In vitro augmentation of cytotoxicity by N-CWS in peritoneal polymorphonuclear leukocytes (PMNs) induced by PSK,OK-432 or N-CWS

Peritoneal polymorponuclear leukocytes (PMNs) were collected from the peritoneal cavity of C3H/He mice 6 hrs after intraperitoneal (i.p.) injection of 2.5 mg/head of PSK, 1 KE (100 µg)/head of OK-432 or 200 µg/head ofNocardia rubra cell wall skeleton (N-CWS). Withoutin vitro stimulation, these PMNs did not show cytotoxicity to syngeneic MM46 mammary carcinoma cells in⁵¹Cr release assay. Cytotoxicity of these PMNs was augmented by the addition of 25 µg/ml of N-CWS but not of PSK or OK-432 to cultures for the assay at the beginning of the culture. H₂O₂ production of PSK-induced PMNs was increased by thein vitro addition of 25 µg/ml of N-CWS but not of PSK. These results suggest that PSK as well as OK-432 and N-CWS can induce PMNs capable of responding further to N-CWS as the second stimulant.     

PGE2 and PGF2α release by human peritoneal macrophages in endometriosis

Objective: To test for differences in the amount and activity of peritoneal macrophages present in the peritoneal fluid of women with, and without endometriosis using prostaglandin release by macrophages in culture as a marker.Patients: Women of reproductive age undergoing laparoscopy for infertility or chronic pelvic pain with postoperative diagnosis of endometriosis and women undergoing laparoscopy for sterilization.Methods: Peritoneal fluid was aspirated during laparoscopy, volume was recorded, macrophages were isolated via a Ficoll Paque gradient and kept in primary culture. PGE₂ and PGF_2α release of the cells were measured before and after stimulation with zymosan.Results: Women with endometriosis had significantly more peritoneal macrophages than controls. Peritoneal macrophages of women with endometriosis released significantly more PGE₂ than those of the control group: 8.4 ± 2.0 versus 1.4 ± 0.4 ng/ml/10⁶cells (mean ± SEM, p=0.0005) and PGF_2α : 10 ± 4.3 (endometriosis) versus 1.8 ± 0.4 (control) ng/ml/10⁶cells (mean ± SEM, p = 0.045).Conclusion: There is a significant increase in the amount of prostaglandins released by peritoneal macrophages from women with endometriosis. These prostaglandins might alter uterine and tubal contractility, thereby affecting fertility.     

Annexin A1 mediates the anti‐adhesive effects of dexamethasone during the cell–cell interaction between the all‐trans retinoic acid‐treated acute promyelocytic leukemic cells and endothelial cells

Annexin A1 (AnxA1) is an important anti‐inflammatory mediator during granulocytic differentiation in all trans‐retinoic acid (ATRA) treated acute promyelocytic leukemic (APL) cells. Dexamethasone has been used successfully to prevent complications in ATRA‐treated APL patients, although its mechanism of action is still not clear. In the present study, we have examined the effect of dexamethasone on the modulation of AnxA1 in ATRA‐APL NB4 (ATRA‐NB4) cells, ATRA‐NB4 cells‐derived microparticles (MPs) and its role during cell–cell interaction between ATRA‐NB4 cells and endothelial cells. Our results have shown that dexamethasone can inhibit the percentage of ATRA‐NB4 cells expressing surface AnxA1 and its receptor FPR2/ALX in a time‐dependent manner based on flow cytometric analysis. However, dexamethasone treatment of ATRA‐NB4 cells has no significant effect on the level of AnxA1 mRNA, the total cellular level of AnxA1 protein or the release of AnxA1 from these cells, as determined by RT‐PCR, Western blotting, and ELISA, respectively. Further studies demonstrate that dexamethasone is able to significantly inhibit the adhesion of ATRA‐NB4 cells to endothelial cells, and this anti‐adhesive effect can be inhibited if the cells were pre‐treated with a neutralizing antibody specific for AnxA1. Finally, dexamethasone also enhances the release of AnxA1‐containing MPs from ATRA‐NB4 cells which can in turn prevent the adhesion of the ATRA‐NB4 cells to endothelial cells. We conclude that biologically active AnxA1 originating from dexamethasone‐treated ATRA‐APL cells and their MPs plays an anti‐adhesive effect and this contributes to inhibit the adhesion of ATRA‐APL cell to endothelial cells. J. Cell. Biochem. 114: 551–557, 2013. © 2012 Wiley Periodicals, Inc.     

Preface

"Although few people die of pain,many people die in pain and even more live in pain"——IASP On October11,2004,International Association for the Study of Pain(IASP)     

Human T cell leukemia virus type I induces DNA synthesis and immunoglobulin secretion in human lymphocyte cultures

Viral particles obtained from HTLV-I (human T cell leukemia virus, type I)-transformed T cell lines induced immunoglobulin production by normal peripheral blood lymphocytes. Conversely, no immunoglobulin could be detected in the supernatant medium in purified B cells cultivated with HTLV-I, suggesting that the presence of T cells is mandatory for HTLV-I to induce B cell polyclonal activation. The T cell help was mediated by soluble factors, as indicated in experiments showing that cell-free conditioned medium from T lymphocytes activated by HTLV-I was able to induce B cell proliferation and differentiation. Furthermore, a direct effect of HTLV-I on B cell proliferation was demonstrated when viral particles were added to purified B cells together with suboptimal doses of Staphylococcus aureus Cowan strain I (SAC). These observations show that an immediate early effect of HTLV-I infection was exerted on B cells, mainly in a T cell-dependent manner. Such an effect may account for the hypergammaglobulinemia observed in HTLV-I seropositive individuals, and in patients with HTLV-I-associated neurological disorders.     

Involvement of hyposialylated immunoglobulins in the inactivation of alpha 1-proteinase inhibitor

The elastase inhibitory capacity of alpha 1-proteinase inhibitor (alpha 1-PI) was measured, using a direct and reproducible method, with phagocytic cells maintained in the tissue culture plate through the assay. The oxidative inactivation of alpha 1-PI is known to be mediated by the action of myeloperoxidase (MPO). The fact that hyposialylated IgG (hs IgG) induce the release of MPO prompted us to investigate the effects of such hs IgG on the inhibitory capacity of alpha 1-PI. The results show that 1-PI inactivation was observed only when phagocytic cells were activated by aggregated hs IgG, and not by unaggregated hs IgG. These observations indicate that hyposialylation should be completed by aggregation to perpetuate the oxidative reactions characteristic of inflammatory diseases.