Release of Polymorphonuclear Leukocytes From the Bone Marrow by Interleukin-8

Blood ◽  
1998 ◽  
Vol 92 (3) ◽  
pp. 1062-1069 ◽  
Author(s):  
Takeshi Terashima ◽  
Dean English ◽  
James C. Hogg ◽  
Stephan F. vanEeden
Keyword(s):  
Bone Marrow ◽  
Transit Time ◽  
Polymorphonuclear Leukocytes ◽  
Interleukin 8 ◽  
Thymidine Analogue ◽  
American Society

Several studies have shown that interleukin-8 (IL-8) causes a rapid granulocytosis with the release of polymorphonuclear leukocytes (PMN) from the bone marrow (BM) partially responsible for the granulocytosis. This study was designed to quantitate the release of PMN from the BM by IL-8 and measure the transit time of PMN through the marrow after IL-8 administration. The thymidine analogue, 5'-bromo-2'-deoxyuridine (BrdU), was used to label dividing PMN in the marrow and follow their release into the circulation after intravenous IL-8. This allowed us to calculate the transit time of PMN through the mitotic and postmitotic pools of BM. BrdU was infused intravenously into rabbits 24 hours before IL-8 (2.5 μg/kg). IL-8 caused a rapid, transient granulocytopenia (5.9 ± 0.4 at baseline v 0.2 ± 0.06 × 10/9L at 5 minutes, P < .05) followed by granulocytosis (8.4 ± 0.1 at 30 minutes, P < .05) associated with an increased number (0.3 ± 0.1 at baseline v1.2 ± 0.6 × 109/L at 30 minutes, P < .05) and percentage of band cells (P < .05), as well as a rapid increase in the number of BrdU-labeled PMN (PMNBrdU) in the circulation (0.09 ± 0.05 at baseline to 1.5 ± 0.6 × 109/L at 60 minutes, P < .05). The transit time of PMN through both the mitotic and postmitotic pools of BM was not affected by IL-8. To determine the marrow compartment from which the PMN were mobilized by IL-8, we quantitated PMN movement from the hematopoietic and sinusoidal compartments into the circulation. The fraction of PMNBrdU in both compartments was higher than in the circulating blood (P < .05) and the fraction and number of PMNBrdU in the sinusoids decreased with IL-8 treatment (P < .05). We conclude that the pool of PMN residing in the BM venous sinusoids are rapidly released into the circulation after administration of IL-8. © 1998 by The American Society of Hematology.

Release of Polymorphonuclear Leukocytes From the Bone Marrow by Interleukin-8

Blood ◽  
1998 ◽  
Vol 92 (3) ◽  
pp. 1062-1069 ◽  
Author(s):  
Takeshi Terashima ◽  
Dean English ◽  
James C. Hogg ◽  
Stephan F. vanEeden
Keyword(s):  
Bone Marrow ◽  
Transit Time ◽  
Polymorphonuclear Leukocytes ◽  
Interleukin 8 ◽  
Thymidine Analogue ◽  
American Society

Abstract Several studies have shown that interleukin-8 (IL-8) causes a rapid granulocytosis with the release of polymorphonuclear leukocytes (PMN) from the bone marrow (BM) partially responsible for the granulocytosis. This study was designed to quantitate the release of PMN from the BM by IL-8 and measure the transit time of PMN through the marrow after IL-8 administration. The thymidine analogue, 5'-bromo-2'-deoxyuridine (BrdU), was used to label dividing PMN in the marrow and follow their release into the circulation after intravenous IL-8. This allowed us to calculate the transit time of PMN through the mitotic and postmitotic pools of BM. BrdU was infused intravenously into rabbits 24 hours before IL-8 (2.5 μg/kg). IL-8 caused a rapid, transient granulocytopenia (5.9 ± 0.4 at baseline v 0.2 ± 0.06 × 10/9L at 5 minutes, P &lt; .05) followed by granulocytosis (8.4 ± 0.1 at 30 minutes, P &lt; .05) associated with an increased number (0.3 ± 0.1 at baseline v1.2 ± 0.6 × 109/L at 30 minutes, P &lt; .05) and percentage of band cells (P &lt; .05), as well as a rapid increase in the number of BrdU-labeled PMN (PMNBrdU) in the circulation (0.09 ± 0.05 at baseline to 1.5 ± 0.6 × 109/L at 60 minutes, P &lt; .05). The transit time of PMN through both the mitotic and postmitotic pools of BM was not affected by IL-8. To determine the marrow compartment from which the PMN were mobilized by IL-8, we quantitated PMN movement from the hematopoietic and sinusoidal compartments into the circulation. The fraction of PMNBrdU in both compartments was higher than in the circulating blood (P &lt; .05) and the fraction and number of PMNBrdU in the sinusoids decreased with IL-8 treatment (P &lt; .05). We conclude that the pool of PMN residing in the BM venous sinusoids are rapidly released into the circulation after administration of IL-8. © 1998 by The American Society of Hematology.

scholarly journals Novel properties of statins: suppression of the systemic and bone marrow responses induced by exposure to ambient particulate matter (PM10) air pollution

2012 ◽  
Vol 303 (6) ◽  
pp. L492-L499 ◽  
Author(s):  
Ryohei Miyata ◽  
Ni Bai ◽  
Renaud Vincent ◽  
Don D. Sin ◽  
Stephan F. Van Eeden
Keyword(s):  
Bone Marrow ◽  
Particulate Matter ◽  
Transit Time ◽  
Polymorphonuclear Leukocytes ◽  
Inflammatory Responses ◽  
Ambient Particulate Matter ◽  
Bone Marrow Stimulation ◽  
Dividing Cells ◽  
Prolonged Retention ◽  
Progression Of Atherosclerosis

Exposure to ambient particulate matter (PM10) elicits systemic inflammatory responses that include the stimulation of bone marrow and progression of atherosclerosis. The present study was designed to assess the effect of repeated exposure of PM10on the turnover and release of polymorphonuclear leukocytes (PMNs) from the bone marrow into the circulation and the effect of lovastatin on the PM10-induced bone marrow stimulation. Rabbits exposed to PM10three times a week for 3 wk, were given a bolus of 5′-bromo-2′-deoxyuridine to label dividing cells in the marrow to calculate the transit time of PMNs in the mitotic or postmitotic pool. PM10exposure accelerated the turnover of PMNs by shortening their transit time through the marrow (64.8 ± 1.9 h vs. 34.3 ± 7.4 h, P < 0.001, control vs. PM10). This was predominantly due to a rapid transit of PMNs through the postmitotic pool (47.9 ± 0.7 h vs. 21.3 ± 4.3 h, P < 0.001, control vs. PM10) but not through the mitotic pool. Lovastatin delayed the transit time of postmitotic PMNs (38.2 ± 0.5 h, P < 0.001 vs. PM10) and shifted the postmitotic PMN release peak from 30 h to 48 h. PM10exposure induced the prolonged retention of newly released PMNs in the lung, which was reduced by lovastatin ( P < 0.01). PM10exposure increased plasma interleukin-6 levels with significant reduction by lovastatin ( P < 0.01). We conclude that lovastatin downregulates the PM10-induced overactive bone marrow by attenuating PM10-induced systemic inflammatory responses.

Polymorphonuclear leukocyte transit times in bone marrow during streptococcal pneumonia

1996 ◽  
Vol 271 (4) ◽  
pp. L587-L592 ◽  
Author(s):  
T. Terashima ◽  
B. Wiggs ◽  
D. English ◽  
J. C. Hogg ◽  
S. F. van Eeden
Keyword(s):  
Bone Marrow ◽  
Streptococcus Pneumoniae ◽  
Transit Time ◽  
Polymorphonuclear Leukocytes ◽  
Nuclear Staining ◽  
Inflammatory Conditions ◽  
Transit Times ◽  
Brdu Injection ◽  
The Mean ◽  
Toxic Potential

The release of polymorphonuclear leukocytes (PMN) from the bone marrow (BM) is a hallmark of acute inflammatory conditions. BM stimulation may increase the toxic potential of these newly released PMN and influence their behavior at inflammatory sites. The present study was designed to measure the transit time of PMN in the mitotic and postmitotic pools of the BM in rabbit using 5'-bromo-2'-deoxyuridine (BrdU). Blood samples were obtained at 2- to 24-h intervals from 24 to 192 h after a single BrdU injection, and BrdU-positive PMN (PMNBrdU) was detected as they appear in the circulating blood, using immunohistochemistry. The intensity of nuclear staining for BrdU was used to define a single generation of PMN and graded as either weakly (G1), moderately (G2), or highly (G3) stained. The mean +/- SE transit time of PMNBrdU through the BM was 95.6 +/- 3.6 h, with 51.1 +/- 5.9 h in the mitotic and 65.4 +/- 5.4 h in the postmitotic pool. Streptococcus pneumoniae instillation in the lung (n = 3) shortened the transit time of PMN through the BM to 54.0 +/- 2.6 h with a shorter time in both the mitotic (36.2 +/- 5.7 h) and the postmitotic pool 34.6 +/- 0.8 h). All these values were shorter than the control values (P < 0.05). We conclude that Streptococcus pneumoniae shortens the transit time of PMN in the mitotic and postmitotic pools in the marrow, which may result in the release of immature PMN with higher levels of lysosomal enzymes into the circulation.

scholarly journals Lactoferrin biosynthesis during granulocytopoiesis

Blood ◽  
1984 ◽  
Vol 64 (5) ◽  
pp. 1103-1109 ◽  
Author(s):  
TA Rado ◽  
J Bollekens ◽  
G St. Laurent ◽  
L Parker ◽  
EJ Jr Benz
Keyword(s):  
Bone Marrow ◽  
Chronic Myelogenous Leukemia ◽  
Messenger Rna ◽  
Polymorphonuclear Leukocytes ◽  
Leukemia Cell ◽  
Myelogenous Leukemia ◽  
Leukemia Cell Line ◽  
Xenopus Laevis Oocytes ◽  
Lineage Infidelity ◽  
Translatable Mrna

Abstract We examined the synthesis of lactoferrin, an iron binding protein that, among hematopoietic cells, is restricted to secondary granules of polymorphonuclear leukocytes. Lactoferrin biosynthesis was absent from leukemic myeloblasts and promyelocytes but abundant in normal bone marrow and both the bone marrow and peripheral blood of patients with chronic myelogenous leukemia (CGL) if the samples contained substantial numbers of myelocytes and metamyelocytes. Lactoferrin was present in the steady state in normal or CGL bands and polymorphonuclear leukocytes, but no lactoferrin biosynthesis was detectable in these samples. Taken together, these results suggest that lactoferrin accumulation begins with the onset of biosynthesis at the myelocyte stage and is largely complete by the beginning of the band stage of maturation. HL-60 cells, a permanent promyelocytic leukemia cell line, synthesized no lactoferrin. Translation of messenger RNA in Xenopus laevis oocytes revealed that mRNA from patients with chronic myelogenous leukemia and abundant myelocytes and metamyelocytes directed the synthesis of readily detectable amounts of lactoferrin, whereas HL-60 cells contained no translatable lactoferrin mRNA. We thus hypothesize that lactoferrin is a useful marker of gene expression restricted to the terminal stages of granulocyte maturation. Biosynthesis of this protein appears to be mediated by appearance of translatable mRNA at the myelocyte stage, coincident with development of secondary granules. Absence of lactoferrin production by HL-60 cells is due to absence of translatable lactoferrin mRNA, either because of lineage infidelity of these transformed cells or because of arrest before the developmental stage at which secondary granules appear.

Erythropoietin-independent erythroid colony formation by bone marrow progenitors exposed to interleukin-11 and interleukin-8

2005 ◽  
Vol 33 (11) ◽  
pp. 1299-1308 ◽  
Author(s):  
Isabelle Corre-Buscail ◽  
Danielle Pineau ◽  
Marjorie Boissinot ◽  
Sylvie Hermouet
Keyword(s):  
Bone Marrow ◽  
Colony Formation ◽  
Interleukin 8 ◽  
Interleukin 11

Interleukin-8 (CXCL8) in Tumor Associated Non-Vascular Extracellular Fluids: Its Diagnostic and Prognostic Values. A Review

2012 ◽  
Vol 27 (3) ◽  
pp. 169-178 ◽  
Author(s):  
Jaromír Kotyza
Keyword(s):  
Tumor Progression ◽  
Polymorphonuclear Leukocytes ◽  
Cell Types ◽  
Interleukin 8 ◽  
Low Grade ◽  
Remission Status ◽  
Cancerous Cell ◽  
Inflammatory Processes ◽  
And Migration ◽  
Proliferation And Migration

Interleukin-8 (IL-8, CXCL8) was originally discovered as a powerful attractor and activator of polymorphonuclear leukocytes. It was soon recognized that IL-8 also affects proliferation and migration of cancer cells, tumor angiogenesis and metastasis, and that it is expressed in many cancerous cell types. IL-8 protein expression is usually increased in serum of cancer patients, but markedly higher concentrations are found in cancer-associated non-vascular extracellular fluids, such as pleural effusion, ascites and cyst fluid. Elevated concentrations of IL-8 are indicative of malignant processes also in cerebrospinal fluid, urine, saliva, interstitial fluid and cervicovaginal secretions. Higher IL-8 levels are typically found in high-grade peritumoral fluids rather than low-grade tumors and benign conditions, with the exception of inflammatory processes. In line with recent molecular biology investigations, it appears that the local IL-8 production is related to its malignant origin and to tumor progression. Hence, IL-8 in peritumoral fluid is to be taken into consideration while assessing tumor character and monitoring the tumor progression/remission status. Besides, the data here collected justify the attempts to find an IL-8-targeted inhibitory therapy.

The effect of interleukin-6 on L-selectin levels on polymorphonuclear leukocytes

2002 ◽  
Vol 283 (3) ◽  
pp. H879-H884 ◽  
Author(s):  
Tatsushi Suwa ◽  
James C. Hogg ◽  
Kevin B. Quinlan ◽  
Stephan F. van Eeden
Keyword(s):  
Transit Time ◽  
Interleukin 6 ◽  
Polymorphonuclear Leukocytes ◽  
Inflammatory Stimuli ◽  
Low Levels

Interleukin-6 (IL-6) shortens the transit time of polymorphonuclear leukocytes (PMN) through the marrow and accelerates their release into the circulation. In contrast to other inflammatory stimuli, this response is associated with a decrease in L-selectin levels on circulating PMN. The present study was designed to determine the effect of IL-6 on L-selectin levels of PMN in rabbits. Recombinant human IL-6 (2 μg/kg) caused a decrease in L-selectin levels on circulating PMN 3 to 12 h after treatment ( P < 0.05). L-selectin levels decreased on PMN already in the circulation for up to 4 h ( P < 0.05), on PMN released from the marrow posttreatment for up to 12 h ( P < 0.01) and on PMN in the marrow for up to 6 h ( P < 0.05) after IL-6 treatment. We conclude that IL-6 decreases L-selectin levels on circulating PMN by demarginating PMN with low levels of L-selectin and by releasing PMN from the marrow with low levels of L-selectin. We postulate that this prolonged downregulation of L-selectin on circulating PMN could influence their recruitment into inflammatory sites.

scholarly journals Transepithelial Migration Process Induced by Interleukin-8 Delays Polymorphonuclear Leukocytes (PMNL) Apoptosis

2001 ◽  
Vol 1 ◽  
pp. 38-38 ◽  
Author(s):  
Gaëlle Le'Negrate ◽  
Phillippe Rostagno ◽  
Bernard Rossi ◽  
Paul Hofman
Keyword(s):  
Polymorphonuclear Leukocytes ◽  
Interleukin 8 ◽  
Migration Process
Sign in / Sign up

Export Citation Format

Share Document