Release of the chloride-dependent arginine aminopeptidase from PMN leukocytes and macrophaces during phagocytosis

Söderling, Eva; Knuuttila, Matti

doi:10.1016/0024-3205(80)90342-2

Cited by 9 publications

(2 citation statements)

References 19 publications

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“…This metabolite is a potent inhibitor of leucine aminopeptidase and aminopeptidase B of mammalian cells [18,29,30] and immune cells both in vitro [17,19,22,36] and in vivo [15]. Aminopeptidase activity has been associated with macrophage activation and differentiation [21,37], the inflammatory process [20,23,28] and was shown in a cell-free system to correlate *This research was sponsored by the National Cancer Institute, DHHS, under contract no. N01-23910 with Program Resources Inc.…”

Section: Introductionmentioning

confidence: 99%

Chemoimmunotherapy with cyclophosphamide and bestatin in experimental metastasis in mice

Abe

Schneider²,

Black

et al. 1989

Cancer Immunol Immunother

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Bestatin has significant therapeutic activity (even following oral administration) for the treatment of metastatic disease, an activity which is limited by tumor burden. Therefore, the therapeutic potential of bestatin was examined in combination with chemotherapy to determine if there is additive activity for heavy tumor burdens. Bestatin significantly increased therapeutic activity and decreased the myelotoxicity of cyclophosphamide following a single injection of cyclophosphamide or split daily doses. In immune function studies, in tumor-bearing animals, bestatin increased the number of colony-forming units (granulocyte-macrophage) (CFU) and alveolar macrophage tumoricidal activity. However, when bestatin was combined with cyclophosphamide, which depressed bone marrow and macrophage activity, it did not show apparent augmentation of macrophage and NK cell activity, but did significantly increase bone marrow CFU activity. Thus, in combined chemoimmunotherapy, bestatin appears to enhance therapeutic activity by accelerating the recovery of hematopoiesis. We suggest, therefore, that a combination chemotherapy protocol, with oral bestatin, may facilitate myelorestoration following aggressive chemotherapy. The majority of biological response modifiers require parental administration; thus, the identification of an orally active, synthetic immunoaugmenting agent with a defined receptor is of particular interest.

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Section: Introductionmentioning

confidence: 99%

Chemoimmunotherapy with cyclophosphamide and bestatin in experimental metastasis in mice

Abe

Schneider²,

Black

et al. 1989

Cancer Immunol Immunother

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“…These cells have a putative role in protecting the host from periodontal pathogens (Attstrom 1971, Cainciola, Genco & Patters 1977, Page & Schroeder 1981, Wilton 1982. Kenney, Saxe & Bowles (1972) and Knuutilla & Soderling (1981) have reported that chlorhexidine causes membrane damage to neutrophils and macrophages with release of intracellular enzymes (Soderling & Knuutilla 1980). On the other hand, Davies et al (1954) were unable to show any effect of a 0.01%…”

Section: Introductionmentioning

confidence: 99%

The effect of chlorhexidine on blood cells

Gabler

Roberts

Harold

1987

J of Periodontal Research

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Chlorhexidine was cytotoxic to both neutrophils and red blood cells over a narrow concentration range of 0.01 to 0.02% drug. Serum provided significant protection against the cytotoxic effects of the antimicrobial agent. At a concentration of 0.01%, chlorhexidine acted as a potent activator of the neutrophil's oxidative burst, stimulating the cells to produce oxygen radicals such as superoxide (O2). Chlorhexidine ranging from 10 ' to 10~-caused spontaneous degranulation of neutrophils. If neutrophils were pretreated with chlorhexidine and then activated by the chemoattractant tripeptide FMLP, chlorhexidine inhibited the induced O2 generation and degranulation. If, on the other hand, neutrophils were activated with phorbol myristate acetate (PMA) following chlorhexidine treatment, the antimicrobial agent enhanced both 02~ synthesis and degranulation. It appears that the responsiveness of chlorhexidine-treated neutrophils to subsequent activators is dependent upon the nature of the activator.

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Substrate specificities of Cl−-activated arginine aminopeptidases from human and rat origin

Söderling¹

1983

Archives of Biochemistry and Biophysics

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Release of the chloride-dependent arginine aminopeptidase from PMN leukocytes and macrophaces during phagocytosis

Cited by 9 publications

References 19 publications

Chemoimmunotherapy with cyclophosphamide and bestatin in experimental metastasis in mice

Chemoimmunotherapy with cyclophosphamide and bestatin in experimental metastasis in mice

The effect of chlorhexidine on blood cells

Substrate specificities of Cl−-activated arginine aminopeptidases from human and rat origin

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