Biomedical subjects

E Shezen

Publications and source records attributed to E Shezen.

25 records · Page 2Linked to original sources

PubMed1986

1 alpha, 25-Dihydroxyvitamin D3 augments clonal growth of macrophages from rat bone marrow progenitor cells and modulates their function.

1 alpha, 25-Dihydroxyvitamin D3 (1,25(OH)2D3) was shown to enhance (approximately 2 fold) the colony-stimulating factor-dependent clonal growth of macrophage colonies and clusters from rat bone marrow progenitor cells. The proliferative capacity of macrophage progenitors in liquid cultures was likewise augmented (2-3 fold). Mononuclear phagocytes (macrophages, for simplicity) developing in the presence of 1,25(OH)2D3 showed a reduced capacity of migration. 1,25(OH)2D3 administered at bone marrow culture initiation led to augmentation of the phagocytic capability of macrophages in four-day cultures and to its suppression in macrophages in seven-day cultures. The observed patterns of modulation of differentiation and function by 1,25(OH)2D3 differ from the patterns we found for mouse bone marrow cells. The results suggest that the differential response to hormones observed in different species may include responses to 1,25(OH)2D3.

Animals↗

PubMed1985

Opposing effects of dexamethasone on the clonal growth of granulocyte and macrophage progenitor cells and on the phagocytic capability of mononuclear phagocytes at different stages of differentiation.

Dexamethasone, a synthetic glucocorticosteroid, was shown to modulate the colony-stimulating factor-dependent clonal growth of myeloid progenitor cells in semisolid agar cultures, enhancing the formation of granulocyte colonies (50-100%) and suppressing the formation of macrophage colonies (75-97%). Modulation of the pattern of myeloid colony formation by dexamethasone (12-125 nM) was brought about when the steroid was administered to 6-day cultures at the time of culture initiation and up to 72 hr later. Dexamethasone inhibited myeloid cell proliferation when administered to 5-day liquid cultures at culture initiation and up to 96 hr later. Dexamethasone (12-250 nM) also enhanced the phagocytic activity of bone marrow-derived mononuclear phagocytes toward heat-killed (HK) yeast cells (up to 100%) and IgG-coated sheep red blood cells (up to 60%). Enhancement of the phagocytic capability depended critically on the stage in culture at which dexamethasone was administered. Exposure to dexamethasone for 28 hr up to 96 hr of 96-hr cultures of bone marrow cells did not lead to a modulation of phagocytic activity of the developing mononuclear phagocytes. The presence of dexamethasone during the critical period of 96 hr to 120 hr after culture initiation led to an enhanced phagocytic capability, which was statistically significant already 12 hr after the administration of the glucocorticoid. Dexamethasone induced an enhanced phagocytic activity when administered at any time after culture initiation provided that it was in culture during this critical period. When added at 120 hr of culture, dexamethasone no longer enhanced the phagocytic capability of mononuclear phagocytes and when added later than 156 hr of culture suppressed it. Dexamethasone also suppressed (up to 68%) the phagocytic capability of resident and elicited peritoneal macrophages. The results suggest that glucocorticoids shift the balance of granulocyte vs. macrophage formation at early stages of precursor cell differentiation. Reduction in mononuclear phagocyte growth and enhancement of its phagocytic capability might reflect accelerated differentiation/maturation steps. The inhibitory effect of dexamethasone on macrophage formation and on the phagocytic capability of mature mononuclear phagocytes and peritoneal macrophages might be a relevant aspect of the in vivo immune suppression encountered after glucocorticoid administration.

Animals↗

PubMed1985

1,25-Dihydroxyvitamin D3 and the regulation of the differentiation and function of macrophages and granulocytes.

1,25-Dihydroxyvitamin D3 (1,25(OH)2D3) exerts a differential inhibitory effect on the formation of granulocyte, granulocyte/macrophage, and macrophage colonies grown from mouse bone marrow precursor cells; 50% inhibition was attained at 1.1, 2.3, and 23 nM 1,25(OH)2D3, respectively. The inhibition of colony formation, as well as phagocyte proliferation in liquid cultures, requires the presence of 1,25(OH)2D3 in the early stages of culture (up to 72 h after culture initiation). 1,25(OH)2D3 induces a dose- and time-dependent augmentation of the phagocytic capability of mononuclear phagocytes (up to 100%) towards both heat-killed yeast cells and IgG-coated sheep red blood cells. The augmentation of the phagocytic capability of the mononuclear phagocytes depends critically on when 1,25(OH)2D3 is added. It is effective when added up to 72 h after culture initiation, while at later stages (greater than or equal to 96 h) the cells are no longer induced to express enhanced phagocytic capability. We suggest that these phenomena may be relevant to hemopoietic processes.

Animals↗

PubMed1982

Enhancement of phagocytosis by neurotensin, a newly found biological activity of the neuropeptide.

Specific binding of neurotensin (NT) to mouse peritoneal thioglycollate-elicited macrophages and macrophages differentiated in vitro from bone marrow cells was demonstrated and characterized. NT binding to these phagocytes modulated their phagocytic capacity in a biphasic manner. At concentrations of 10(-14) to 10(-9) M NT, a dose-dependent augmentation of phagocytosis (up to 2-fold) was observed. Further increases in the concentration of NT resulted in a gradual decrease of the augmented response until the basal phagocytic activity (in the absence of NT) was reached. Three partial sequences of NT, NT (8-13), NT (6-13) and NT (1-10), were also effective in augmenting the phagocytic response of thioglycollate elicited macrophages, but the maximal effect was attained at about 10(-7) M and stayed at that level up to a concentration of 10(-5) M. The activity of the three NT partial sequences was comparable to that of substance P and tuftsin. Scatchard analysis of (3H)NT binding to macrophages suggested the existence of two populations of binding sites, a major population of relatively low affinity binding sites and a small population of high affinity binding sites. NT (8-13), NT (6-13), substance P and tuftsin competed with (3H)NT binding to the low affinity sites with a comparable KI to that of NT. NT (1-10) did not compete for the binding at the low affinity sites. It is suggested that NT binding to the high affinity sites leads to enhancement of phagocytosis, whereas its binding to the low affinity sites leads to inhibition of the augmented response. However, the low affinity sites are the sites of interaction of NT (8-13), NT (6-13), substance P and tuftsin with the phagocytes and their saturation with the peptides leads to augmentation of phagocytosis.

Amino Acid Sequence↗

PubMed1981

Combined treatment of Lewis lung carcinoma by tumor excision and levan.

A combined treatment modality including surgical excision and daily injections of high molecular levan seemed to be effective against Lewis lung carcinoma in C57BL mice. The inhibitory effect of levan on tumor growth in mice treated by resection of the primary tumor was demonstrated as follows: (1) recurrence of primary tumors was less in levan-treated mice compared to untreated animals; (2) metastases were less numerous in the levan-treated animals; (3) levan treatment partly prevented loss in body weight, and (4) it increased the survival rate. Recurrence of primary tumors appeared to be more efficiently inhibited by local levan treatment, while systemic (i.p.) administration was more effective than local treatment in preventing metastases. The mechanism of inhibition of tumor growth was related to accumulation of macrophages around the metastases.

Animals↗

PubMed1978

Modification of the tuberculin reaction by levan.

High molecular levan (polyfructoside) inhibits the skin tuberculin reaction in guinea pigs as judged by the degree of induration and erythema. The effect is dose-dependent. No effect on cellular infiltration was observed in histological studies. The lymph nodes of levan-treated animals were smaller and exhibited a much milder granulomatous reaction than those of non-treated animals.

Animals↗

PubMedDate not supplied

YAC-Lymphoma bearing induces functional changes in bone marrow derived mononuclear phagocytes.

Bone marrow derived mononuclear phagocytes (BMDMP) differentiated in vitro from bone marrows of YAC-lymphoma bearing mice and Corynebacterium parvum (CP)-inflamed mice shown to differ in several functional parameters from those derived from bone marrows of control mice. The former 2 BMDMP populations expressed: (a) an increased level of acid phosphatase activity; (b) an increased degree of zymosan-induced chemiluminescence reaction; (c) a lower sensitivity of the proliferative capacity to prostaglandin E2 (PGE2), as compared to the BMDMP population from normal mice. These data suggest that YAC-lymphoma bearing in A/J mice induces similarly to inflammatory stimuli changes in the functional capacity of bone marrow mononuclear phagocyte precursor cells.

Acid Phosphatase↗