature mast cells characterized by well-developed Golgi apparatus, many ribosomes and a few electron-dense secretory granules in the peripheral cytoplasm were also observed at the same time. The present results clarified the ultrastructural features of mast cells in the course of PCL-induced contact dermatitis in IQI/Jic mice.

Anaphylaxis↗
PubMed1980

Differential effects of 5-fluorouracil analogs on humoral and cell-mediated responses in mice: augmentation of delayed hypersensitivity response against picryl chloride by 1,3-bis(tetrahydro-2-furanyl)-5-fluoro-2,4-pyrimidinedione (FD-1), a new anti-tumor drug.

The inhibitory effects of three fluorinated pyrimidines, i.e., 5-fluorouracil (FU), N1-(2-tetrahydrofuryl)-5-fluorouracil (ftorafur, FT), and 1,3-bis(tetrahydro-2-furanyl)-5-fluoro-2,4-pyrimidinedione (FD-1), on humoral and cell-mediated responses were compared. Both primary and secondary humoral responses against sheep red blood cells were strongly suppressed, and the suppressive activities of FD-1, FT and FU were directly proportional to the plasma level of active substance, FU. However, allogeneic skin graft rejection was not suppressed by FD-1 and FT. Furthermore, the delayed hypersensitivity response (DHR) against picryl chloride (PCl) was augmented by FD-1 but not by FT and FU if they were administrated for 3 days after PCl immunization. Spleen cells from mice immunized 7 days previously with PCl were able to suppress the occurrence of the DHR when they were transfused intravenously to normal syngeneic mice simultaneously immunized with PCl. The suppressor activity of spleen cells was due to B cells since the activity was abrogated by treatment with anti-IgG serum plus complement, but not by anti-T cell serum plus complement. However, the suppressor activity disappeared when donor mice were administrated with FD-1 and FU. It is suggested that FD-1 has a great inhibitory effect on suppressor cells than effector cells induced by PC1, and then the immunosuppressive potency of these drugs is not always reflected in the level of FU.

Animals↗
PubMed1979

Suppressor cells for the afferent phase of contact sensitivity to picryl chloride: inhibition of DNA synthesis induced by T cells from mice injected with picryl sulfonic acid.

Previous reports have shown that picryl sulfonic acid (PSA) induces suppressor T cells that inhibit the effector phase of contact sensitivity, whereeas its DNP counterpart, dinitrobenzenesulfonate (DNBS) induces cells that inhibit the afferent phase of sensitization. Accordingly, cells from mice injected with DNBS, but not PSA, could be shown to inhibit the DNA synthesis in the lymph nodes that occurs during sensitization. It is now shown that PSA does induce T cells that suppress DNA synthesis but this can only be detected with enriched T cells or by using a regimen of PSA injection different frm previously used to induce suppressor cells for the effector phase. The T cells did not affect responses to oxazolone or dinitrofluorobenzene (DNFB) and were distinguishable from suppressors of the efferent phase in that they could be produced in adult thymectomized but not cyclophosphamide-treated mice. T cells from mice injected with DNBS that inhibited DNA synthesis to DNFB had the same properties.

Animals↗
PubMed2002

Inhibition of contact hypersensitivity reaction to picryl chloride: effect of small molecular weight peptidomimetic compounds possessing inhibitory activity against metalloproteinases.

We have studied the effect of small molecular weight inhibitors of snake venom metalloproteinases (SVMP) and matrix metalloproteinases (MMPs) on the induction and effector phase of the contact hypersensitivity reaction (CHR) in a mouse model. Identification of nonsteroid small molecules is very important for the development of new anti-inflammatory drugs. The compounds that we tested were synthetically modified tripeptides (peptidomimetic compounds) POL-257, POL-509, POL-443, POL-491, and POL-647, with structures based on natural occurring peptides in snake venom. A well-known hydroxamate-based inhibitor of the MMPs, Batimastat (BB-94), was also used. We have shown that these peptidomimetics possess in vitro inhibitory activity against the MMP-2 (gelatinase-A), MMP-9 (gelatinase-B), and MMP-3 (stromelysin). They also inhibit metalloproteinases purified from the venom of Crotalus adamanteus and C. atrox snakes, which are very similar to the so-called A Desintegrine, A Metalloproteinase (ADAMs) enzymes. When injected intraperitonealy before the topical application of the contact sensitizer (picryl chloride) or before the challenge, these compounds significantly inhibited the development of CHR. BB-94 at doses 0.4 and 4 mg/kg before the sensitization or before the challenge almost completely abrogated the reaction. POL-257 and POL-443 were among the most active peptidomimetics tested. They inhibited the inflammatory reaction up to 70-80%, when applied either immediately before sensitization or before challenge. POL-509, a methylated derivative of POL-257, inhibited the CHR to 40-50% when administered at either challenge or sensitization. However, when applied 24 h before the challenge, it completely abrogated the inflammatory reaction. The results show that these small molecular weight peptidomimetic compounds, as well as BB-94, are able to significantly inhibit the CHR. This finding opens possibilities for using metalloproteinase inhibitors in the treatment of allergic contact dermatitis and other inflammatory diseases.

Animals↗