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Eosinophils peripheral blood

Melani, C., Mattia, G.F., Silvani, A., Care, A., Rivoltini, L., Parmiani, G. and Colombo, M.P. (1993). Interleukin-6 expression in human neutrophil and eosinophil peripheral blood granulocytes. Blood 81, 2744-2749. [Pg.96]

Liu LY, Jarjour NN, Busse WW, Kelly EA. Chemokine receptor expression on human eosinophils from peripheral blood and bronchoalveolar lavage fluid after segmental antigen challenge. J Allergy Clin Immunol 2003 112(3) 556-562. [Pg.252]

Microscopic examination of nasal scrapings typically reveals numerous eosinophils. The peripheral blood eosinophil count may be elevated, but it is nonspecific and has limited usefulness. [Pg.911]

Hematology. Hemacytometers or electronic cell counters can be used to assess the numbers of lymphocytes, neutrophils, monocytes, basophils, and eosinophils in the peripheral blood, while changes in relative ratios of the various cell types can be assessed by microscopic differential evaluation. Similar evaluations can be... [Pg.560]

Ohkawara Y, Lim KG, Glibetic M, Nakano K, Dolovich J, Croitoru K, et al CD40 expression by human peripheral blood eosinophils. J Clin Invest 1996 97 1761-1766. [Pg.174]

Clinical studies of cotton mill workers who had previously demonstrated a decreased expiratory flow measured by flow volume curves and FEV during cotton dust exposure showed an increase in WBC to 25.5% after 4 hours of exposure. Segmented neutrophils increased most (33%), while eosinophil mean counts did not change. The ratio of segmented neutrophils to epithelial cells from nasal mucosal swabs increased from 0.56 before to 1.84 after 4 hours of exposure. Peripheral blood and PMN counts increased upon exposure to cotton dust, and PMN were recruited to the nasal mucosa. Chest tightness and decreased flow were temporarily correlated with leukocyte recruitment following cotton dust exposure (2). [Pg.179]

Previous studies have reported that ERKs are characteristically associated with cell proliferation and protection from apoptosis (Bl, XI), while activation of JNK and p38 MAPK can promote apoptosis in many systems, including B lymphocytes (G5), cerebellar granule cells (K3), hematopoietic cells (K8), and neuronal cells (M3, XI). On the other hand, a recent report found that a pyridinyl imidazole, SB 202190, the specific inhibitor of p38 MAPK, by itself was sufficient to induce apoptosis in T lymphocyte Jurkat cells (N2). Moreover, Th-2-derived cytokine IL-5, the ERK activator and antiapoptotic factor for eosinophils, could also activate p38 MAPK in human eosinophils (BIO). We recently reported that cytokine IL-3, IL-5, and GM-CSF could prolong survival of human eosinophilic leukemic (EoL-1) cells through the transient activation of ERK (W15). On the other hand, activation of p38 MAPK in EoL-1 cells by the NSAID sodium salicylate (NaSal) could lead to apoptosis (W15). We also found that the suppression of ERK using ERK antisense phosphorothioate oligodeoxynucleotides could promote the apoptosis of peripheral blood eosinophils (W16). Moreover, we found that dexamethasone-induced apoptosis and activation of JNK and p38 MAPK activity in eosinophils are regulated by caspases (Z2). [Pg.78]

Fig. 4. An apoptotic peripheral blood eosinophil observed under EM. The apoptotic cell displays the characteristic condensation of nuclear chromatin into large, electron-dense masses surrounding the central, relatively electron-lucent nuclear matrix. The swelling and breakage of plasma and perinuclear membranes and the release of the contents of granules from swollen, enlarged, electron-lucent granule containers within secretory cells are also observed. A single osmiophilic lipid body is found in the cytoplasm (x 18,500) (D6). Reproduced with permission from Dvorak, A. M., Images in clinical medicine, an apoptotic eosinophil. N. Engl. J. Med. 340, 437 (1999). Fig. 4. An apoptotic peripheral blood eosinophil observed under EM. The apoptotic cell displays the characteristic condensation of nuclear chromatin into large, electron-dense masses surrounding the central, relatively electron-lucent nuclear matrix. The swelling and breakage of plasma and perinuclear membranes and the release of the contents of granules from swollen, enlarged, electron-lucent granule containers within secretory cells are also observed. A single osmiophilic lipid body is found in the cytoplasm (x 18,500) (D6). Reproduced with permission from Dvorak, A. M., Images in clinical medicine, an apoptotic eosinophil. N. Engl. J. Med. 340, 437 (1999).
W16. Wong, C. K., Zhang, J. P., Lam, C. W. K., Ho, C. Y, and Hjelm, N. M., Sodium salicylate-induced apoptosis of human peripheral blood eosinophils is independent of the activation of c-Jun N-terminal kinase and p38 mitogen-activated protein kinase. Int. Arch. Allergy Immunol. 121, 44-52 (2000). [Pg.107]

Due to the low number of eosinophils in peripheral blood, especially in guinea pigs, eosinophils are elicited in the peritoneal cavity by repeated injection of horse serum. Eosinophils are then purified to >95% by use of a discontinous Percoll gradient. The yield of eosinophils varies but we usually use 1 exbreeder donor for every 2 4 recipients. [Pg.277]

Sedgwick JB, Jansen KJ, Kennedy JD, Kita H, Busse WW. Effects of the very late adhesion molecule 4 antagonist WAY103 on human peripheral blood eosinophil vascular cell adhesion molecule 1-dependent functions. J. Allergy CUn. Immunol. 2005 16 812-819. [Pg.2333]

There has also been a report of an acute eosinophilic pneumonia associated with peripheral blood eosinophilia in a patient with follicular lymphoma (5). [Pg.1391]

Braun, RK., Franchini, M., Erard, F., Rihs, S., De Vries, I.J.M., Blaser, K., Hansel, T. T. and Walker, C. (1993). Human peripheral blood eosinophils produce and release interleukin-8 on stimulation with calcium ionophore. Eur. J. Immunol. 23, 956-960. [Pg.93]

Kita, H., Ohnishi, T., Okubo, Y., WeUer, D., Abrams, J. S. and Gleich, G.J. (1991). Granulocyte/macrophage colony-stimulating factor and interleukin 3 release from human peripheral blood eosinophils and neutrophils. J. Exp. Med. 174, 745-748. [Pg.95]

Moqbel, R, Lacy, P., Levi-Schafler, F., Manna, M., North, J., Gomperts, B. and Kay, A.B. (1995). Interleukin-6 as a granule-associated pre-formed mediator in peripheral blood eosinophils from asthmatic subjects. Am. J. Resp. Crit. Care Med., in press. [Pg.96]

Taylor, K.J. and Luksza, A.R (1987). Peripheral blood eosinophil counts and bronchial responsiveness. Thorax 42, 452-456. [Pg.98]

Despite the negative findings of in vitro studies, there is evidence that cytokines may play a role in the pathogenesis of EMS. It is known that IL-3, IL-5, and GM-CSF can each induce eosinophil production and enhance in vitro survival. In one study, EMS patients had significantly elevated serum levels of IL-5 and a higher proportion of hypodense eosinophils compared to normal controls. Elevated levels of IL-3 and GM-CSF were not observed. Their results suggest that IL-5 is the cytokine that triggers eosinophilia and converts peripheral blood eosinophils to the hypodense phenotype. The mechanism... [Pg.1032]


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