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At least 415 records · Page 23Linked to original sources
PubMed1989

Leukocytosis in mice following therapy with a novel antitumor agent, RA-700.

Nine daily intravenous (iv) injections of RA-700 (an antitumor cyclic hexapeptide) at doses of 2 to 6 mg/kg/day caused increases of WBC counts at 4-6 days after treatment in normal C57BL/6 X DBA/2 (BDF1) mice. The percentages of neutrophils and lymphocytes were modified. There was a decrease of colony-forming units in culture (CFUc) in bone marrow to 40% of the control value on day 1 but CFUc rapidly returned to normal values on day 3. The colony-forming units in spleen (CFUs) in bone marrow decreased during treatment. On the other hand, CFUc and CFUs in spleen were increased from the initiation of treatment to the time prior to the increase of WBC count. Spleen weight increased after treatment, and histologically, increases of immature and also mature granulocytes and megakaryocytes were observed. However, RA-700 did not stimulate the progress of hematoprogenitors in vitro. The results indicated that RA-700 stimulates the progress of hematoprogenitors in the spleen, but this effect is probably indirect.

Animals↗
PubMed2005

Short term changes in lung function, leukocytosis in blood, and lachrymal fluid among bacterial single cell protein workers after an episode with high exposure to endotoxins.

AIMS: To study possible effects of endotoxin exposure among bacterial single cell protein workers on pulmonary function, blood parameters, and lachrymal fluid before and after a work shift. METHODS: The study included 23 men and five women who were examined at the start and at the end of a work shift. Most workers performed a task with unusually high exposure levels. Twelve of the workers were re-examined the day after. The workers were divided into three exposure groups: production workers with the highest assumed exposure levels (n = 18), engineers (n = 5), and clerks (n = 2). The median endotoxin level during a work shift was 34000 EU/m3 in the high exposure group (range 3300-89000 EU/m3 ), 11000 EU/m3 (range 350-27000 EU/m3) among the engineers, and 180 EU/m3 (range 60-300 EU/m3) for the clerks. The workers answered a questionnaire about work related symptoms. Assessment of lung function included dynamic lung volumes and flows. The blood analysis included cell count of leukocytes and mediators of inflammation, fibrinogen, interleukin-6 (IL-6), D-dimer, and C-reactive protein (CRP). Cells in lachrymal fluid were counted with a microscope. RESULTS: The forced vital capacity (FVC) changed significantly (p<0.05) from 5.34 l (SD 0.9) to 5.25 l (SD 0.9) and forced expired volume in one second (FEV1) from 4.15 l (SD 0.7) to 4.07 l (SD 0.7) during the work shift. The leukocytes increased significantly (p<0.05) from 6.9 10(9)/l (SD 1.2) to 7.7 10(9)/l (SD 1.5) and IL-6 from 1.5 ng/l (SD 0.6) to 3.31 ng/l (SD 2.7). Except for fibrinogen, which had a borderline increase and PEF that decreased, the parameters were normalised the day after. Four of the workers had an increase of neutrofile granulocytes in the lachrymal fluid during the shift. There was a significant association between the endotoxin concentration and decrease of FEV1 despite the use of powered respirators. CONCLUSIONS: During a work shift with unusual high levels of endotoxins at a plant manufacturing bacterial single cell protein the results show that FVC and FEV1 were reduced. Mediators of inflammation increased along with leucocytosis in blood and lachrymal fluid among the workers.

Adult↗
PubMed1980

Bronchoscopy and lung lavage induced bilateral pulmonary neutrophil influx and blood leukocytosis in dogs and monkeys.

Investigators have previously determined that repetitive lung washes attract neutrophils to the lungs. They ascribed this attraction to the release of chemotactic factors. Our studies demonstrate that lavage of one lobe of a lung attracts neutrophhils to unwashed lobes as well; therefore, the attraction of neutrophils cannot be entirely due to the local release of chemotactic agents. Further experiments showed that influx of neutrophils also occurred after bronchoscopy without lung lavage but not after the anesthesia alone. These studies suggest that the lungs have mechanisms that regulate and control neutrophil influx both locally and contralaterally. It is not yet clear whether the controlling mechanisms represent an integrated system in the control of leukocyte traffic through the lungs. In addition, lung lavage and bronchoscopy without lung lavage cause an increase in the blood leukocyte count, with an increase in the number of young neutrophil forms. Lung wash concentrates cause a dramatic increase in the number of blood leukocytes when instilled into a bronchus. These data indicate that lungs contain a material that can stimulate the bone marrow to release leukocytes from its reserves.

Anesthesia↗
PubMed1975

Comparison of agents producing a neutrophilic leukocytosis in man. Hydrocortisone, prednisone, endotoxin, and etiocholanolone.

To study the potential application of glucocorticosteroid administration for the measurement of the bone marrow neutrophil reserve response, blood neutrophil count changes were measured in normal subjects after the administration of intravenous hydrocortisone (25, 50, 100, 200, and 400 mg) and oral prednisone (5, 10, 20, 40, and 80 mg). The upper three doses of both steroids increased the blood neutrophil count by approximately 4,000 cells/mm3. The neutrophilia occurring after hydrocortisone (200 mg) and/or prednisone (40 mg) was compared with that observed after endotoxin (0.8 ng/kg) and etiocholanolone (0.1 mg/kg) in 14 normal subjects, 7 patients with Wegener's granulomatosis on cyclophosphamide therapy and 10 patients with chronic idiopathic neutropenia. The normal responses (mean increase of blood neutrophils/mm3 above base line +/- 1 SEM) were: hydrocortisone 4,220 +/- 320, prednisone 4,610 +/- 360, endotoxin 6,060 +/- 880, and etiocholanolone 3,780 +/- 440. In the patient studies, etiocholanolone gave the smallest mean responses, but, in general, the results were similar for all agents. These data indicate that these glucocorticosteroids can be used as equivalent agents to endotoxin and etiocholanolone for measuring the neutrophil reserve response.

Adult↗
PubMed2003

Myeloproliferative disease in transgenic mice expressing P230 Bcr/Abl: longer disease latency, thrombocytosis, and mild leukocytosis.

P230 Bcr/Abl has been associated with indolent myeloproliferative disease (MPD). We generated transgenic mice expressing P230Bcr/Abl driven by the promoter of the long terminal repeat of the murine stem cell virus of the MSCV neo P230 BCR/ABL vector. Two founder mice exhibited mild granulocytosis and marked thrombocytosis and developed MPD. The disease of one founder mouse, no. 13, progressed to extramedullary myeloblastic crisis in the liver at 12 months old. The other founder mouse, no. 22, was found to have chronic-phase MPD with large populations of megakaryocytes and granulocytes in an enlarged spleen. The transgenic progeny of no. 22 clearly exhibited MPD at 15 months old. These results showed that P230Bcr/Abl had leukemogenic properties and induced MPD. The phenotype of the MPD caused by P230Bcr/Abl was characterized by mild granulocytosis, a high platelet count, infiltration of megakaryocytes in some organs, and a longer disease latency compared with the MPD caused by P210Bcr/Abl.

Animals↗
PubMed2004

Anemia, thrombocytopenia, leukocytosis, extramedullary hematopoiesis, and impaired progenitor function in Pten+/-SHIP-/- mice: a novel model of myelodysplasia.

The myeloproliferative disorder of mice lacking the Src homology 2 (SH2)-containing 5' phosphoinositol phosphatase, SHIP, underscores the need for closely regulating phosphatidylinositol 3-kinase (PI3K) pathway activity, and hence levels of phosphatidylinositol species during hematopoiesis. The role of the 3' phosphoinositol phosphatase Pten in this process is less clear, as its absence leads to embryonic lethality. Despite Pten heterozygosity being associated with a lymphoproliferative disorder, we found no evidence of a hematopoietic defect in Pten(+/-) mice. Since SHIP shares the same substrate (PIP(3)) with Pten, we hypothesized that the former might compensate for Pten haploinsufficiency in the marrow. Thus, we examined the effect of Pten heterozygosity in SHIP(-/-) mice, predicting that further dysregulation of PIP(3) metabolism would exacerbate the pheno-type of the latter. Indeed, compared with SHIP(-/-) mice, Pten(+/-)SHIP(-/-) animals developed a myelodysplastic phenotype characterized by increased hepatosplenomegaly, extramedullary hematopoiesis, anemia, and thrombocytopenia. Consistent with a marrow defect, clonogenic assays demonstrated reductions in committed myeloid and megakaryocytic progenitors in these animals. Providing further evidence of a Pten(+/-)SHIP(-/-) progenitor abnormality, reconstitution of irradiated mice with marrows from these mice led to a marked defect in short-term repopulation of peripheral blood by donor cells. These studies suggest that the regulation of the levels and/or ratios of PI3K-derived phosphoinositol species by these 2 phosphatases is critical to normal hematopoiesis.

Anemia↗