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Biomedical subjects

J C Hogg

Publications and source records attributed to J C Hogg.

At least 37 records · Page 2Linked to original sources
PubMed2001

Dynamic changes in neutrophil defensins during endotoxemia.

Bacterial endotoxin or lipopolysaccharide (LPS) is an important causative agent of sepsis. This study determines the expression of defensins NP-2 and NP-5 and the function of polymorphonuclear leukocytes (PMN) in rabbits treated with LPS. PMN functional activity was assessed by measuring CD18 expression and H(2)O(2) production and by examining the lungs. NP-2 and, to a minor extent, NP-5 of circulating PMN increase during endotoxemia. This early increase is concomitant with neutrophilia and elevated CD18 expression and H(2)O(2) production, as well as with enhanced NP-2 immunoreactivity in pulmonary microvessels. A decline in defensins, shortly after the last LPS treatment, is associated with a decrease in the circulating activated PMN and enhanced immunoreactivity in the inflammatory cells, as well as with lung tissue damage. This study shows that LPS-induced changes in the defensins of circulating PMN correlate with the number and activated condition of these cells and suggests that PMN-derived products implement the inflammatory reaction that leads to lung injury and sepsis.

Animals↗
PubMed2001

Adenoviral E1A primes alveolar epithelial cells to PM(10)-induced transcription of interleukin-8.

The presence of the adenoviral early region 1A (E1A) protein in human lungs has been associated with an increased risk of chronic obstructive pulmonary disease (COPD), possibly by a mechanism involving amplification of proinflammatory responses. We hypothesize that enhanced inflammation results from increased transcription factor activation in E1A-carrying cells, which may afford susceptibility to environmental particulate matter < 10 microm (PM(10))-mediated oxidative stress. We measured interleukin (IL)-8 mRNA expression and protein release in human alveolar epithelial cells (A549) transfected with the E1A gene (E1A+ve). Both E1A+ve and -ve cells released IL-8 after incubation with TNF-alpha, but only E1A+ve cells were sensitive to LPS stimulation in IL-8 mRNA expression and protein release. E1A+ve cells showed an enhanced IL-8 mRNA and protein response after treatment with H(2)O(2) and PM(10). E1A-enhanced induction of IL-8 was accompanied by increases in activator protein-1 and nuclear factor-kappa B nuclear binding in E1A+ve cells, which also showed higher basal nuclear binding of these transcription factors. These data suggest that the presence of E1A primes the cell transcriptional machinery for oxidative stress signaling and therefore facilitates amplification of proinflammatory responses. By this mechanism, susceptibility to exacerbation of COPD in response to particulate air pollution may occur in individuals harboring E1A.

Adenovirus E1A Proteins↗
PubMed2001

Effect of mechanical deformation of neutrophils on their CD18/ICAM-1-dependent adhesion.

Mechanical deformation of polymorphonuclear leukocytes (PMN) changes their expression of the surface adhesion molecule CD11b/CD18. We tested the hypothesis that mechanical deformation of PMN enhances their adhesiveness. Purified human PMN were deformed through either 5- or 3-microm polycarbonate membrane filters and allowed to adhere to 96-well plates coated with human recombinant intercellular adhesion molecule-1 (ICAM-1). Flow cytometric studies showed that deformation of PMN increased CD11b/CD18 expression (P < 0.01). PMN adhesion to ICAM-1-coated plates was dependent on the magnitude of cell deformation (5 microm, 63.8 +/- 8.1%, P < 0.04; 3 microm, 232.4 +/- 20.9%, P < 0.01). Priming of PMN (0.5 nM N-formyl-methionyl-leucyl-phenylalanine) before deformation (5 microm) increased PMN adhesion (63.8 +/- 8.1 vs. 105.3 +/- 16.4%; P < 0.04). Stimulation (5% zymosan-activated plasma) of PMN after deformation resulted in increased adhesion, and the degree of increase was dependent on the magnitude of PMN deformation (stimulation, 50.6 +/- 4%; 5-microm filtration and stimulation, 62.9 +/- 6.6%; 3-microm filtration and stimulation, 249.9 +/- 24.2%; P < 0.01). This study shows that mechanical deformation of PMN causes an increase in PMN adhesiveness to ICAM-1 that was enhanced by both priming of PMN before deformation and stimulation after cell deformation.

CD18 Antigens↗
PubMed2001

The effect of repeated exposure to particulate air pollution (PM10) on the bone marrow.

Studies have shown that exposure to ambient particulate matter is related to an increased cardiopulmonary morbidity and mortality. The present study was designed to measure the effect of repeated exposure to urban air particles (PM10) on the rate of production and release of polymorphonuclear leukocytes (PMN) from the bone marrow into the peripheral blood. Rabbits exposed to PM10 (5 mg) twice a week for 3 wk, were given a bolus of 5'-bromo-2'-deoxyuridine (BrdU) to label dividing cells in the marrow that allows us to calculate the transit time of PMN in the bone marrow mitotic and postmitotic pools. The PM10 exposure (n = 8) causes a persistent increase in circulating band cells (p < 0.05) and a shortening of the transit time of PMN through the postmitotic pool in the marrow (64.4 +/- 2.2 h to 56.3 +/- 2.2 h, p < 0.05) if compared with vehicle-exposed control subjects (n = 6). PM10 exposure increases the bone marrow pool of PMN particularly the mitotic pool of PMN (p < 0.05). The PM10 were distributed diffusely in the lung and caused a mild mononuclear inflammation. The percentage of alveolar macrophages containing PM10 correlated significantly with the bone marrow PMN pool size (total pool r2 = 0.56, p < 0.012, mitotic pool r2 = 0.61, p < 0.007) and the transit time of PMN through the postmitotic pool (r2 = -0.42, p < 0.043). We conclude that repeated exposure to PM10 stimulates the bone marrow to increase the production of PMN in the marrow and accelerate the release of more immature PMN into the circulation. The magnitude of these changes was related to the amount of particles phagocytosed by alveolar macrophages.

Air Pollution↗
PubMed2001

Interleukin-6 changes deformability of neutrophils and induces their sequestration in the lung.

Interleukin-6 (IL-6) is an important mediator of both the hepatic and the bone marrow components of the acute-phase response. Previous studies from our laboratory have shown that cells released into the circulation from the marrow preferentially sequester in the lung. The present study was designed to examine the mechanism of this sequestration using a single dose of recombinant human IL-6 to stimulate the marrow in rabbits. Marrow release was monitored by labeling polymorphonuclear leukocyte (PMN) precursors in the marrow with the thymidine analogue, 5'-bromo-2-deoxyuridine (BrdU), 24 h before IL-6 treatment. This treatment caused a neutrophilia that was associated with the increase of circulating BrdU- labeled PMN (PMN(BrdU)) and morphometric studies confirmed that PMN(BrdU) released from the marrow preferentially sequestered in the lung microvessels compared to unlabeled PMN. IL-6 treatment increases PMN F-actin content (p < 0.05) that was not due to cell activation by IL-6. In vitro studies show that IL-6 treatment decreased the deformability of circulating PMN (p < 0.05). These studies confirm that IL-6 treatment causes an accelerated release of PMN from the bone marrow and shows that these newly released PMN have high levels of F-actin, are less deformable, and preferentially sequester in lung microvessels.

Actins↗
PubMed2001

Particulate matter induces cytokine expression in human bronchial epithelial cells.

The present study was designed to determine cytokines produced by primary human bronchial epithelial cells (HBECs) exposed to ambient air pollution particles (EHC-93). Cytokine messenger RNA (mRNA) was measured using a ribonuclease protection assay and cytokine protein production by enzyme-linked immunosorbent assay. Primary HBECs were freshly isolated from operated lung, cultured to confluence, and exposed to 10 to 500 microg/ml of a suspension of ambient particulate matter with a diameter of less than 10 microm (PM(10)) for 2, 8, and 24 h. The mRNA levels of leukemia inhibitory factor (LIF), granulocyte macrophage colony-stimulating factor (GM-CSF), interleukin (IL)-1alpha, and IL-8 were increased after exposure to PM(10), and this increase was dose-dependent between 100 (P < 0.05) and 500 (P < 0.05) microg/ml of PM(10) exposure. The concentrations of LIF, GM-CSF, IL-1beta, and IL-8 protein measured in the supernatant collected at 24 h increased in a dose- dependent manner and were significantly higher than those in the control nonexposed cells. The soluble fraction of the PM(10) (100 microg/ml) did not increase these cytokine mRNA levels compared with control values and were significantly lower compared with HBECs exposed to 100 microg/ml of PM(10) (LIF, IL-8, and IL-1beta; P < 0.05), except for GM-CSF mRNA (P = not significant). We conclude that primary HBECs exposed to ambient PM(10) produce proinflammatory mediators that contribute to the local and systemic inflammatory response, and we speculate that these mediators may have a role in the pathogenesis of cardiopulmonary disease associated with particulate air pollution.

Aged↗
PubMed2001

BAL induces an increase in peripheral blood neutrophils and cytokine levels in healthy volunteers and patients with pneumonia.

STUDY OBJECTIVES: To examine the peripheral effects of BAL on the neutrophil counts and cytokine levels in the circulation. DESIGN AND METHODS: WBC counts and plasma cytokines were measured before and 4 h after fiberoptic bronchoscopy (FOB) without further interventions (n = 6), or combined with BAL in normal volunteer subjects (n = 6), and in patients with bacterial pneumonia (n = 4). The bronchus of the right middle lobe was wedged, and three 50-mL aliquots of sterile saline solution was instilled. There was no endotoxin contamination in the saline solution or the fluid obtained through the working channel of bronchoscope. RESULTS: In volunteers, peripheral WBC counts and the number of nonsegmented and segmented neutrophils increased after the BAL procedure (p < 0.05) associated with the increase in plasma concentration (mean +/- SEM) of interleukin (IL)-6 (0.99 +/- 0.32 pg/mL before BAL and 20.38 +/- 13.42 pg/mL after BAL; p < 0.05) and granulocyte colony-stimulating factor (G-CSF; 14.1 +/- 1.7 pg/mL before BAL and 38.5 +/- 9.7 pg/mL after BAL; p < 0.05). The increase in WBC counts and neutrophil counts was positively correlated to the increase in IL-6 (p < 0.05) and the increase in G-CSF (p < 0.05). In patients with pneumonia, IL-6 and G-CSF levels were higher after BAL than in normal volunteer subjects (p < 0.05). There was no increase in plasma concentration of IL-1beta, tumor necrosis factor-alpha, or IL-8 after BAL in normal volunteer subjects or in patients with pneumonia. FOB without BAL did not increase the WBC count, neutrophil count, or plasma cytokine levels. CONCLUSION: The BAL procedure increases the number of WBCs, and segmented and nonsegmented neutrophils in the peripheral circulation as well as circulating IL-6 and G-CSF levels.

Adult↗
PubMed2000

Neutrophils released from the bone marrow by granulocyte colony-stimulating factor sequester in lung microvessels but are slow to migrate.

Inflammatory mediators such as granulocyte colony-stimulating factor (G-CSF) release polymorphonuclear leukocytes (PMNL) from the bone marrow. This growth factor is used to promote the host response to infection but its effect on the behaviour of leukocytes at the inflammatory site is unclear. This study examined the sequestration and migration of PMNL released from the bone marrow by G-CSF in a model of streptococcal pneumonia. Eight hours following the administration of either human G-CSF (n=6) or saline (n=3) in rabbits, a focal Streptococcus pneumoniae pneumonia was induced and the animals were followed for 2 h. The thymidine analogue 5'-bromo-2'-deoxyuridine (BrdU) was used to label PMNL (PMNL(BrdU)) in the marrow and as a marker of PMNL newly released by the bone marrow. The PMNL(BrdU) in the lung and blood were identified using immunohistochemistry. G-CSF pretreatment elevated the circulating PMNL (3.6+/-0.4 (mean+/-SEM) to 8.3+/-1X10(9) x L(-1), p<0.05) and PMNL(BrdU) (5.4+/-2.1 to 12.5+/-3.1%, p<0.05) counts at 8 h with little further increase caused by the subsequent 2 h pneumonia. These counts did not change in the control group. Morphometric studies of the lung showed that the total number of PMNL sequestered in lung capillaries were increased in the G-CSF group and the percentage of the these PMNL that were BrdU-labelled, was higher than in circulating blood (p<0.05). In the G-CSF group, only 11.2+/-2.6% of the PMNL that migrated into the airspaces were PMNL(BrdU) compared to 50.8+/-8% PMNL(BrdU) in the pulmonary capillaries. In vitro studies showed PMNL(BrdU) released from the bone marrow by G-CSF are less deformable than unlabelled circulating PMNL (p<0.01). It is concluded that granulocyte colony-stimulating factor treatment causes the marrow to release polymorphonuclear leukocytes that preferentially sequester in lung microvessels but are slow to migrate out of the vascular space into the airspace at the pneumonic site.

Animals↗
PubMed2000

The response of human bone marrow to chronic cigarette smoking.

Chronic cigarette smoking in humans causes leukocytosis. Animal studies show that chronic smoking shortens the transit time of polymorphonuclear leukocytes (PMNLs) through the bone marrow. The present study examines the response of human bone marrow to chronic cigarette smoking. Three characteristics of peripheral blood PMNLs that indicate active bone marrow release (band cell counts, surface L-selectin expression and myeloperoxidase (MPO) content), were measured in 38 healthy chronic smokers (23+/-5 pack-yrs) and 15 age- and sex-matched nonsmoking controls. The total white cell (6.8+/-0.3x10(9) versus 5.3+/-0.2x10(9) cells x L(-1), p<0.0001) and PMNL (4.2+/-0.18x10(9) versus 3.2+/-0.1x10(9) cells x L(-1), p<0.003) counts were higher in smokers as were the percentage (4.8+/-0.6 versus 1.1+/-0.2, p<0.0001) and total number (0.21+/-0.04x10(9) versus 0.03+/-0.001x10(9) cells x L(-1), p<0.01) of band cells. Flow cytometry showed that the mean fluorescence intensity (MFI) of L-selectin (3.2+/-0.2 versus 2.6+/-0.1, p<0.05) on PMNLs was higher in smokers. There was no difference in the baseline or N-formyl-methionyl-leucyl-phenylalanine-stimulated expression of CD63 or CD18/CD11b (surface markers of PMNL activation) between smokers and controls. The MPO content of PMNLs was higher in smokers (3.4+/-0.3 versus 1.7+/-0.2 MFI, p<0.05). Smokers with a low (<75% of the predicted value) diffusing capacity of the lung for carbon monoxide had higher PMNL MPO levels than smokers with a diffusing capacity of >75% pred (p<0.05). In conclusion, chronic smoking causes phenotypic changes in circulating polymorphonuclear leukocytes that are characteristic of chronic stimulation of the bone marrow and it is speculated that the increased number of immature polymorphonuclear leukocytes contributes to the chronic lung inflammation associated with cigarette smoking.

Adult↗
PubMed2000

Flow cytometric analysis of defensins in blood and marrow neutrophils.

Polymorphonuclear neutrophils (PMN) are vital in host defense against microbial infections. This study provides a flow cytometric method for the quantitative analysis of microbicidal peptides (defensins) in cells of PMN lineage. Rabbit neutrophil peptides, NP-2 and NP-5, were measured in all PMN and in subpopulations of PMN expressing 1-selectin. PMN lineage counts were made on Wright's-stained blood smears and marrow cytospins. Immunoreactivity for NP-2, and NP-5 was detected by using the alkaline phosphatase anti-alkaline phosphatase technique. The results show that marrow PMN express higher levels of NP-2 and NP-5 than blood PMN, p < 0.001 and that these levels are associated with elevated numbers of myeloid precursors. In both blood and marrow, NP-2 occurs in two PMN subpopulations and the mean fluorescence intensity of NP-2 is consistently higher than that of NP-5. Increased levels of defensins are observed in circulating PMN depicting the most 1-selectin p < 0.05. Immunocytochemical results indicate that PMN defensins reside in cytoplasmic granules and are not constitutively expressed on the cell surface. Furthermore, defensins are not detected in monocytes, eosinophils, lymphocytes and erythrocytes. The flow cytometric method described here provides a novel means of quantitating host natural defenses, allows the characterization of PMN subpopulations and has clinical applications.

Alkaline Phosphatase↗
PubMed2000

Polymorphonuclear leukocytes released from the bone marrow by granulocyte colony-stimulating factor: intravascular behavior.

INTRODUCTION: Granulocyte-colony stimulating factor (G-CSF) treatment stimulates the bone marrow and releases polymorphonuclear leukocytes (PMN) into the circulation. This study was designed to measure the intravascular margination, demargination and survival of PMN released from the marrow by G-CSF. MATERIALS AND METHODS: To trace PMN in the circulation, dividing PMN in the bone marrow of rabbits were labeled with 5'-bromo-2'-deoxyuridine (BrdU) and the effects of a single dose of G-CSF (12.5 microg/kg) on the behavior of these labeled cells in the circulation were measured. RESULTS: The results show that G-CSF induced a granulocytosis that peaked 12 h after treatment. This granulocytosis was associated with stimulation of the bone marrow characterized by shortening of the transit time of PMN through the marrow (97.3+/-2.5 h n=4 control vs 78.9+/-3.6 h n=5 G-CSF) particularly in the post-mitotic pool (P<0.01). Morphometric studies of the lung show a reduced sequestration of BrdU-labeled PMN in lung microvessels in G-CSF-treated animals (P<0.05) and a approximately 14-fold (G-CSF-group) vs a approximately 65-fold (control-group) enrichment of BrdU-labeled PMN in lung tissue if compared to circulating blood. The effect of G-CSF on demargination of PMN was measured by transferring BrdU-labeled PMN from donor animals treated with G-CSF to recipients. G-CSF did not cause demargination of intravascular PMN but delayed the clearance of G-CSF-treated PMN in the circulation. This delayed clearance was associated with inhibition of apoptosis in circulating PMN when measured both by morphology (17.7+/-2.3 vs 7.5+/-1.4%, P<0.01) and flow cytometry (16.2+/-1.1 vs 5+/-1.9%, P<0.01) using a DNA end-labeling method (control vs G-CSF group). CONCLUSION: We conclude that PMN released from the bone marrow by G-CSF sequestered less in the lung microvessels and have a prolonged intravascular life span.

Animals↗
PubMed2000

Chronic bronchitis: the role of viruses.

Mucus is produced by the epithelial cells in the glands, gland ducts, and the cells lining the airway lumen in the lower airways. The chronic cough and sputum production that defines chronic bronchitis is associated with an inflammatory reaction involving this mucus-secreting apparatus. Respiratory viral infections target the epithelial cells of the lung producing desquamation, microvascular dilatation, edema, and an inflammatory cell infiltrate. These changes predispose the lower airways to bacterial infection by interfering with mucociliary clearance and reducing bacterial killing by macrophages. The exact role of those infections in the pathogenesis of chronic bronchitis has not been clearly determined but they probably play a critical role in inducing bacterial colonization and initiating acute exacerbations of COPD. This article reviews the classification of the viral agents responsible for respiratory tract infection and the nature of the changes they produce in the normal airways and in the airways of patients with chronic bronchitis during acute infections.

Bronchitis↗
PubMed2000

Increased number of glucocorticoid receptor-beta-expressing cells in the airways in fatal asthma.

BACKGROUND: We have recently demonstrated an increased number of glucocorticoid receptor-beta (GRbeta)-positive cells in steroid-insensitive subjects with severe asthma. Insensitivity to steroids may be a major contributing factor in fatal asthma; however, no such direct evidence has been report previously. OBJECTIVE: Our aims were to investigate the expression of GRbeta immunoreactivity, an endogenous inhibitor of steroid action previously associated with steroid insensitivity, within the airways of patients who died of slow-onset fatal asthma and to compare its expression in patients with emphysema and in nonasthmatic subjects who died of unrelated causes. Sections from airways, both large and small, were obtained from 7 patients who died of asthma, 6 who died from emphysema, and 8 who died from nonpulmonary diseases. Sections from lungs of 6 patients with mild asthma whose lungs were resected for carcinoma were also included as controls. METHODS: Tissue samples were processed for immunocytochemistry with a polyclonal antibody to GRbeta with use of the avidin-biotin technique and with monoclonal CD3, major basic protein, CD68, and elastase antibodies with the alkaline phosphatase-anti-alkaline phosphatase technique. Sequential immunocytochemistry was performed to phenotype the GRbeta immunoreactive cells. Tissue sections from both large (>2 mm) and small (<2 mm) airways were examined. RESULTS: There was a significantly greater number of GRbeta immunoreactive cells in fatal asthma compared with emphysema and controls (P <.001 and P <.05, respectively). There was no difference in the expression of GRbeta in emphysema compared with controls. GRbeta immunoreactivity was also significantly higher in fatal asthma compared with mild asthma. The expression of GRbeta in the small airways of patients with severe asthma did not differ significantly from that in the large airways. The majority of GRbeta-positive cells were T cells and to a lesser extent eosinophils, macrophages, and neutrophils. CONCLUSION: The results of this study support the association of GRbeta expression with fatal asthma and suggest that alternative anti-inflammatory agents need to be considered in the acute setting for patients who are not responding to steroid therapy.

Asthma↗
PubMed2000

Latent adenoviral infection modifies the steroid response in allergic lung inflammation.

BACKGROUND: Steroid-resistant asthma develops after adenoviral bronchiolitis. OBJECTIVE: We sought to determine the effect of steroids on allergic lung inflammation in the presence of latent adenoviral infection. METHODS: Guinea pigs with latent adenoviral (n = 12) or sham (n = 12) infections were sensitized and challenged with ovalbumin (OA) or sham sensitized and challenged with saline solution. The effect of steroids (20 mg/kg administered intraperitoneally) on OA-induced lung inflammation was examined by using quantitative histology as the outcome measure. RESULTS: Latent adenoviral infection increased CD8(+) cells in the airway wall and CD8(+) cells, macrophages, B cells, and CD4(+) cells in the lung parenchyma. Ovalbumin challenge, on the other hand, increased eosinophils, macrophages, B cells, and CD4(+) cells in both the airway wall and lung parenchyma independent of the effect of latent adenoviral infection. In the sham-infected groups steroid treatment caused the expected reduction in the eosinophilic infiltrate induced by OA challenge in the airways without affecting the other cells. In the presence of both latent adenoviral infection and OA challenge, steroid treatment had no effect on allergen-induced eosinophilia but reduced CD8(+) cells in the airways and CD8(+) cells, CD4(+) cells, and B cells in the parenchyma. CONCLUSION: Latent adenoviral infection and OA challenge result in different types of lung inflammation, and the presence of latent adenoviral infection causes OA-induced eosinophilic airway inflammation to become steroid resistant.

Adenoviridae Infections↗
PubMed2000

Interleukin-6 induces demargination of intravascular neutrophils and shortens their transit in marrow.

Recombinant human interleukin-6 (IL-6) causes both a thrombocytosis and leukocytosis. The thrombocytosis is caused by an accelerating thrombocytopoiesis, but the mechanism of the leukocytosis is unknown. This study was designed to determine the relative contributions of marrow stimulation and intravascular demargination to the IL-6 induced neutrophilia. IL-6 (2 microgram/kg), administered intravenously to rabbits, caused a biphasic neutrophilia with an initial peak at 3 h and a second peak at 9 h. Using the thymidine analog 5'-bromo-2'-deoxyuridine (BrdU) to label dividing polymorphonuclear leukocytes (PMNs) in the bone marrow, we showed that IL-6 treatment mobilizes PMNs from the marginated pool into the circulating pool at 2-6 h with a decrease in L-selectin expression on PMNs and also accelerates the release of PMNs from the postmitotic pool in the bone marrow at 12-24 h. We have concluded that IL-6 causes a biphasic neutrophilia wherein the first peak results from the mobilization of PMNs into the circulating pool from the marginated pool and the second peak results from an accelerated bone marrow release of PMNs.

Animals↗
PubMed2000

Phagocytosis of particulate air pollutants by human alveolar macrophages stimulates the bone marrow.

Epidemiologic studies have shown an association between the level of ambient particulate matter < 10 microm (PM(10)) and cardiopulmonary mortality. We have shown that exposure of rabbits to PM(10) stimulates the bone marrow. In this study, we determined whether human alveolar macrophages (AMs) that phagocytose atmospheric PM(10) produce mediators capable of stimulating the bone marrow. AMs incubated with PM(10) for 24 h produced tumor necrosis factor-alpha in a dose-dependent manner (86.8 +/- 53.29 pg/ml with medium alone; 1,087.2 +/- 257.3 pg/ml with 0.1 mg/ml of PM(10); P < 0.02). Instillation of the supernatants from AMs incubated with 0.1 mg/ml of PM(10) into the lungs of rabbits (n = 6) increased circulating polymorphonuclear leukocyte (PMN) and band cell counts as well as shortened the PMN transit time through the bone marrow (87.9 +/- 3.3 h) compared with unstimulated human AMs (104.9 +/- 2.4 h; P < 0.01; n = 5 rabbits). The supernatants from rabbit AMs incubated with 0.1 mg/ml of PM(10) (n = 4 rabbits) caused a similar shortening in the PMN transit time through the bone marrow (91.5 +/- 1.6 h) compared with human AMs. We conclude that mediators released from AMs after phagocytosis of PM(10) induce a systemic inflammatory response that includes stimulation of the bone marrow.

Air Pollutants↗
PubMed2000

The human bone marrow response to acute air pollution caused by forest fires.

Atmospheric pollution increases cardiopulmonary morbidity and mortality by unexplained mechanisms. Phagocytosis of fine particles (PM(10)) by rabbit alveolar macrophages elevates white blood cells (WBC) by releasing precursors from the bone marrow and this could contribute to the pathogenesis of cardiopulmonary disease. The present study examined the association between acute air pollution caused by biomass burning and peripheral WBC counts in humans. Serial measurements of the WBC count made during the 1997 Southeast Asian Smoke-haze (Sep 29, Oct 27) were compared with a period after the haze cleared (Nov 21, Dec 5) using peripheral blood PMN band cells to monitor marrow release. The results showed that indices of atmospheric pollution were significantly associated with elevated band neutrophil counts expressed as a percentage of total polymorphonuclear leukocytes (PMN), with maximal association on zero and 1 lag day for PM(10) and 3, and 4 lag days for SO(2) (p value < 0.000). We conclude that atmospheric pollution caused by biomass burning is associated with elevated circulating band cell counts in humans because of the increased release of PMN precursors from the marrow. We speculate that this response contributes to the pathogenesis of the cardiorespiratory morbidity associated with acute air pollution.

Adult↗