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PubMed1989

Independent release of peptide YY (PYY) into the circulation and ileal lumen of the awake dog.

Peptide YY (PYY) is a recently discovered polypeptide found in the endocrine cells of the distal small intestine, colon, and rectum. This study was designed to evaluate the postprandial release of PYY into the peripheral blood and the ileal lumen in response to different ingested nutrients. Six adult conditioned mongrel dogs had 25-cm distal ileal Thiry-Vella segments surgically constructed. After a 2-week postoperative recovery period the animals were fed meals consisting of protein (2 g/kg), fat (5 g/kg), or glucose (1.5 g/kg). Circulating and ileal intraluminal PYY concentrations were measured by a sensitive radioimmunoassay developed in our laboratory. Significant increases in circulating PYY levels were seen only after the fat meal in dogs. Ileal intraluminal PYY concentrations were significantly greater than those concentrations seen in the peripheral blood. A significant rise in ileal intraluminal PYY was seen only after the glucose meal without concomitant changes in circulating PYY. These findings document independent release mechanisms of PYY into the circulation and ileal lumen of the awake dog. We believe that the release of PYY into the canine circulation and into the ileal lumen after feeding may be dependent on the type of nutrient ingested and may serve to regulate the diverse physiologic roles of PYY in the gastrointestinal tract.

Animals↗
PubMed1991

Vagal cooling blocks circulating neuropeptide Y (NPY), peptide YY (PYY), and pancreatic polypeptide (PP) release.

Neuropeptide Y (NPY), peptide YY (PYY), and pancreatic polypeptide (PP) are regulatory peptides that constitute a new family of gastrointestinal and neural peptides. The influence of vagal integrity on NPY, PYY, and PP basal and postprandial release was evaluated using a new technique of reversible cryogenic cervical vagal blockade in an awake canine model. Cooling coils were placed around bilateral cervical vagal trunks in five dogs along with omocervical arterial catheters. Vagal transmission was monitored by pulse and arterial pressure monitoring. Cryogenic blockade of vagal nerves was performed by circulating a mixture of 0 degrees C ethanol and water through the cooling coils. NPY, PYY, and PP were measured using standard radioimmunoassays. Vagal cooling decreased basal NPY and PYY levels (P less than 0.05) but not PP. After a standard meal, vagal cooling blocked the postprandial rise seen in circulating NPY and PP (P less than 0.05). These data demonstrate a technique of reversible vagal blockade to evaluate the role of cervical vagal integrity in gastrointestinal endocrinology. Cryogenic vagal blockade inhibits the postprandial rise of circulating PP into the circulation. Vagal pathways appear to contribute to fasting activity of PYY and NPY releasing cells. Inhibited meal-stimulated release of NPY supports a role for vagal modulation of postprandial NPY release into the circulation.

Animals↗
PubMed1992

Effect of tryptophan administration on circulating melatonin levels in chicks and rats: evidence for stimulation of melatonin synthesis and release in the gastrointestinal tract.

The administration of L-tryptophan (Trp, 150-300 mg/kg) to rats and chicks causes a rapid and dose-dependent elevation of circulating melatonin. The elevation of serum melatonin was greater after oral compared to the intraperitoneal route of administration of the same dose of Trp (150 mg/kg). The Trp-induced increase of circulating melatonin was unaffected by prior pinealectomy but was almost abolished by a partial ligature of the portal vein. The Trp-induced increase of melatonin in the portal blood preceded that in the systemic circulation. The gut contains considerable amounts of melatonin and the Trp-induced elevation of melatonin was greater in the duodenum compared to the pineal or the blood. The enterochromaffin cells of the gastrointestinal tract appear to be the major source of the Trp-induced increment of circulating melatonin. The possibility is discussed that the sedating, sleep inducing effects of Trp are mediated by the Trp-induced elevation of circulating melatonin.

Administration, Oral↗
PubMed1985

Circulating concentrations of di(2-ethylhexyl) phthalate and its de-esterified phthalic acid products following plasticizer exposure in patients receiving hemodialysis.

The degree of exposure to the plasticizer di(2-ethylhexyl) phthalate (DEHP) was assessed in 11 patients undergoing maintenance hemodialysis for the treatment of renal failure. The amount of DEHP leached from the dialyzer during a 4-hr dialysis session was estimated by monitoring the DEHP blood concentration gradient across the dialyzer. Circulating concentrations of the biologically active products of DEHP de-esterification, viz., mono(2-ethylhexyl) phthalate (MEHP) and phthalic acid, were also determined during the dialysis session. On the average, an estimated 105 mg of DEHP was extracted from the dialyzer during a single dialysis session, with a range of 23.8 to 360 mg. The rate of extraction of DEHP from the dialyzer was correlated with serum lipid content as expressed by the sum of serum cholesterol and triglyceride concentrations (r = +0.65, p less than 0.05). Time-averaged circulating concentrations of MEHP during dialysis (1.33 +/- 0.58 micrograms/ml) were similar to those of DEHP (1.91 +/- 2.11 micrograms/ml). Blood concentrations of phthalic acid (5.22 +/- 3.94 micrograms/ml) were higher than those of the esters. The length of time patients had been receiving regular dialysis treatment was not a determinant of circulating concentrations of DEHP or MEHP. In contrast, time-averaged circulating concentrations of phthalic acid correlated strongly with the duration (in years) of dialysis treatment (r = +0.92, p less than 0.001). The results indicated substantial exposure to DEHP during hemodialysis and that the de-esterified products of DEHP are present in significant concentrations in the systemic circulation. Further study is needed to assess the contribution of these metabolites to the biological actions of DEHP in man.

Adult↗
PubMed1983

Glomerular and vascular IgG deposits in HgCl2 nephritis: role of circulating antibodies and of immune complexes.

The respective roles of circulating anti-glomerular basement membrane antibodies and of circulating immune complexes in the appearance of glomerular linear and granular IgG deposition during HgCl2-induced glomerulonephritis in the Brown-Norway rat has been studied. Syngeneic kidney transplantations have been performed at various phases of the disease. Results show that circulating antibodies are responsible for linear IgG deposition which did not change to granular deposits during the course of the disease. Electron-dense subepithelial deposits occurred only when circulating immune complexes were detected. These experiments strongly suggest that, in the mercury model, circulating immune complexes are responsible for granular IgG deposits observed in arteries and in the subepithelial space of glomeruli.

Animals↗
PubMed1984

Distribution of activated B lymphocytes in the circulation and synovial fluid in rheumatoid arthritis.

The circulating peripheral blood of 13/28 patients with definite or classical rheumatoid arthritis (RA) had increased numbers of spontaneous in vivo active immunoglobulin-producing B lymphocytes detected by a reverse hemolytic PFC assay (mean = 3000 (1310-7920) Ig PFC/10(6) B cells) compared to an age/sex-matched control population (mean = 550 (300-900) Ig PFC/10(6) B cells). Among the remaining 16 RA patients who had normal numbers (less than 900 Ig PFC/10(6)) of such circulating B cells, 5 patients had increased numbers of activated B cells in the synovial fluid and 6 patients had no increase. Extraarticular features (nodules and vasculitis) in 11/13 patients and advanced but relatively inactive synovitis characterized those RA patients with increased numbers of active circulating B cells. In contrast, extraarticular features were seldom observed (1/16) among the remaining patients with normal numbers of active circulating B cells. Among these patients, more active generalized synovitis characterized those patients with increased numbers of active synovial fluid B cells compared to those patients with normal numbers. These studies imply that in RA patients, whose disease is primarily articular, active Ig synthesis is limited to the synovial compartment, while in those with extraarticular features active Ig-producing B cells also appear in the circulation.

Adolescent↗
PubMed1989

Circulating immune complexes and kidney lesions following 131I administration in mice with thyroglobulin antibodies.

Immune complexes containing thyroglobulin have been described in kidneys of some patients with thyroid disease. We investigated the circulating immune complexes (with the Raji cell radioassay) and the kidney histopathology (by immunofluorescence and electron microscopy) in mice that received radioiodine to release thyroglobulin in the circulation, 2 or 4 weeks after immunization with mouse thyroglobulin in Freund's complete adjuvant. Circulating immune complexes and thyroglobulin, antibodies were found in all mice. Granular deposition of IgG, IgM, C3, and thyroglobulin, mainly in the mesangium but also in the capillary walls of the glomeruli, were observed in most of the mice. These experiments suggest that circulating immune complexes composed of thyroglobulin are responsible for the glomerular lesions. Hyperthyroid patients should be tested for thyroglobulin antibodies before treatment with radioiodine to avoid formation of thyroglobulin-containing circulating immune complexes.

Animals↗
PubMed1987

Relationship between circulating thyroid hormones and cell-mediated immunity in immature male chickens.

The objective of this experiment was to examine the relationship between circulating triiodothyronine (T3), thyroxine (T4) and cell-mediated immunity in immature male chickens. Three week old Single Comb White Leghorn male chicks were used as the experimental animals. In order to produce a wide range of circulating thyroid hormone concentrations, birds were divided into groups and received one of nine treatments including surgical thyroidectomy; 0.1% propylthiouracil (PTU) in the feed; 1 ppm T3 and 10 ppm T4 in the feed. The graft versus host (GvH) response and response to phytohemagglutinin (PHA) were measured at 6 weeks of age. Total and differential white blood cells were counted. Birds were bled, weighed, sacrificed, and the lymphoid organs were removed and weighed. Concentrations of T3 and T4 were measured in the birds from all treatment groups. There were positive correlations between thyroid hormones, mainly T3, and weights of thymus and spleen. T4 but not T3 was positively correlated with number of circulating lymphocytes. There were no significant correlations between circulating T3 and T4 and either PHA or GvH responses. It was concluded that physiological levels of thyroid hormones are needed to maintain normal weights of thymus and spleen and a normal level of circulating lymphocytes. Furthermore, we conclude that lower than physiological levels might be sufficient to maintain normal cell-mediated immunity. Finally, in order to enhance cell-mediated immune responses using thyroid hormones, different doses than were used might be required.

Animals↗
PubMed1987

Stress-induced changes of circulating neuropeptide Y in the rat: comparison with catecholamines.

Circulating concentrations of neuropeptide Y-like immunoreactivity (NPY), noradrenaline (NA) and adrenaline (AD) were measured in conscious, chronically catheterized rats submitted to various stress protocols. Basal plasma levels of NPY, NA and AD (194 +/- 52 fmol/ml, 0.90 +/- 0.11 pmol/ml and 0.52 +/- 0.07 pmol/ml) were increased by handling (+132%, +76% and +629%, respectively) and rose further during electric shock treatment. Adrenalectomy resulted in the complete disappearance of circulating adrenaline but did not alter either control or stress values of noradrenaline. In comparison circulating levels of NPY were reduced, but not significantly in adrenalectomized animals. Insulin stress induced a large increase in plasma AD levels and cold stress induced an increase in plasma NA levels, without any parallel change in NPY concentrations. These results demonstrate that NPY, which is colocalized with catecholamines in the peripheral nervous systems, is also released during stress responses and that its release parallels more closely changes in circulating NA than AD. Furthermore, stress-induced changes in circulating NPY-like immunoreactivity do not originate from the adrenal gland but mainly from the peripheral nervous system, and the release of NPY is dependent upon the nature of the stimulus.

Adrenalectomy↗
PubMed1993

Circulating alpha-actin protein in acute myocardial infarction.

We used Western-blot analysis to investigate the possible presence in the bloodstream of the contractile protein alpha-actin in 70 patients diagnosed with acute myocardial infarction on the basis of clinical, electrocardiographic and laboratory (creatine kinase and lactate dehydrogenase) criteria. Circulating protein was identified with a monoclonal antibody specific for cardiac alpha-actin. Of the 70 control samples of blood, the immunoblot results were negative for alpha-actin in 98% of the cases. Of the 30 patients with skeletal muscle damage caused by surgery, 26 were negative for circulating alpha-actin. Of the 70 patients with acute myocardial infarction, circulating alpha-actin was found in 67 (95%) as a 43 kDa band in immunoblots; the highest circulating concentrations (0.0580 micrograms/microliters) were found in those with anterior acute myocardial infarction. Circulating alpha-actin was detected in samples taken between 1 and 180 h after the onset of pain, and showed a biphasic pattern of appearance. Our findings for serum alpha-actin, together with the relationship between serum concentrations of this protein and sex (p = 0.001), tobacco use (p = 0.007) and postepisode complications (p = 0.002), should make it possible to gain a deeper understanding of acute myocardial infarction as a clinical entity.

Actins↗
PubMed1984

The effect of steroids on the circulating lymphocyte population--VI. Studies of the thoracic duct T- and B-lymphocyte populations after neonatal thymectomy and prednisolone treatment. An immunofluorescence study in the rat.

The corticosteroid effect on circulating lymphocytes in a steroid-sensitive species (rat) was studied by immunofluorescence. Both normal and neonatally thymectomized animals were injected with a high dose of prednisolone. T- and B-lymphocytes as well as T-lymphocyte subsets were analyzed in thoracic duct lymph during the involution phase (3 h after injection) and the restitution phase (17 h after injection) using conventional and monoclonal antisera. Neonatal thymectomy significantly reduced the number of circulating T-helper and T-non helper cells. In the involution phase, after a corticosteroid injection, there was a 64% reduction of lymph cell content in normal rats, affecting both T- and B-lymphocytes. Thymectomized animals showed an even more pronounced disappearance of cells. Counted in percentage, more B- than T-lymphocytes disappeared from the circulation. The T-non helper cells disappeared to a greater extent than the T-helper cells did. Cells with Ia-antigen showed about the same values as the B-lymphocytes. During the restitution phase all cells types were restored to normal levels. It seems that a high prednisolone dose has a more pronounced effect on the circulation of B- than of T-lymphocytes, and the T-non helper cells are probably more sensitive than the T-helper subpopulation. These data support the hypothesis that a major corticosteroid effect is a trapping and redistribution of circulating lymphocytes, more pronounced for certain cell types.

Animals↗
PubMed1994

Hyperthermia induces doxorubicin release from long-circulating liposomes and enhances their anti-tumor efficacy.

PURPOSE: To examine the possibility that hyperthermia would accelerate drug release from long-circulating liposomes, and enhance their antitumor activity. METHODS AND MATERIALS: Liposomes were prepared by thin film hydration technique. Hyperthermia was induced by ultrasound apparatus and a water bath heating system. The antitumor efficacy of treatment against RIF-1 tumor in C3H mice was evaluated by the tumor growth delay assay. RESULTS: In vitro drug release experiments demonstrated that increase in temperature from 37 degrees C to 41 degrees C resulted in about a sixfold increase in doxorubicin (DOX) release in a 1-h period. Increasing the temperature to 43 degrees C, resulted in only a modest additional drug release. Drug uptake studies showed that local hyperthermic treatment immediately following the drug administration dramatically enhanced Stealth liposome-encapsulated doxorubicin (S-DOX) uptake by tumors, but did not do so for free DOX. At 42 degrees C and at a dose of 10 mg/kg, the accumulation of S-DOX was about 10-fold and 2.5-fold higher than that with free drug and S-DOX at 37 degrees C, respectively. The antitumor efficacy study confirmed our hypothesis that the addition of hyperthermia to the treatment of RIF-1 tumors with doxorubicin encapsulated in long-circulating liposomes would enhance antitumor effects. Two hyperthermia treatments given at 24-h intervals appeared to be the most promising method of combining heat and long-circulating liposomes. The increased antitumor activity was not accompanied by increased toxicity, as determined by the body weight of the mice. CONCLUSION: Local hyperthermic treatment is able to accelerate DOX release from long-circulating liposomes, increase tumor uptake, and enhance their antitumor efficacy. The combination of local hyperthermia and long-circulating liposomes appears to show considerable promise in the treatment of localized diseases.

Animals↗
PubMed1986

Circulating insulin-like growth factor I levels in newborn premature and full-term infants followed longitudinally.

Longitudinal circulating levels of insulin-like growth factor I (IGF-I) were measured by radioimmunoassay after acid/ethanol extraction of serum or plasma in 44 appropriate-for-gestational age (AGA) premature infants, 7 small-for-gestational age (SGA) premature infants and 9 AGA full-term infants. The subjects were divided into cohorts with gestational age at birth 26-29 weeks, 30-33 weeks, 34-37 weeks and 38-42 weeks (full-term). The premature infants in this study exhibited diminished growth as compared with normal intrauterine growth. In all but the earliest premature infant cohort there was an immediate fall from the mean fetal IGF-I level, as reflected by the cord value, to a basal postnatal circulating level of IGF-I. The basal level of circulating IGF-I in premature infants was related only to gestational age. It increased slowly from 25 weeks gestation until four weeks after full-term equivalent and was independent of time of birth. Full-term infants were distinguished from early premature infants by the occurrence of a prominent postnatal surge in circulating IGF-I levels that was characterised by a significant (P less than 0.02) increase between day 1 and days 10-15. The SGA and AGA infants in the 34-37 week cohort showed similar profiles of circulating IGF-I with no significant difference in cord values between the two groups.

Gestational Age↗
PubMed1995

Tissue IGFBP-3 proteolysis: contrasting pathophysiology to that in the circulation.

Endogenous IGFBP-3 has been examined in the circulation and in four different extravascular fluids in normal healthy adults and in patients with psoriasis or arthritis. In all of these cases there was no apparent increase of IGFBP-3 protease activity in the circulation. In contrast, endogenous IGFBP-3 from normal skin interstititial fluid and synovial fluid from healthy adults was found to be predominantly in the 29 kDa proteolytically modified form. This indicated that in these extravascular fluids in normal healthy adults a protease was active which was similar, if not identical, to that found in the circulation in pregnancy and other conditions. This was confirmed by the fragmentation of recombinant IGFBP-3 when incubated with these fluids. When the skin interstitial fluid or synovial fluid were taken from abnormal tissues (psoriasis in the former and osteoarthritis or rheumatoid arthritis in the latter) there was a considerable reduction in the amount of endogenous IGFBP-3 in the 'clipped' form and a reduction in the protease activity. In psoriatic lesions, this reduction in IGFBP-3 protease activity was shown to be due to the presence of an inhibitor in the interstitial fluid but not in the circulation. In both peritoneal and follicular fluid, the ratio of intact to fragmented IGFBP-3 appeared to relate to the oestrogen status. In peritoneal fluid there was a decrease in intact IGFBP-3 during the late proliferative/early secretory phase of the endometrial cycle. In the ovary there was an increase in the amount of fragmented IGFBP-3 in the follicular fluid from the dominant follicle in comparison with atretic follicles from the same ovary. There is normally little proteo-lysis of IGFBP-3 in the circulation but this increases in many conditions where there is increased metabolic activity. The same enzyme(s) appear to be active in many extravascular fluids but under very different regulation. The activity in these extravascular fluids is normally high but can be decreased with local tissue inflammation; this decrease appears to be mediated by the induction of a local inhibitor.

Adult↗
PubMed2006

Circulating angiogenic proteins in trisomy 13.

OBJECTIVE: Women who are carrying a trisomy 13 fetus are more prone to develop preeclampsia. Excess circulating soluble fms-like tyrosine kinase-1 has been implicated recently in the pathogenesis of preeclampsia. Since the fms-like tyrosine kinase-1/soluble fms-like tyrosine kinase-1 gene is located on chromosome 13q12, we hypothesized that the extra copy of this gene in trisomy 13 may lead to excess circulating soluble fms-like tyrosine kinase-1, reduced free placental growth factor level, and increased soluble fms-like tyrosine kinase-1/placental growth factor ratio. This may then contribute to the increased risk of preeclampsia that has been observed in these patients. Our objective was to characterize the maternal circulating angiogenic proteins in trisomy 13 pregnancies. STUDY DESIGN: Maternal serum samples of trisomy 13, 18, 21 and normal karyotype pregnancies were obtained from first and second trimester screening programs. We chose 17 cases of trisomy 13 that were matched for maternal age, freezer storage time, and parity with 85 normal karyotype control samples. Additionally, 20 cases of trisomy 18 and 17 cases of trisomy 21 were included. Cases and control samples were assayed for levels of soluble fms-like tyrosine kinase-1 and placental growth factor by enzyme-linked immunosorbent assay in a blinded fashion. Because of the skewed distributions of soluble fms-like tyrosine kinase-1 and placental growth factor, nonparametric analytic techniques were used, and the results are reported as median and ranges. RESULTS: In early pregnancy trisomy 13 cases and control samples, the median circulating soluble fms-like tyrosine kinase-1/placental growth factor ratios were 17.0 (range, 1.2-61.3) and 6.7 (range, 0.8-62.9), respectively (P = .003). The median soluble fms-like tyrosine kinase-1/placental growth factor ratios in trisomy 18 and 21 were 4.8 (range, 0.9-53.9) and 5.1 (range, 1.0-18.1), which were not significantly different than the control samples. Furthermore, the differences between trisomy 13 and control samples were more pronounced in the second trimester specimens than in the specimens from the first trimester. CONCLUSION: These data suggest that alterations in circulating angiogenic factors may be involved intimately in the pathogenesis of preeclampsia in trisomy 13. A larger clinical study that measures these factors longitudinally and correlates them with pregnancy outcomes is needed to further establish the link between trisomy 13, altered angiogenic factors, and preeclampsia.

Angiogenic Proteins↗
PubMed2004

Comparison of suppression of the circulating and vascular renin-angiotensin system by enalapril versus trandolapril in chronic heart failure.

Experimental studies suggest that angiotensin-converting enzyme (ACE) inhibitors with high tissue affinity confer a greater degree of vascular renin-angiotensin system suppression than those with low tissue affinity despite similar suppression of the circulating renin-angiotensin system. To test this hypothesis in a clinical setting, we randomized subjects with chronic heart failure to receive the low tissue affinity ACE inhibitor enalapril or the high tissue affinity ACE inhibitor trandolapril, and assessed the degree of circulating and vascular renin-angiotensin system suppression. Vascular renin-angiotensin system suppression was determined by measuring the pressor response to intravenous injections of angiotensin I. Circulating renin-angiotensin system suppression was determined by measuring plasma angiotensin II. Vascular and circulating renin-angiotensin system suppression, endothelial function (flow-mediated vasodilation), and maximal exercise capacity (peak oxygen uptake) were assessed after a 4-week run-in period on open-label enalapril 40 mg/day and after 8 weeks of randomized double-blind treatment with enalapril 40 mg/day or trandolapril 4 mg/day. Twenty-six men and 4 women (mean age 52 +/- 11 years; mean left ventricular ejection fraction 25 +/- 9%; New York Heart Association class II [n = 16] and III [n = 14]) were studied. After a 2-month randomized treatment period, vascular renin-angiotensin system suppression, circulating renin-angiotensin system suppression, endothelial function, and exercise capacity did not differ between subjects treated with enalapril and those treated with trandolapril. Despite substantial differences in the tissue affinity of enalapril and trandolapril, the degree of vascular renin-angiotensin system suppression achieved with these agents did not differ in subjects with chronic heart failure during long-term therapy.

Angiotensin II↗
PubMed2004

Increased circulating malondialdehyde-modified LDL in the patients with familial combined hyperlipidemia and its relation with the hepatic lipase activity.

Familial combined hyperlipidemia (FCHL) is characterized by elevated levels of serum total cholesterol (TC), triglyceride (TG), or both. The increased incidence of coronary artery diseases (CAD) in the patients with FCHL is believed to be caused by circulating atherogenic lipoproteins associated with the complex phenotype. Recent establishment of sensitive detection system for malondialdehyde-modified (MDA)-LDL, which is one of oxidized lipoproteins, showed its increased circulating level in the patients with CAD. In order to know the atherogenic lipoproteins resulted from the dyslipidemia observed in FCHL, we measured the serum MDA-LDL level in the patients. The circulating MDA-LDL level and the ratio of MDA-LDL and LDL-C in FCHL were significantly higher (P<0.05) than those in control, which are adjusted about the age, serum TC, LDL-C and HDL-C levels, respectively. Furthermore, the circulating MDA-LDL level and the ratio of MDA-LDL and LDL-C were negatively correlated (R=-0.635, P<0.01 and R=-0.702, P<0.01, respectively) with hepatic lipase (HL) activity in FCHL. The serum MDA-LDL level and the ratio of MDA-LDL and LDL-C were in the subjects with T/T genotypes in the HL C-514T polymorphism were significantly increased compared to those with C/C genotype, respectively. The subjects with T/T genotype showed the activities to 65 and 79% of those in the subjects with C/C genotype in male and female, respectively. The intima-media thickness (IMT) of carotid artery was significantly higher (P<0.05) in the subjects with T/T genotype than those with C/C genotype in male. These findings indicate that the circulating MDA-LDL level is possibly contributing the atherogenic process in FCHL, and the common HL polymorphism might be a determinant of the serum level of oxidized LDL in the patients with FCHL.

Cholesterol↗
PubMed2004

Enhanced glucocorticoid sensitivity of cytokine release from circulating leukocytes stimulated with lipopolysaccharide in healthy male smokers.

Smoking is a strong cardiovascular risk factor that promotes inflammation. The source of elevated pro-inflammatory cytokines in the circulation of smokers is not fully understood. We investigated the release of pro-inflammatory cytokines from circulating leukocytes stimulated with lipopolysaccharide (LPS) and its inhibition by glucocorticoids in smokers and non-smokers. Ninety-three middle-aged apparently healthy men were categorized as smokers (> 10 cigarettes/day; n = 41) or life-long non-smokers (n = 52). Peripheral cortisol was assessed from overnight urine. C-reactive protein (CRP) and tumor necrosis factor (TNF)-alpha were measured in plasma. LPS-stimulated interleukin (IL)-6 and TNF-alpha release from harvested circulating leukocytes were assessed using an in vitro whole blood assay with and without co-incubation of increasing concentrations of either dexamethasone or hydrocortisone. Glucocorticoid sensitivity was defined as the concentration of glucocorticoids required that inhibits LPS-stimulated cytokine release by 50%. Smokers had higher CRP levels (p = .005) and a trend for higher basal TNF-alpha levels (p < .07), and they also showed lower IL-6 and TNF-alpha release after LPS-stimulation than non-smokers (p's < .001). While peripheral cortisol concentration showed no significant group difference, inhibition of LPS-stimulated leukocyte IL-6 and TNF-alpha release by either glucocorticoid was enhanced in smokers as compared to non-smokers (p's < .022). The finding suggests that, in spite of a low-grade systemic inflammation, smokers have decreased LPS-stimulated cytokine release from circulating leukocytes and greater glucocorticoid sensitivity of this cytokine release than non-smokers. Circulating leukocytes unlikely contribute to the elevated pro-inflammatory cytokine levels in the blood of smokers.

Adult↗