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Biomedical subjects

I Iwamoto

Publications and source records attributed to I Iwamoto.

At least 127 records · Page 7Linked to original sources
PubMed1993

Interferon gamma regulates antigen-induced eosinophil recruitment into the mouse airways by inhibiting the infiltration of CD4+ T cells.

We have previously shown that antigen-induced eosinophil recruitment into the tissue of sensitized mice is mediated by CD4+ T cells and interleukin 5. To determine whether interferon gamma (IFN-gamma) regulates antigen-induced eosinophil recruitment into the tissue, we studied the effect of recombinant (r) murine IFN-gamma and of anti-IFN-gamma monoclonal antibody (mAb) on the eosinophil infiltration of the trachea induced by antigen inhalation in mice. The intraperitoneal administration of rIFN-gamma prevented antigen-induced eosinophil infiltration in the trachea of sensitized mice. The administration of rIFN-gamma also decreased antigen-induced CD4+ T cell but not CD8+ T cell infiltration in the trachea. On the other hand, pretreatment with anti-IFN-gamma mAb enhanced antigen-induced eosinophil and CD4+ T cell infiltration in the trachea. These results indicate that IFN-gamma regulates antigen-induced eosinophil recruitment into the tissue by inhibiting CD4+ T cell infiltration.

Animals↗
PubMed1993

Right common iliac arterio-intestinal fistula caused by tubercular peritonitis: report of a case.

A 59-year-old female was admitted with massive hematemesis and melena. A hematological examination revealed that the red blood cell count was 1.31 x 10(6)/mm3, Hb 3.4 g/dl, and Hct 12%. No source of bleeding was found by an emergency endoscopic examination of the esophagus, stomach and duodenum, or by superior mesenteric angiography. At laparotomy a right common iliac arterio-intestinal fistula was found. The microscopic examination of this part of the ileum, including the fistula, revealed the presence of tubercular peritonitis. An extra-anatomic bypass graft using a prosthetic graft was performed between the left and right femoral arteries because reconstruction of the right common iliac artery was impossible.

Blood Vessel Prosthesis↗
PubMed1993

In vitro interleukin-5 production of peripheral blood mononuclear cells is increased in patients with asthma.

To determine whether the capacity of interleukin-5 (IL-5) production is increased in patients with asthma, we studied in vitro IL-5 production from peripheral blood mononuclear cells (PBMC) in 27 asthmatics (16 allergic asthmatics and 11 nonallergic asthmatics) and 10 normal subjects. IL-5 production of phytohemagglutinin (PHA)-stimulated PBMC was significantly greater in asthmatics than in normal subjects (p < 0.02). IL-5 production of PBMC by IL-2 stimulation was also significantly increased in asthmatics compared with that of normal subjects (p < 0.05). In contrast, IL-2 production of PHA-stimulated PBMC did not significantly differ between asthmatics and normal subjects. In addition, the number of CD4+ and CD8+ T cells in PBMC or CD4+/CD8+ ratio did not significantly differ between asthmatics and normal subjects, whereas CD25+ T cells were significantly increased in asthmatics compared with those of normal subjects (p < 0.02). Finally, there was no significant correlation between the in vitro IL-5 production of PBMC and blood eosinophil counts in asthmatics and normal subjects. Our results indicate that the capacity of IL-5 production, but not of IL-2 production, is increased in asthmatics. The increased capacity of IL-5 production might be involved in the migration and activation of eosinophils in the airways of asthmatics.

Adolescent↗
PubMed1993

Aerosolized recombinant interferon-gamma prevents antigen-induced eosinophil recruitment in mouse trachea.

In a murine model of airway late-phase reaction we have previously shown that antigen-induced eosinophil recruitment into the airways of sensitized mice is mediated by CD4+ T cells and interleukin-5. To determine whether interferon-gamma (IFN-gamma) regulates antigen-induced eosinophil recruitment into the airways, we studied the effect of aerosolized recombinant murine IFN-gamma on the eosinophil infiltration of the trachea induced by antigen inhalation in mice. The administration of aerosolized rIFN-gamma prevented antigen-induced eosinophil infiltration in the trachea of sensitized mice. The administration of aerosolized rIFN-gamma also decreased antigen-induced CD4+ but not CD8+ T-cell infiltration in the trachea. However, there were no significant changes in the number of blood eosinophils or of splenic CD4+ and CD8+ T cells in the treatment with rIFN-gamma. These results indicate that locally administered IFN-gamma prevents antigen-induced eosinophil recruitment into the airways by inhibiting CD4+ T cell infiltration.

Administration, Inhalation↗
PubMed1993

Experimental toxoplasmosis in pregnant cats.

Cysts of the K strain of Toxoplasma gondii were administered orally to nine pregnant cats having no antibody to the organism at each of the three stages of gestation, namely early (14 days), middle (30 days), and late (40 and 51 days). Premature and weak or deformed fetuses were observed in the offsprings delivered by mother cats infected with Toxoplasma in the early or middle stage of gestation, while the cats infected at the late stage were delivered of apparently healthy fetuses. Mother cats developed parasitemia excreting Toxoplasma oocysts in their feces and formed the antibody to the organism after the oral administration. Toxoplasma was recovered from the organs or tissues of all fetuses delivered by the mother cats infected in the early stage of gestation. All kittens born healthy from the cats infected in the middle stage of gestation were free from Toxoplasma, but 80% of the premature kittens were found to be infected. Toxoplasma was isolated also from the organs of about half the offsprings born healthy from the mother cats infected in the late stage of gestation. These results indicate that congenital infection with Toxoplasma may occur commonly and cause damage to the fetuses when pregnant cats are infected orally with Toxoplasma cysts in the early or middle stage of gestation.

Animals↗
PubMed1993

[Effect of cytokines on eosinophil differentiation and proliferation].

IL-3, IL-5, and GM-CSF are eosinopoietic cytokines that induce the proliferation and differentiation of eosinophils. However, the regulatory mechanism of eosinopoiesis is largely unknown. A combination of IL-3 and IL-5 induces selective proliferation and differentiation of eosinophils from mononuclear cell fractions of human cord blood. IFN-gamma decreases the IL-3- and IL-5-induced eosinophil differentiation in a dose-dependent manner. IL-4 and IL-2 also decrease the IL-3- and IL-5-induced eosinophil differentiation. These observations indicate that IL-2, IL-4, and IFN-gamma have a direct or indirect inhibitory effect on eosinopoiesis.

Cell Differentiation↗
PubMed1993

[Episodic angioedema with eosinophilia].

In 1984, Gleich et al. originally reported a novel syndrome of episodic angioedema with eosinophilia. The syndrome is characterized by recurrent angioedema, urticaria, weight gain, elevated IgM levels, marked blood eosinophilia, and eosinophil infiltrates in the dermis. It has also been observed that activated CD4+ T cells are present in the dermis of patients with this syndrome, suggesting that T cell-derived cytokines especially IL-5 might be involved in the migration and activation of eosinophils in the skin. Indeed, it has recently been reported that serum IL-5 levels elevate during clinical exacerbation of this syndrome. However, it still remains to be elucidated what antigen periodically activates CD4+ T cells, what factor(s) determine selective migration of eosinophils into the skin, and so on.

Angioedema↗
PubMed1992

The development of hypercalcemia in a patient with an ovarian tumor producing parathyroid hormone-related protein.

Hypercalcemia developed in a 34-year-old woman with a clear cell carcinoma of the ovary. Osseous involvement with the tumor cells was not present. Primary hyperparathyroidism was absent. Operative partial resection of the metastatic supraclavicular lymph node, followed by radiation therapy, decreased her serum calcium concentrations. This case belongs to the category of humoral hypercalcemia of malignancy (HHM). Detection of a significant quantity of immunoreactive parathyroid hormone-related protein (PTH-rP) in the metastatic lymph node suggested that the HHM of the patient was induced by PTH-rP produced by the tumor. From a review of 17 cases of ovarian tumors showing HHM-like morbidity, it was found that clear cell carcinoma and cystadenocarcinoma were the major types of ovarian tumors associated with HHM.

Adenocarcinoma↗
PubMed1992

Role of CD4+ T lymphocytes and interleukin-5 in antigen-induced eosinophil recruitment into the site of cutaneous late-phase reaction in mice.

Previous studies suggested that the eosinophil recruitment into the site of cutaneous late-phase reaction (LPR) was dependent on IgE antibody and mast cells. In this study, we determined the role of CD4+ T cells and CD8+ T cells in causing antigen-induced eosinophil recruitment of LPR in mouse skin. Eosinophil infiltration into the subcutaneous tissue of ovalbumin (OVA)-sensitized BALB/c mice was biphasic, reaching the first peak at 6 h after the subcutaneous challenge with OVA and the second peak at 24 to 48 h. The in vivo depletion of CD4+ T cells by pretreatment with anti-L3T4 monoclonal antibody (mAb) significantly decreased the second peak (at 24 h and 48 h), but not the first peak (at 6 h), of OVA-induced eosinophil infiltration into the skin of OVA-sensitized mice. However, the depletion of CD8+ T cells by pretreatment with anti-Lyt-2 mAb had no significant effect on either the first peak or second peak of OVA-induced cutaneous eosinophilia. Pretreatment with anti-murine interleukin-5 (IL-5) mAb also decreased the second peak, but not the first peak, of OVA-induced cutaneous eosinophilia. In contrast to the inhibitory effects of depletion of CD4+ T cells and of anti-IL-5 mAb on the second peak of antigen-induced cutaneous eosinophilia, disodium cromoglycate and a selective antagonist for platelet activating factor (PAF) CV-6209 decreased the first peak of OVA-induced cutaneous eosinophilia in the mouse. These results indicate that CD4+ T cells, but not CD8+ T cells, cause the second peak of antigen-induced eosinophil recruitment of cutaneous LPR and that IL-5 mediates this eosinophil recruitment. In contrast, the first peak of antigen-induced eosinophil recruitment of cutaneous LPR is mediated by mast cells and PAF.

Animals↗
PubMed1992

Substance P-induced granulocyte infiltration in mouse skin: the mast cell-dependent granulocyte infiltration by the N-terminal peptide is enhanced by the activation of vascular endothelial cells by the C-terminal peptide.

Previous studies have shown that substance P induces granulocyte infiltration in mouse skin, which is mediated through mast cell degranulation. However, it is not yet known whether the direct effect of substance P on vascular endothelial cells is involved in the granulocyte infiltration in the skin. To solve this issue, we used the N-terminal peptide substance P1-9 (SP1-9), which is active for mast cells but inactive for vascular endothelial cells, and the C-terminal peptide SP6-11, which is active for vascular endothelial cells but inactive for mast cells, since substance P activates both mast cells and vascular endothelial cells. The subcutaneous administration of substance P (10(-7)-10(-5)M) caused granulocyte (neutrophil and eosinophil) infiltration in the skin of BALB/c mice 6 h after the injection. SP1-9 (10(-5)-10(-4) M) also caused granulocyte infiltration of mouse skin which was associated with mast cell degranulation. In contrast, SP6-11 (10(-7)-10(-4) M), which was found to increase the vascular permeability of endothelial cells in mouse skin, induced no significant granulocyte infiltration nor mast cell degranulation. However, SP6-11 (10(-5)-10(-4) M) enhanced SP1-9-induced granulocyte infiltration in the skin without any significant increase in mast cell degranulation. We conclude that substance P causes granulocyte infiltration in mouse skin through both mast cell degranulation induced by the N-terminal peptide of substance P and the activation of vascular endothelial cells induced by the C-terminal peptide of substance P.

Animals↗
PubMed1992

Comparison of substance P-induced and compound 48/80-induced neutrophil infiltrations in mouse skin.

It has recently been shown that substance P induces neutrophil infiltration in the skin, which is mediated through mast cell degranulation. Since substance P activates both skin mast cells and vascular endothelial cells, we compared the potencies of substance P and a mast cell-degranulating agent, compound 48/80, which is inactive for vascular endothelial cells, in inducing neutrophil infiltration in mouse skin. We also examined the effect of the C-terminal peptide of substance P, SP6-11, which is active for vascular endothelial cells, on compound 48/80-induced neutrophil infiltration in the skin. Subcutaneous administrations of substance P (10(-7) to 10(-5) M; 0.1 ml) and compound 48/80 (0.5-50 micrograms/ml) induced neutrophil infiltrations and mast cell degranulations in mouse skin in a concentration-dependent fashion. Moreover, substance P induced more neutrophil infiltrations than compound 48/80 in terms of the magnitude of mast cell degranulations. SP6-11 (10(-6) to 10(-4) M) induced no significant neutrophil infiltration or mast cell degranulation, but increased the vascular permeability of endothelial cells in the skin. Furthermore, SP6-11 enhanced compound 48/80-induced neutrophil infiltration without any increase in mast cell degranulation. Our results indicate that, in addition to mast cell degranulation, the activation of vascular endothelial cells is involved in substance P-induced neutrophil infiltration in the skin.

Analysis of Variance↗
PubMed1992

CD4+ T-lymphocytes and interleukin-5 mediate antigen-induced eosinophil infiltration into the mouse trachea.

In order to determine the role of CD4+ and CD8+ T-cells and of interleukin-5 (IL-5) in causing antigen-induced eosinophil infiltration into the site of airway late-phase reaction, we examined the effect of the in vivo depletion of CD4+ and CD8+ T-cells on the eosinophil infiltration of the trachea induced by antigen inhalation in mice. We also studied the effect of anti-murine IL-5 monoclonal antibody (mAb) on the antigen-induced eosinophil infiltration in the trachea. The eosinophil infiltration into the trachea of ovalbumin (OVA)-sensitized BALB/c mice began to increase 9 h after OVA inhalation and persisted for more than 48 h. The in vivo depletion of CD4+ T-cells by pretreatment with anti-L3T4 mAb significantly decreased the eosinophil infiltration induced by OVA inhalation in the trachea of sensitized mice. However, the in vivo depletion of CD8+ T-cells by pretreatment with anti-Lyt-2 mAb had no significant effect on OVA-induced eosinophil infiltration in the trachea. Pretreatment with anti-murine IL-5 mAb also decreased OVA-induced eosinophil infiltration in the trachea. In contrast, neither disodium cromoglycate nor a selective antagonist for platelet-activating factor CV-6209 decreased OVA-induced airway eosinophilia in the mouse. Our results provide direct evidence that CD4+ but not CD8+ T-cells mediate antigen-induced eosinophil recruitment in the airways and that IL-5 mediates this eosinophil recruitment.

Administration, Inhalation↗
PubMed1992

[Effect of a leukotriene B4 antagonist on substance P-induced granulocyte infiltration in mouse skin].

Substance P causes granulocyte (neutrophil and eosinophil) infiltration in mouse skin by inducing mast cell degranulation. However, the mediator responsible for this granulocyte infiltration has not been determined. In this study, we examined the effect of a leukotriene B4 (LTB4) antagonist ONO-4057 on substance P-induced granulocyte infiltration in the skin of BALB/c mice. Pretreatment with the LTB4 antagonist decreased substance P-induced neutrophil and eosinophil infiltrations in mouse skin at 6 h to the same extent that an inhibitor of mast cell degranulation disodium cromoglycate decreased those responses. The LTB4 antagonist also decreased substance P-induced neutrophil, but not eosinophil, infiltration in mouse skin at 24 h. We conclude that LTB4 is a major mast cell-derived chemotactic mediator for initiating substance P-induced neutrophil and eosinophil infiltrations in mouse skin.

Animals↗
PubMed1992

[Effects of growth factors on proliferation of cultured human peritoneal mesothelial cells].

Loss of ultrafiltration during continuous ambulatory peritoneal dialysis (CAPD) is often caused by the structural peritoneal membrane alteration, namely the disappearance of mesothelial cells and the proliferation of peritoneal collagen fibers. The interleukin hypothesis has been proposed to explain the etiology of peritoneal fibrosis. The CAPD procedure has been shown to induce macrophages and lymphocytes in the peritoneum, resulting in the production of interleukin-1 (IL-1) and interferon-gamma (IFN-gamma), which may be promote to the development of peritoneal fibrosis. On the other hand, the mesothelial defect can be rapidly restored by proliferation of mesothelial cells implanted on the wound surface. In this study, we demonstrated that IL-1 beta, IFN-gamma, epidermal growth factor (EGF) and platelet derived growth factor (PDGF) enhance to the growth of cultured human peritoneal mesothelial (CHPM) cells. The cell cultures were derived from surgically removed omentum using the enzymatic disaggregation method. CHPM cells were cultured with Ham's F-12 medium containing 10% FCS up to third generation. At a concentration of 1x10(4) cells/well were cultured with various concentrations of IL-1 beta, IFN-gamma, EGF, PDGF and IL-6. [3H] TdR (37MBq/well) was added to the cultures during the last 12hr of the 48hr culture period and then radioactivity was measured to determine the uptake of [3H] TdR. It was shown that IL-1 beta, IFN-gamma, EGF and PDGF induced the proliferation of CHPM cells in a dose dependent manner when cultured in medium containing 3% FCS.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Division↗