Biomedical subjects

F Sendo

Publications and source records attributed to F Sendo.

At least 55 records · Page 3Linked to original sources

PubMed1995

Modulation of rat neutrophil functions by administration of granulocyte colony-stimulating factor.

Neutrophil function was examined in rats treated with recombinant human granulocyte colony-stimulating factor (G-CSF) using peripheral blood neutrophils (PBNs) and peritoneal exudate neutrophils (PENs) as sources of cells examined in vitro. Adherence to plastic plates containing fetal calf serum of nonstimulated or N-formylmethionyl-leucyl-phenylalanine (fMLP)- or tumor necrosis factor-alpha-stimulated PBNs obtained from G-CSF-injected rats was lower than that of control rats. In contrast, this adherence was higher in G-CSF-treated rats than in the control group when PENs were used. Neutrophil adherence of G-CSF-injected and noninjected groups was identical when phorbol myristate acetate was used to stimulate neutrophils. Superoxide production of PBNs stimulated with fMLP in vitro was lower in G-CSF-treated rats than in control rats but higher than in the controls when PENs were used. Furthermore, in vitro tumor cell growth inhibition by PBNs was lower in G-CSF-treated rats than in control rats, but when PENs were used inhibition was higher than in the controls.

Amino Acid Sequence↗

PubMed1995

Inhibition by bacterial lipopolysaccharide of spontaneous and TNF-alpha-induced human neutrophil apoptosis in vitro.

In the previous paper (Takeda et al, Int. Immunol., 5, 691-694, 1993), we demonstrated that tumor necrosis factor-alpha (TNF-alpha) promptly accelerates apoptosis of human neutrophils in vitro. In order to determine the role of neutrophil apoptosis in defending against bacterial infection, we studied the effect of bacterial lipopolysaccharide (LPS) on this process. LPS inhibited spontaneous and TNF-alpha-induced human neutrophil apoptosis in vitro, as determined by 1) light and electron microscopy, 2) flow cytometry, and 3) agarose gel electrophoresis of DNA. Low concentrations of cycloheximide, a protein synthesis inhibitor, which alone did not affect neutrophil apoptosis, were able to reduce spontaneous apoptosis inhibition by LPS, suggesting the involvement of newly synthesized protein in this phenomenon.

Apoptosis↗

PubMed1995

Inhibition by dexamethasone of human neutrophil apoptosis in vitro.

We investigated in this study the effect of a synthetic glucocorticoid hormone, dexamethasone (Dex), on apoptosis of human peripheral blood neutrophils. Dex inhibited spontaneous and tumor necrosis factor-alpha (TNF-alpha)-induced neutrophil apoptosis in a concentration- and time-dependent manner. This effect of Dex on neutrophil apoptosis was completely reversed by a glucocorticoid receptor antagonist, RU38486, and by cycloheximide. The decrease in sensitivity to TNF-alpha-induced apoptosis cannot be ascribed to a down-modulation of TNF receptors on these cells. These observations suggest that a glucocorticoid hormone participates in the regulation of neutrophil apoptosis and that inhibition of human neutrophil apoptosis by Dex is mediated through glucocorticoid-receptor-induced de novo synthesis of macromolecules. Possible mechanisms and implications of this phenomenon are discussed.

Apoptosis↗

PubMed1994

Modulation of the in vivo immune response by selective depletion of neutrophils using a monoclonal antibody, RP-3. III. Enhancement by RP-3 treatment of the anti-sheep red blood cell plaque-forming cell response in rats.

Because recent work has shown that neutrophils produce various cytokines and are activated by these agents, this study was undertaken to examine neutrophil participation in immune networks. In our previous work, we demonstrated that delayed type hypersensitivity to SRBC and accompanying mononuclear leukocyte recruitment are inhibited in vivo by selective depletion of neutrophils using a mAb designated RP-3. To elucidate the function of these cells in Ab production, we assessed the splenic plaque-forming cell response to SRBC in a rat model through selective depletion of circulating neutrophils by RP-3. This depletion which occurred at the time of immunization resulted in an increase in the number of anti-SRBC Ab producing cells, as determined by the direct and indirect plaque-forming cell response. This phenomenon was observed only when the Ag was administered i.p. and not with i.v. immunization. These results suggest that neutrophils suppress Ab production in certain situations.

Animals↗

PubMed1994

Characterization of the recognition specificity of autoreactive, polyspecific monoclonal antibodies obtained from spleen cells of parasite-infected BALB/c mice.

We examined the specificity of four monoclonal antibodies (MoAbs) obtained from Schistosoma japonicum (1D, GAO3), Trypanosoma cruzi (TSLO), and Trichinella spiralis (TSY2) infected BALB/c mice. All four MoAbs reacted not only with autologous parasite antigens but also with various heterologous parasite antigens and normal tissues. The antigen recognition pattern seen on Western blots was almost identical in 1D and GAO3, and in TSLO and TSY2. Furthermore, certain bands were identical among all four MoAbs. The mechanisms responsible for these phenomena are discussed.

Animals↗

PubMed1994

Effects of supernatant from tonsillar cell culture on neutrophil functions.

The palatine tonsil is the most important element of Waldeyer's ring as a defense mechanism against various microorganisms. The neutrophils are the initial active participants in bacterial infection and inflammation, but their interaction with other cellular participants is poorly understood. To clarify this point, the effects of culture supernatant from human tonsillar cells on the peripheral neutrophil function were investigated. Supernatants from tonsillar cells were incubated in the presence or absence of streptococcal preparation (OK-432) enhanced chemiluminescence, adherence, phagocytosis, chemotaxis, and superoxide production of human peripheral neutrophils. The results suggest that tonsils play an important role in the regulation of neutrophil function.

Bacterial Infections↗

PubMed1994

Neutrophil activating activity of tonsillar cells from patients with tonsillitis.

The previous paper demonstrated that tonsillar cells cultured in vitro in the presence or absence of a streptococcal preparation, OK-432, produce factors that activate various neutrophil functions. In the present study, examination was made of the factor productivity of tonsillar cells from patients with chronic tonsillitis of varying severity, and palmoplantar pustulosis (PPP). Tonsillar cells from patients with severe tonsillitis and PPP incubated with culture medium alone produced a much greater amount of active factors compared with those from patients with mild tonsillitis. When tonsillar cells were incubated in the presence of OK-432, augmentation in factor production by the addition of OK-432 was less in former than latter cases, suggesting that factor production from tonsils correlates with the course of inflammation in this organ.

Adolescent↗

PubMed1993

Modulation of in vivo immune response by selective depletion of neutrophils using a monoclonal antibody, RP-3. I. Inhibition by RP-3 treatment of the priming and effector phases of delayed type hypersensitivity to sheep red blood cells in rats.

Recent studies on neutrophils have revealed that these cells produce various cytokines, and may be involved in regulation of the immune response. We examined whether neutrophils are involved in delayed type hypersensitivity (DTH) to SRBC in rats by selective depletion of in vivo neutrophils using a mAb designated RP-3. When the rats had been treated with RP-3 at the time of priming with SRBC, DTH to these cells was inhibited. Furthermore, RP-3 treatment was effective in inhibiting the effector phase of the DTH response to SRBC. When spleen cells from rats that had been treated with RP-3 at the time of immunization were used for local transfer of DTH, footpad swelling was significantly less than that induced by spleen cells from the RP-3-untreated immune rats.

Animals↗

PubMed1993

Modulation of in vivo immune response by selective depletion of neutrophils using a monoclonal antibody, RP-3. II. Inhibition by RP-3 treatment of mononuclear leukocyte recruitment in delayed-type hypersensitivity to sheep red blood cells in rats.

We demonstrated in our previous paper that treatment of rats with RP-3, a mAb that depletes in vivo neutrophils selectively, resulted in inhibition of both the priming and effector phases of delayed type hypersensitivity (DTH) to SRBC. In order to clarify the mechanisms of this phenomenon, we examined the effect of RP-3 treatment on mononuclear leukocyte (MNL) recruitment in DTH. When rats had been treated with RP-3 at the time of Ag priming, MNL migration, which accompanies DTH, was inhibited. The prior infiltration of neutrophils was also partially required for MNL recruitment because migration was inhibited when the immune rats were treated with RP-3 at the time of DTH elicitation.

Animals↗

PubMed1993

Abrogation of tumor-inhibitory MRC-OX8+ (CD8+) effector T-cell generation in rats by selective depletion of neutrophils in vivo using a monoclonal antibody.

These studies were designed to examine the role of neutrophils in transplantation immunity to syngeneic rat tumors. We have earlier reported that specific transplantation immunity to syngeneic transplanted tumors is abrogated by selective depletion of peripheral-blood neutrophils by administration of a monoclonal antibody (MAb) (RP-3) at the time of immunization with X-irradiated tumor cells. In order to elucidate the mechanisms of this phenomenon, we have now examined whether induction of the sensitized spleen cells that inhibit the growth of tumor cells is inhibited by RP-3 treatment at the time of in vivo priming with tumor-associated antigen (TAA). Neutrophils were required to induce the sensitized T cells responsible for tumor inhibition with Winn's assay. In addition, CD8+ T cells are proved to be effector cells in an assay system of tumor-growth inhibition using a diffusion chamber. Our results indicate that neutrophils are required for priming rats with TAA to induce CD8+ effector T cells in tumor inhibition.

Animals↗

PubMed1993

Inhibition of Corynebacterium parvum-primed and lipopolysaccharide-induced hepatic necrosis in rats by selective depletion of neutrophils using a monoclonal antibody.

To examine whether neutrophils are involved in the pathogenesis of experimental liver dysfunction, we observed the effect of selective in vivo neutrophil depletion by a monoclonal antibody (RP-3) on the pathogenesis of acute experimental hepatic necrosis in rats induced by a preparative injection of heat-killed Corynebacterium parvum and a challenging dose of lipopolysaccharide (LPS) (positive control group). The serum transaminase titer 8 h after LPS injection was reduced by selective depletion of peripheral blood neutrophils as a result of RP-3 treatment (RP-3 group). A kinetic study showed that the serum transaminase titer of the RP-3 group was significantly lower than that of the positive control group from 4 to 24 h after LPS injection. The transaminase level was significantly lower in the group with less than 400/mm3 peripheral blood neutrophils than in the group with a greater number. The effect of RP-3 on the transaminase level was due neither to the injection of cancer ascites nor to RP-3 injection with the accompanying decrease in complement titer. These results suggest that neutrophils play an important role in the induction of liver dysfunction in this system.

Animals↗

PubMed1993

Rapid acceleration of neutrophil apoptosis by tumor necrosis factor-alpha.

We demonstrate here that human necrosis factor-alpha, a potent neutrophil activator, induces rapid (within 3 h) apoptosis of these cells, i.e. neutrophils treated with this cytokine exhibit (i) light and electron microscopic changes characteristic to apoptotic cells, (ii) reduced propidium iodide binding to DNA, and (iii) the ladder form of DNA, as shown by agarose gel electrophoresis. These results suggest that apoptosis acceleration may be involved in processes by which neutrophils are prevented from damaging tissues.

Apoptosis↗

PubMed1993

Immunohistochemical localization of Gnathostoma spinigerum larval antigens by monoclonal antibodies: I. Light microscopy.

Immunohistochemical localization of antigens in advanced third-stage larvae of Gnathostoma spinigerum (GsAL3) was studied by indirect enzyme immunostaining using 7 G. spinigerum specific monoclonal antibodies, FS-3D11, SS-5H5, SK-6C4, SK-4E1, SK-7G6, SD-8D4 and SA-9B5. All these MAb belong to the IgG1 subclass and only FS-3D11 and SS-5H5 recognize carbohydrate determinants. Each MAb exhibited a different reaction pattern and staining intensity in sectioned GsAL3. FS-3D11 bound primarily to the intestinal brush border whereas SS-5H5 reacted with various tissues of the parasite including intestinal epithelium and brush border, lateral cords, muscle, pseudocoel, and cuticle. SK-6C4 predominantly stained muscle, however, SK-4E1 and SK-7G6 exhibited a lack of labeling. SD-8D4 bound to the cuticle and the lateral cords whereas SA-9B5 reacted primarily with the pseudocoel. These results suggest that antigens sharing common epitopes are present in various structures of the larvae with the intestine being the most antigenic site. The present data also suggest that certain GsAL3 antigens recognized by the MAb obtained in this study are sensitive to formalin fixation and/or paraffin embedding since for 2 out of the 7 MAb staining was negative.

Animals↗

PubMed1993

Purification of Gnathostoma spinigerum larval antigens by monoclonal antibody affinity chromatography.

An immunoaffinity column was prepared by coupling a partially purified Gnathostoma spinigerum-specific IgG1, MAb SK-6C4 (5 mg/ml) to CNBr-activated Sepharose 4B. Ten milliliters of approximately 0.3 mg/ml of crude soluble G. spinigerum larval antigens (GsAL3) were loaded onto the affinity column at a flow rate of about 5 ml/hour. Elution of the bound antigens was accomplished using 50 mM diethylamine-HCI containing 0.15 M NaCL, pH 11.5. The average amount of eluted antigens obtained by one passage of crude GsAL3 (1-4 mg) through 4 to 8 ml of column matrix was 143 micrograms (range, 67 - 414 micrograms). The minimal amount of purified GsAL3 detectable by ELISA using MAb SK - 6C4 (100 micrograms/ml) was 50 ng/ml. The SK - 6C4 affinity-purified GsAL3 was found to be relatively pure and immunologically specific as determined by SDS-PAGE and Western blotting, respectively.

Animals↗

PubMed1993

Schistosoma japonicum soluble egg antigens activate naive B cells to produce antibodies: definition of parasite mechanisms of immune deviation.

This study analysed the effect of Schistosoma japonicum egg antigens (SEA) on the activation of lymphocytes from naive mice. T cells were found to be unaffected by SEA. B cells, however, were activated by SEA without participation of adherent cells such as macrophages. B-cell activating factor(s) in SEA were distributed into a fraction of M(r) 120,000 and a fraction of M(r) 650,000 by gel filtration. However, a fraction of M(r) 120,000 demonstrated the presence of a limited number of components by polyacrylamide gel electrophoresis (PAGE) under non-denaturing conditions. These activating factor(s) were destroyed by peroxidase oxidation, heat treatment, chymotrypsin and trypsin digestion. These results indicate that the B-cell activating factor(s) in SEA contain both carbohydrate and protein. IgM antibodies were detected in the culture supernatant of SEA-activated B cells after 48 hr in culture, but IgG antibodies were undetected in culture. These antibodies did not react with SEA but reacted with sheep, horse, mouse red blood cells, carbonic anhydrase and autoantigens in myelinated nerve fibres of cerebrum as well as luminal surface and parietal cells of the stomach of naive mice. Thus our data demonstrated that SEA directly stimulates naive B cells to produce antibodies against heterophile and autologous antigens.

Animals↗

PubMed1992

Correlation between reduction of polymorphonuclear leucocytes in glomeruli injected with a newly developed monoclonal antineutrophil antibody and proteinuria in Masugi nephritis.

The effects of the reduction of neutrophils in glomeruli on the improvement of proteinuria and glomerular injuries were determined in the first (heterologous) phase of Masugi (nephrotoxic) nephritis. Male (6-week-old) WKA/Hkm rats were initially injected with 2.0 ml of a newly developed monoclonal antineutrophil antibody and then injected with 1.0 ml of nephrotoxins. This monoclonal anti-neutrophil antibody was found to have selectively reduced the number of neutrophils in the glomerular capillary lumen in cases of Masugi nephritis by light microscopy. Malondialdehyde (MDA) levels or superoxide dismutase (SOD) activities in renal tissues of such rats were also examined. However, there were no significant differences in the levels of proteinuria and the number of glomerular cells containing resident cells and infiltrated mononuclear cells in the first phase of Masugi nephritis with or without pretreatment with antineutrophil antibody. No significant differences were observed in the levels of MDA or SOD activities in renal tissues of Masugi nephritis with or without pretreatment with such an antibody either. It appeared that infiltration of neutrophils in the glomeruli might not be related to proteinuria and glomerular injuries in the first phase of Masugi nephritis. It was postulated that the massive proteinuria in the first phase of Masugi nephritis might be correlated with the activities of reactive oxygen species induced by the glomerular cells, i.e. glomerular resident cells and infiltrated mononuclear cells.

Animals↗

PubMed1992

Decreased natural killer cell activity in women with endometriosis.

Natural killer (NK) cell activity is characterized by the spontaneous capacity of lymphoid cells derived from nonimmunized hosts to recognize and lyse certain tumor cell lines, virus-infected cells and transplanted tumor cell lines. Endometriosis is characterized by implantation and proliferation of autologous ectopic tissue in the pelvic cavity. Therefore, we focused on examining NK cell activity in women with endometriosis. NK cell activity in peripheral blood from women with endometriosis was lower than in women without endometriosis. On the basis of this finding, we analyzed also the effect of peripheral sera of women with endometriosis on NK cell activity. In the presence of peripheral sera of women with endometriosis, NK cell activity was significantly suppressed as compared with the sera of women without endometriosis. The suppressive effect of sera of women with endometriosis on NK cell activity showed dose-dependent curves. These studies provide the speculation that natural immunity mediated by NK cells may modulate the development of endometrial implants.

Cytotoxicity, Immunologic↗

PubMed1991

Inhibition of IL-8-induced W3/25+ (CD4+) T lymphocyte recruitment into subcutaneous tissues of rats by selective depletion of in vivo neutrophils with a monoclonal antibody.

IL-8 recruits both neutrophils and lymphocytes in vitro and in vivo. To elucidate the mechanisms of lymphocyte recruitment in vivo by IL-8, we examined the role of neutrophil infiltration through selective depletion of circulating neutrophils using a mAb, RP-3. Selective depletion of neutrophils inhibited the IL-8 induced in vivo migration of the W3/25+ (CD4+) T cell subset but did not inhibit that of the MRC-OX8+ (CD8+) subset. These results suggest that CD4+ T cell migration into IL-8-injected s.c. tissues depends on the prior infiltration of neutrophils chemoattracted directly by IL-8.

Animals↗