Increase In Number Of Leukocytes Research Articles

Serum IL-6 Is Increased During Performance Cycling After Energy Drink Consumption

Energy Drinks have become a popular preexercise supplement due to the combination of caffeine and carbohydrate. Other ingredients such as glucuronolactone and taurine may play a role in performance enhancement. PURPOSE: The purpose of this study was to investigate the influence of a common energy drink on cycling performance, substrate oxidation and immune-related variables. METHODS: This study was a blinded, randomized, cross-over design. Eleven trained male cyclists (mean age 33.4 ± 8.9 yr, body mass 81 ± 7.6 kg, maximal VO2 51.72 ± 3.4 ml*kg-1*min-1) consumed either 500 ml of Red Bull Energy Drink (ED1- 2.0g taurine, 1.2 g glucoronolactone, 160 mg caffeine, 54 g carbohydrate (CHO), 40 mg niacin, 10 mg pantothenic acid, 10 mg vitamin B6, and 10 μg vitamin B12), Coke-a-Cola Classic matched for caffeine and CHO (ED2), or flavored placebo (ED3- crystal light and Perrier) 55 min prior to racing. Performance was measured as time to complete a 25-mile simulated road race. Blood was collected pre-drink (PrD), 30 minutes after drink (pre-exercise, PrEx), during exercise at mile 5 (M5), mile 15 (M15), and immediately (PoEx) & 30 min post-exercise (30min). RESULTS: Performance time was not different among trials (ED1 4117 ± 161 s, ED2 4132 ± 230 s, ED3 4173 ± 225 s). PrEx IL-6 was not different among PD1, 2 or 3 (0.61±0.09, 0.78±0.1, 0.56±0.07, pg*mL-1). PoEx IL-6 was greatest after ED1 while ED2 IL-6 response was greater than ED3 (10.2±1.6, 6.7±0.6, 4.8±0.7 pg*ml-1, p<0.001). IL-6 declined after ED1 & ED2 by 30min, but remained significantly greater than baseline after all trials (5.3±1, 4.1±0.5, 3.6±0.7, 30min ED1, 2 and 3, p<0.001). Cycling increased leukocyte number in all conditions with ED1 leukocyte number greater than that of ED3 at M15 (9.8±0.6, 8.5±0.3 ×10∧6 cells/mL). Mean fat oxidation was greater in ED3 compared to ED2 (0.43±0.06, 0.28±0.04 g*min-1, p=0.033) but did not differ between ED1 (0.32±0.06) and ED3. CHO oxidation did not differ among trials. Lactate was greater for ED1 & ED2 at PrEx, M5, M15 and PoEx (p=0.003). CONCLUSION: Coingestion of caffeine and CHO prior to endurance cycling significantly increased the IL-6 response to exercise, and the additional ingredients of ED1 appear to have further augmented this response. ED1 also appears to have influenced leukocyte number and fat oxidation during performance cycling.

Leukocyte profile in sows during lactation period

During prepartum and postpartum period, there occurs in sows a significant change in the values of haematologic and biochemical parameters. The objective of this research paper was to examine the change in the count of the cells of white blood line in the course of lactation period. The trial was conducted on ten Swedish Landrace breed sows, having the blood taken on the first day postpartum (1-6h), and in the third and fourth week of lactation. The results obtained for haemotologic analyses have suggested the increase in total number of leukocytes and neutrophilic granulocytes, and the decrease in the number of lymphocytes, monocytes and eosinophils on the first day postpartum. In the third and fourth week of lactation a statistically significant fall in the number of leukocytes and granulocytes in relation to the first day was observed, along with a significant increase in limphocytes, monocytes and eosinophils. In examined time intervals the number of basophils did not change significantly. The neutrophil-limphocyte index was highest on the first day postpartum, while in the third and fourth week it was significantly lower.

Inhibitory effect of eupatilin and jaceosidin isolated from Artemisia princeps on carrageenan-induced inflammation in mice

Ethnopharmacological relevance Artemisia princeps Pampanini (family Asteraceae) is an herbal medicine widely used as a hepatoprotective, antioxidative, anti-inflammatory, and antibacterial agent in Korea, China, and Japan. Aim of the study This study aimed to elucidate the anti-inflammatory effect of the main constituents, eupatilin and jaceosidin, isolated from Artemisia princeps. Materials and methods We used carrageenan-induced inflammation in an air pouch on the back of mice and carrageenan-induced hind paw edema in rats to determine the anti-inflammatory effects of eupatilin and jaceosidin. Inflammatory makers, such as expression of pro-inflammatory cytokines and cyclooxygenase (COX)-2, and activation of nuclear factor-kappa B (NF-κB), were measured by enzyme-linked immunosorbent assays and immunoblot analyses. Results Eupatilin and jaceosidin blocked carrageenan-induced increase in leukocyte number and protein levels in air pouch exudates. Eupatilin and jaceosidin inhibited COX-2 expression and NF-κB activation, and markedly reduced TNF-α, IL-1β, and prostaglandin E2 (PGE 2) levels. They also inhibited hind paw edema induced by carrageenan. Eupatilin and jaceosidin had similar activity. Conclusions These findings suggest that eupatilin and jaceosidin may reduce inflammation by inhibiting NF-κB activation, and that Artemisia princeps inhibits inflammation because of these constituents.

Temporal patterns of soluble adhesion molecules in cerebrospinal fluid and plasma in patients with the acute brain infraction.

The aim of this study was to define concentration changes of soluble adhesion molecules (sICAM-1, sVCAM-1 and sE-Selectin) in cerebrospinal fluid and plasma, as well as, number of peripheral blood leukocytes and the albumin coefficient in the patients with the acute brain infarction. We also, analyzed the correlation between the measured levels, the infarct volume and the degree of neurological and the functional deficit. The study included 50 patients with the acute cerebral infarction and the control group consisted of 16 patients, age and sex matched. Obtained results showed significant increase in number of leukocytes, the albumin coefficient and the level of soluble adhesion molecules within the first seven days in patients. The highest values of measured parameters were noted within the third and the fourth day after the insult, which is the suggested period of maximal intensity of inflammatory reactions. Significant correlation was found between measured parameters and the infarct volume, the degree of neurological and the functional deficit. The results suggest that investigated parameters in CSF and blood represent a dynamic index of inflammatory events as one of the fundametal mechanisms responsible for neuron damage during acute phase of brain infarction.

Temporal Patterns of Soluble Adhesion Molecules in Cerebrospinal Fluid and Plasma in Patients with the Acute Brain Infraction

The aim of this study was to define concentration changes of soluble adhesion molecules (sICAM-1, sVCAM-1 and sE-Selectin) in cerebrospinal fluid and plasma, as well as, number of peripheral blood leukocytes and the albumin coefficient in the patients with the acute brain infarction. We also, analyzed the correlation between the measured levels, the infarct volume and the degree of neurological and the functional deficit. The study included 50 patients with the acute cerebral infarction and the control group consisted of 16 patients, age and sex matched. Obtained results showed significant increase in number of leukocytes, the albumin coefficient and the level of soluble adhesion molecules within the first seven days in patients. The highest values of measured parameters were noted within the third and the fourth day after the insult, which is the suggested period of maximal intensity of inflammatory reactions. Significant correlation was found between measured parameters and the infarct volume, the degree of neurological and the functional deficit. The results suggest that investigated parameters in CSF and blood represent a dynamic index of inflammatory events as one of the fundametal mechanisms responsible for neuron damage during acute phase of brain infarction.

Calprotectin in Myeloid and Epithelial Cells of Laminae from Horses with Black Walnut Extract‐Induced Laminitis

Laminar inflammation is one of the earliest events in equine laminitis. Calprotectin (CP), a Damage-Associated Molecular Pattern protein, is overexpressed in inflammatory conditions of human skin. CP is overexpressed in the laminar epidermis of horses with black walnut extract (BWE)-induced laminitis. Twenty adult horses. Experimental study. Horses were allocated to one of 4 groups. BWE was administered to horses in 3 groups, which were sampled 1.5, 3, and 12 hours (LAM) later. CP was visualized by immunohistochemistry. Laminar leukocyte counts and intensity of laminar epithelial staining were scored for all animals and statistically analyzed. Laminar epidermal CP signal was significantly increased (P= .02) at the LAM time point, compared with other groups. Rare leukocytes were detected in laminae with CP staining in CON group, but there were marked increases in number of leukocytes in BWE-treated groups (P= .003). Sequential hematoxylin and eosin staining demonstrated that the majority of CP-positive leukocytes were perivascular polymorphonuclear neutrophils (PMN) at each of the developmental time points. CP-positive PMN and mononuclear cells were detected in perivascular locations and close to the epidermal basement membrane in the LAM group. CP expression in the laminar epidermis occurs after extravasation of leukocytes, indicating that leukocyte emigration might be an initiating factor in laminar epithelial stress and inflammation in BWE-induced laminitis. These results indicate a possible role of CP in laminitis pathophysiology and laminar failure.

005. PREPARING FERTILE SOIL: THE IMPORTANCE OF ENDOMETRIAL RECEPTIVITY

The human endometrium is receptive for implantation of a blastocyst, for only 4–5 days in each menstrual cycle. Failure of implantation is a major reason for infertility in women, and the inability to achieve endometrial receptivity is responsible for much of the failure of reproductive technologies. Endometrial receptivity requires alterations in the uterine luminal and glandular cells, particularly in terms of their secretory capacity and altered expression of adhesion molecules, along with decidualization of the endometrial stroma, which in women is initiated during the receptive phase, regardless of the presence of a blastocyst. Increased leukocyte numbers are also important. The microenvironments provided by the endometrium during the receptive phase and which support implantation are highly complex and constantly changing. The present review summarizes work from our laboratories and others, regarding these microenvironments, how they impact on receptivity and how they are disturbed in infertile women. Such microenvironments can also be manipulated to provide new contraceptive strategies for women.

Histopathology and cellular response in Enteromyxum leei (Myxozoa) infections of Diplodus puntazzo (Teleostei)

Enteromyxum leei is an intestinal parasite responsible for serious outbreaks in Mediterranean sharpsnout sea bream Diplodus puntazzo. E. leei infection was experimentally transmitted to healthy D. puntazzo (R) by cohabitation with infected donor fish. Haematological changes and histopathological damage were evaluated in relation to the course of infection. The prevalence of infection in R fish was 100% from day 10 post-exposure (p.e.) onwards, and the infection intensity and histopathological damage increased progressively. Different developmental stages were found in the infected intestines, including proliferative (stages 1–3) and sporogonic (stages 4 and 5) stages. Intestinal damage consisted of vacuolation, necrosis, detachment and sloughing of epithelium, and was correlated with the progression of the infection and with the development of the parasite. Sporogonic stages appeared from day 20 p.e. onwards. Initially, D. puntazzo seems to counteract the infection through the increase in leucocyte numbers, respiratory burst activity, haematopoietic activity and MMC. Two types of eosinophilic granular cells (EGC1 and EGC2) were detected in the intestinal epithelium and lamina propria. EGC1 numbers decreased with the progression of infection, whereas an increase in EGC2 occurred, mainly in the lamina propria. The involvement of the cellular immunity in the response of D. puntazzo to E. leei was demonstrated. The depletion of this response at a certain point of the infection could contribute to the high virulence of this myxozoan in this fish species.

CAMP-PKA Signaling Plays an Important Role in Augmented Neutrophil Adhesion and Chemotaxis in Sickle Cell Disease.

A chronic inflammatory state is now thought to underlie much of the pathophysiology of sickle cell disease (SCD). Increased leukocyte numbers are associated with increased morbidity and mortality in SCD and the adhesion of leukocytes to the vascular endothelium and sickle red cells may play an initiating role in the vaso-occlusive process. We sought to better understand the signaling events that lead to alterations in SCD neutrophil adhesive and chemotactic abilities. Neutrophils were isolated from the peripheral blood of healthy controls and SCD individuals in steady state by separation over a ficoll-paque gradient. Following washing and lysis of contaminating red cells, adhesion to fibronectin (FN) and chemotaxis of control and SCD neutrophils (4×106 cells/ml in RMPI medium) were assessed using static adhesion assays and a 96-well chemotaxis chamber assay (ChemoTX, Neuroprobe). Cell adhesion to FN (20mg/ml; 30 min, 37°C, 5% CO2) or IL-8-induced migration (2h, 37°C, 5% CO2) was calculated using a standard curve of the original cell suspension and expressed as the percentage of cells adhered or the number of cells migrated. As previously shown, SCD neutrophils demonstrate a greater ability to adhere to FN-coated plates than control individual leukocytes (13.1±1.48 % neutrophils adhered compared to 5.0±0.6 %; n=11; P<0.001 Mann-Whitney test). Interestingly, SCD neutrophils demonstrate significantly higher levels of the secondary messenger, cAMP, than control neutrophils (4.76±0.38 pMol/106 cells compared to 1.91±0.34 pMol/106 cells; n≥12; P<0.001). When neutrophils were incubated on FN-coated plates in the presence of the cAMP-dependent kinase (PKA) inhibitor, KT5720 (3μM), increased SCD neutrophil adhesion was significantly reversed to levels approaching those of control neutrophils (7.73±1.3 %; n=11; P=0.001). In contrast, control neutrophil adhesion to FN was not significantly affected by the PKA inhibitor (P>0.05). Furthermore, activation of primed SCD neutrophils by the chemokine, IL-8 (500ng/ml), resulted in a significant increase in SCD neutrophil adhesion to FN (19.3±2.2 %; P=0.02; n=7) with a concomitant increase in intracellular cAMP levels (335.8±17.1 % increase, P<0.05, n=3) that could also be reverted by co-incubation with the PKA inhibitor, KT5720 (11.8 ± 0.8 %; P=0.02; n=7). Interestingly, in vitro chemotaxis of SCD neutrophils in response to a stimulus of IL-8 (100 ng/ml) was found to be significantly increased when compared to control neutrophil IL-8-stimulated chemotaxis (14.3±1.1 x105 cells/ml migrated compared to 8.8±0.8x105 cells/ml; P=0.005; n=8). Once again, KT5720 (3 μM, pre-incubation for 15 min, 37°C), was able to significantly reverse (8.5±1.1 x105/ml; P=0.03; n=6) this enhanced IL-8-dependent SCD neutrophil chemotaxis. Results suggest that an up-regulated PKA-dependent pathway may play an important role in the altered adhesive and chemotactic properties of SCD neutrophils and their further activation by cytokines/chemokines such as IL-8, found in increased levels in the serum of SCD patients. Thus, upregulation of the cAMP-PKA pathway in SCD neutrophils may have important consequences for the chronic inflammatory state in SCD patients and may characterize a novel target for the control of altered neutrophil function in SCD.

Leukocyte Apoptosis and Inflammation in Iron-Overloaded Patients with Sickle Cell Disease or β-Thalassemia: A Mechanism for Increased Stroke and Disease Severity in Sickle Cell Disease.

Sickle cell disease (SCD) is a hemoglobinopathy characterized by micro-vascular hypoxia-reperfusion, inflammation and leukocytosis. Studies in SCD have shown that leukocytosis is a strong predictor of stroke and disease severity. It is known that leukocytosis and inflammation contribute to increased leukocyte-endothelial adhesion and vasoocclusive events. Leukocytosis or increased leukocyte number is determined by the balance between cell death programs (apoptosis) and proliferation. In this study, we examine markers of apoptosis and proliferation in SCD as compared to thalassemia (a hemoglobinopathy that is vasculitis negative) and a control group. Methods: Markers of leukocyte turnover, inflammation and free iron (NTBI, non-transferrin bound iron) were compared in 11 patients with SCD (7M, 13 ± 4 yrs), 18 with thalassemia (7M, 24 ± 9 yrs) and 10 disease-free controls (5M, 27 ± 12 yrs). All SCD and thalassemia patients were healthy and event free in the previous 4 months. Blood was obtained fasting and prior to RBC transfusion; and plasma, serum and cells were separated by centrifugation. The pro-apoptotic markers nucleosome protein (DNA laddering) and Bax (initiator of mitochondrial permeability) and inflammatory marker, high-sensitivity C Reactive Protein (hsCRP) were determined by ELISA. NTBI (DNA damage inducing, pro-apoptotic) was measured by HPLC. Plasma levels of cytokines (anti-apoptotic, proliferation stimulating) were determined by using a multiplex bead-based immunoassay. Plasma lactate dehydrogenase (LDH), a marker of hemolysis, was also measured because hemolysis products have been shown to inhibit apoptosis. Results: Leukocyte number and absolute neutrophil count were 1.8 and 2.2 fold higher in SCD compared to thalassemia (P<0.01). Evidence for decreased apoptosis in SCD included reduced nuleosome protein as compared to thalassemia and reduced Bax as compared to controls. In addition, LDH was significantly increased 1.9 fold in SCD relative to thalassemia (p=0.012). In contrast, NTBI was 2 fold higher in thalassemia than SCD and correlated with nucleosome protein (R=0.45; p=0.013). Finally, high levels of the cytokines IL-6 and IL-10 in SCD relative to thalassemia may be stimulating leukocyte proliferation and survival. These cytokines and hsCRP are also positively correlated with leukocyte number. Conclusions: These preliminary findings demonstrate that the balance of apoptosis vs. proliferation favors delayed cell death and enhanced cell proliferation in SCD, leading to increased circulating leukocytes. These changes may be related to hemolysis, increased levels of inflammatory cytokines, and lower amounts of NTBI in SCD. This leukocytosis increases the potential for vasoocclusive events that contribute to stroke, acute chest syndrome or renal tubule damage.

Degeneration and apoptosis of endometrial cells in the bitch

The relationships between changes in plasma progesterone concentrations, degeneration of the luminal epithelium, the occurrence of apoptosis of endometrial cells and endometrial leucocyte populations in the bitch were determined. Mature bitches ( n = 15) were euthanized and necropsied when in diestrus (Days 7–75, n = 12) or in anestrus (Days 10, 32 and 53). Degeneration of the luminal epithelium was observed in bitches in late diestrus (Days 38–75, n = 5) when plasma progesterone concentrations were decreasing and in anestrus (Days 10 and 32, n = 2) when plasma progesterone concentrations were <0.5 ng/mL. Endometrial leucocyte populations increased after degeneration of the luminal epithelium (around Day 42 of diestrus). Apoptosis was mainly observed in the basal glandular epithelial cells and endothelial cells of blood capillaries in all except anestrous bitches. Very few apoptotic cells were found in the superficial glandular epithelial cells and stromal cells. Higher apoptotic indices were detected in the basal glandular epithelium on Days 12–42 of diestrus than at other stages. Therefore, apoptosis of glandular basal epithelial cells occurred mainly in early diestrus, degeneration of cells of the luminal epithelium occurred from mid-diestrus to early anestrus, and the increase in leucocyte numbers may have been a consequence and not a cause of luminal epithelial degeneration.

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To investigate whether selective COX 2 inhibitors (celecoxib, rofecoxib) would play a role in a model of leukocyte migration in rats. Bacterial endotoxin (Escherichia coli LPS) was intraperitoneally injected at time zero in rats that were previously treated with unspecific and selective cyclooxygenase inhibitors. LPS induced a dose and time-dependent increase in leukocyte number, which was predominantly related to the presence of PMN neutrophils. Only rats treated with selective COX 2 inhibitors and indomethacin showed a significant reduction in leukocyte numbers following LPS administration. Prostaglandins E(2) and F(2alpha) were injected into the peritoneum and the chemoatractant effect was studied. Only PGF(2alpha) was able to induce neutrophil increase following injection. Intraperitoneal reposition of PGF(2alpha) restored the abrogated leukocyte response to LPS, shown by rats pretreated with rofecoxib. It can be concluded that COX 2, through PGF(2alpha) release, is the isoform responsible for neutrophil recruitment in the rat model of LPS-induced inflammation.

α2-Adrenoceptor Stimulation Transforms Immune Responses in Neuritis and Blocks Neuritis-Induced Pain

Neuropathic pain may be primarily driven by immune responses in peripheral nerves. Peripherally released catecholamines may exacerbate neuropathic pain and also modulate immune responses in a complex and sometimes opposing manner by actions on multiple adrenoceptor subtypes. We showed previously that injection of the alpha2-adrenoceptor agonist clonidine at the site of peripheral nerve injury reduces pain behavior and local tissue pro-inflammatory cytokine content in rats. The current study used a model of acute inflammatory neuritis to test the efficacy and mechanisms of action of alpha2-adrenoceptor stimulation to reduce pain. Zymosan, injected on the sciatic nerve, caused hypersensitivity to mechanical stimuli ipsilateral to injection and contralaterally, so-called mirror image pain. Ipsilateral hypersensitivity was inhibited dose-dependently by perineural injection of clonidine. Zymosan increased leukocyte number at the site of injection 3 d later as well as their content of interleukin 1alpha (IL-1alpha), IL-1beta, and IL-6. Perineural clonidine prevented both the increase in leukocyte number and cytokine expression induced by zymosan. Additionally, clonidine reduced the capacity of leukocytes to express pro-inflammatory cytokines as assessed by treatment of cells ex vivo with lipopolysaccharide, whereas no repression of IL-10 production occurred. Clonidine reduced the number of macrophages and lymphocytes as well as their expression of tumor necrosis factor alpha. All of the effects of clonidine were prevented by coadministration of an alpha2A-adrenoceptor-preferring antagonist. These results suggest that alpha2-adrenoceptor stimulation transforms cytokine gene expression, especially in macrophages and lymphocytes from a pro- to an anti-inflammatory profile in the setting of neuritis, likely relieving neuritis-induced pain by this mechanism.

Neurokinin-1 receptor mediates stress-exacerbated allergic airway inflammation and airway hyperresponsiveness in mice.

A wealth of clinical observation has suggested that stress and asthma morbidity are associated. We have previously established a mouse model of stress-exacerbated allergic airway inflammation, which reflects major clinical findings. The aim of the current study was to investigate the role of the neurokinin- (NK-)1 receptor in the mediation of stress effects in allergic airway inflammation. BALB/c mice were systemically sensitized with ovalbumin (OVA) on assay days 1, 14, and 21 and repeatedly challenged with OVA aerosol on days 26 and 27. Sound stress was applied to the animals for 24 hours, starting with the first airway challenge. Additionally, one group of stressed and one group of nonstressed mice received the highly specific NK-1 receptor antagonist RP 67580. Bronchoalveolar lavage fluid was obtained, and cell numbers and differentiation were determined. Airway hyperreactivity was measured in vitro by electrical field stimulation of tracheal smooth-muscle elements. Application of stress in sensitized and challenged animals resulted in a significant increase in leukocyte number in the bronchoalveolar lavage fluid. Furthermore, stressed animals showed enhanced airway reactivity. The increase of inflammatory cells and airway reactivity was blocked by treatment of animals with the NK-1 receptor antagonist. These data indicate that the NK-1 receptor plays an important role in mediating stress effects in allergen-induced airway inflammation.

Acute psychological stress: effects on chemotaxis and cellular adhesion molecule expression.

Activation of a psychological stress response increases autonomic activity and enhances immune function by inducing a significant increase in numbers of leukocytes at sites of inflammation. Chemotaxis and cellular adhesion are thought to mediate leukocyte trafficking. In this study, we examine the effects of an acute psychological stress on chemotactic responses of PBMCs and on CAM expression in relation to measures of sympathetic activation. Subjects underwent either a public speaking task (N = 24) or a control condition (N = 13). Blood was drawn before the task, immediately after, and 20 minutes after, the task for changes in percentage of cells expressing cellular adhesion molecules, chemotaxis to chemokines, HR, blood pressure, and E and NE levels. In response to the laboratory stressor, increases of PBMC chemotaxis to FMLP and SDF-1 were found, which were coupled with increases in the percentages of lymphocytes expressing the integrin Mac-1. Autonomic activity, including blood pressure and circulating levels of catecholamines, increased after administration of the stressor, and correlated with increases of Mac-1. These data show that acute stress induces increase of chemotaxis and expression of CAM expression, which may contribute to increased migration and recruitment of immune cells to sites of infection and/or inflammation.

Dietary Betaine Increases Intraepithelial Lymphocytes in the Duodenum of Coccidia-Infected Chicks and Increases Functional Properties of Phagocytes

Betaine is used by cells to defend against changes in osmolarity. We examined relationships among betaine, osmolarity and coccidiosis. In the first experiment, chicks were fed corn-soy diets containing 0.0, 0.5 or 1.0 g/kg betaine; half were challenged with Eimeria acervulina (Cocci). Cocci decreased weight gain and feed efficiency and increased the osmolarity of the duodenal and jejunal mucosa (P < 0.01). Betaine decreased osmolarity of the duodenum (P < 0.01), especially in Cocci-challenged birds. Cocci increased the thickness (P = 0.04) of and number (P < 0.01) of leukocytes in the duodenal lamina propria especially at high betaine levels (interaction P = 0.05). Villi height was decreased by Cocci (P = 0.05) and this was ameliorated by 1.0 g/kg betaine (interaction P = 0.04). Intraepithelial leukocyte numbers were increased by Cocci (P < 0.01) especially at 0.5 and 1 g/kg betaine. Peritoneal macrophages or peripheral blood heterophils were incubated in media with an osmolarity of 200, 310, 600 or 900 mOsmol and 0.0, 0.1, 0.5 or 1.5 mmol/L betaine (4 x 4 factorial) for 6 h and then E. acervulina were added. In general, phagocytosis and NO release were decreased and interleukin (IL)-1 and IL-6 release were increased in hyperosmotic media compared with isosmotic media. Betaine (0.1 mmol/L) increased NO release by heterophils (P = 0.04) and tended to increase (P < 0.1) NO release from macrophages. The chemotaxis of monocytes toward chemotactic factors released by heterophils was increased by betaine. Increased chemotaxis of monocytes and NO release by macrophages may explain the decreased intestinal pathology but increased leukocyte numbers that were observed when betaine was fed during a Cocci infection.

Experimental peritonitis in horses: peritoneal fluid composition

Sixteen adult horses were randomly divided into four equal groups of four animals and each group was injected intraperitoneally with one of the following suspension: Group I, 100×10(7) colony-forming units (CFU) of E. coli diluted in 500ml of 0.9% saline; Group II, 100×10(7) CFU of Bacteroides fragilis in 500ml of 0.9% saline; Group III, 100×10(7) CFU of E. coli in combination with 100×10(7) CFU of B. fragilis in 500ml of 0.9% saline; Group IV, 500ml of 0.9% saline. A significant increase in leukocyte number was observed in the peritoneal fluid by four hours after the inoculations in animals of Group I and II, and by eight hours in animals of Group III. The highest cell count observed was 516×10³ leukocytes/mm³. Significant increases in peritoneal fluid fibrinogen (1g/dl) and total protein (9.1%) concentrations were also observed. Horses inoculated with pure cultures of either E. coli or B. fragilis demonstrated mild and self-limiting peritonitis, while those inoculated with a combination of both bacteria demonstrated laboratory findings of higher intensity and duration.

A controlled study of leukocyte activation in septic patients.

Qualitative and quantitative evaluation of leukocyte activation in septic patients in comparison to two control groups. A prospective clinical study in which the leukocyte oxidative output of whole blood was measured in three groups of patients. Two chemiluminescence markers (luminol or lucigenin), indicative of either total oxidant output or superoxide production, and three stimuli (opsonized zymosan, formyl-methionyl-leucyl-phenylalanine (fMLP), phorbol myristate acetate) (PMA), representing different pathways of leukocyte activation, were used. Tumor necrosis factor, interleukin-6 and C-reactive protein (TNF, IL-6, and CRP) were determined to evaluate the severity of the inflammatory process. Intensive care and surgical units of a university hospital. Seventy-four healthy patients, ten ICU patients without signs of sepsis or systemic inflammatory response syndrome and 19 septic patients were studied. With all three stimuli, whole blood total oxidative output and superoxide production were generally increased in septic patients. This was most likely due to the increased leukocyte numbers in these patients. When the chemiluminescence values were normalized per phagocyte (granulocytes and monocytes), the total oxidative output of septic phagocytes decreased with opsonin and fMLP but increased with PMA, while superoxide output decreased regardless of the stimuli used. TNF, IL-6 and CRP, although increased in septic patients as compared to ICU controls, correlated weakly with oxidant output. The oxidative output of whole blood was increased in septic patients compared to controls because of elevated leukocyte numbers. However, oxidant output normalized for phagocyte numbers generally decreases during sepsis for most stimuli. Cytokines and CRP do not appear to be associated with the extent of oxidant output during sepsis.

Cellular and humoral immune response to exercise among gymnasts and untrained girls.

Recent studies reported reduced immunity in athletes following exercise. Physical activity affects both cellular and humoral immune functions. Scant information exists on exercise-induced changes in the immune system among children. The purpose of the present study was to investigate the effect of aerobic exercise on several aspects of cellular and humoral functions among 10-12 year-old highly trained female gymnasts (n = 7) and untrained girls (n = 6). All girls were pre-pubertal. Venous blood samples were drawn before, immediately after and 24 h following 20 min of treadmill running (heart rate 170-180 beats.min-1). White blood cells' number rose significantly following exercise and remained elevated for 24 h. The increase in leukocyte number was due to an increase in granulocytes as well as an increase in lymphocytes and monocytes. While neutrophil count returned to basal values after 24 h, lymphocytes and monocytes number remained elevated 24 h following exercise. Exercise resulted in a significant elevation of T cell lymphocytes, T helpers, T suppressors and natural killer cells. All values returned to normal after 24 h. There were no changes in B cell lymphocytes following exercise. Exercise had no effect on serum IgA, IgM, IgE, IgG and sub-types of IgG (IgG1, IgG2, IgG3 and IgG4). No differences were observed between gymnasts and untrained girls. In summary, the exercise-induced changes in cellular and humoral immune functions among the girls were generally similar to those described in adults. Whether the transitory effects of exercise on the immune system are related to increased susceptibility to illness is still questionable.

COMPLEX RELATIONS BETWEEN CORTICOSTEROIDS AND THE ADHESIVE STATE OF THE WHITE BLOOD CELLS IN THE PERIPHERAL BLOOD: FURTHER ANALYSIS OF THE STATE OF LEUKOCYTE/ADHESIVENESS AGGREGATION IN THE PERIPHERAL BLOOD AS A MARKER OF STRESS

Stress is associated with an increment in the concentration of cortisol, a leukocytotic response and increased state of leukocyte adhesiveness/aggregation (LAA) in the peripheral blood. We investigated the interrelationship between these three parameters in individuals under various conditions of stress. These included 123 emergency room patients with chest pain who were also classified in regard to the presence or absence of heart failure; 15 men in the fertility clinic donating semen and 16 women in the operating room before induction of anaesthesia for dilatation and curettage. A low (r=0.35) but significant (p<0.001) correlation was noted between cortisol level, leukocyte count, and per cent of aggregated leukocytes in the peripheral blood in the first group (ischaemic heart disease) but not the fertility clinic or operating room patients. A complementary study in dogs which received an intravenous hydrocortisone injection revealed neither an increased leukocyte number in the peripheral blood nor an increment in the adhesive state. In vitro studies confirmed the depressant effect of high concentrations of hydrocortisone on cell adhesiveness despite an increment in the expression of various adhesive proteins on the surface of the peripheral blood leukocytes. We concluded that the increased state of leukocyte adhesiveness noted by us in the past in patients under stress is not necessarily related to the presence of an increased cortisol concentration, and that factors other than corticosteroid level should be explored as possible triggers of the LAA response during stress. © 1997 by John Wiley & Sons, Ltd.