Effects of acute exercise on expressions of functional receptors on CD56dim and CD56bright natural killer cells

PURPOSE: Mobilization and cytotoxicity of natural killer (NK) cells are regulated by cell surface receptors such as adhesion molecules and activating/inhibitory receptors. In this study, we examined the effects of acute exercise on the expression of these cell surface molecules and receptors. METHODS: Six healthy male college students (22.8 ± 0.8 years olds) exercised on the cycle ergometer for 30 min at intensities corresponding to the individual onset of blood lactate accumulation level (70-85%VO2max). Venous blood samples were collected at rest (PRE); just before the end of exercise (END) and 30 (POST 30), 60 (POST 60), 120 (POST 120) and 180 (POST 180) min post exercise. The densities of cell surface molecules and receptors on CD56dim and CD56bright NK cells were determined by flow cytometry. One-way ANOVA and MANOVA were used for statistical analyses. RESULTS: At PRE, expressions of CD16, CD56, CD44, CD62L, CD314, CD335, CD159a and CX3CR1 differed between CD56dim and CD56bright NK cells. Expressions of adhesion molecules CD62L and CX3CR1 changed significantly in both subsets during and after exercise. The expressions of CD62L tended to decrease at END, and then they increased significantly at POST 30. These changes were mainly due to the proportional changes in CD62Lnegative cells. The opposite patterns of changes were seen in the expressions of CX3CR1. Additionally, the expressions of CX3CR1 decreased at POST 120 and 180 only in CD56dim NK cells. The changes in the expressions of CD44 were similar to those seen in the expressions of CD62L. Although changes in the expression of adhesion molecules were statistically significant, they were relatively unclear in histogram analyses. With regard to the expressions of NK cell activating/inhibitory receptors, most changes were observed in CD56dim NK cells. The expressions of CD16 decreased at END and returned at POST 30. The expressions of CD212 dropped from END to POST 30. In contrast, the expressions of CD335 increased from END to POST 30. Exceptionally, changes in the expressions of CD226 were found in both subsets. The expressions decreased at POST180. CONCLUSION: These results suggest that acute exercise influences the expressions of cell surface molecules and receptors. Changes were mainly observed at END and POST 30 in CD56dim NK cell. However, the delayed changes were also seen in some receptors. The changes in several receptors were related to cell mobilization. In contrast, the changes in other receptors were not directly related to mobilization and cytotoxicity

Prehospital resuscitation with hypertonic saline-dextran modulates inflammatory, coagulation and endothelial activation marker profiles in severe traumatic brain injured patients

<p>Abstract</p> <p>Background</p> <p>Traumatic brain injury (TBI) initiates interrelated inflammatory and coagulation cascades characterized by wide-spread cellular activation, induction of leukocyte and endothelial cell adhesion molecules and release of soluble pro/antiinflammatory cytokines and thrombotic mediators. Resuscitative care is focused on optimizing cerebral perfusion and reducing secondary injury processes. Hypertonic saline is an effective osmotherapeutic agent for the treatment of intracranial hypertension and has immunomodulatory properties that may confer neuroprotection. This study examined the impact of hypertonic fluids on inflammatory/coagulation cascades in isolated head injury.</p> <p>Methods</p> <p>Using a prospective, randomized controlled trial we investigated the impact of prehospital resuscitation of severe TBI (GCS < 8) patients using 7.5% hypertonic saline in combination with 6% dextran-70 (HSD) <it>vs </it>0.9% normal saline (NS), on selected cellular and soluble inflammatory/coagulation markers. Serial blood samples were drawn from 65 patients (30 HSD, 35 NS) at the time of hospital admission and at 12, 24, and 48-h post-resuscitation. Flow cytometry was used to analyze leukocyte cell-surface adhesion (CD62L, CD11b) and degranulation (CD63, CD66b) molecules. Circulating concentrations of soluble (s)L- and sE-selectins (sL-, sE-selectins), vascular and intercellular adhesion molecules (sVCAM-1, sICAM-1), pro/antiinflammatory cytokines [tumor necrosis factor (TNF)-α and interleukin (IL-10)], tissue factor (sTF), thrombomodulin (sTM) and D-dimers (D-D) were assessed by enzyme immunoassay. Twenty-five healthy subjects were studied as a control group.</p> <p>Results</p> <p>TBI provoked marked alterations in a majority of the inflammatory/coagulation markers assessed in all patients. Relative to control, NS patients showed up to a 2-fold higher surface expression of CD62L, CD11b and CD66b on polymorphonuclear neutrophils (PMNs) and monocytes that persisted for 48-h. HSD blunted the expression of these cell-surface activation/adhesion molecules at all time-points to levels approaching control values. Admission concentrations of endothelial-derived sVCAM-1 and sE-selectin were generally reduced in HSD patients. Circulating sL-selectin levels were significantly elevated at 12 and 48, but not 24 h post-resuscitation with HSD. TNF-α and IL-10 levels were elevated above control throughout the study period in all patients, but were reduced in HSD patients. Plasma sTF and D-D levels were also significantly lower in HSD patients, whereas sTM levels remained at control levels.</p> <p>Conclusions</p> <p>These findings support an important modulatory role of HSD resuscitation in attenuating the upregulation of leukocyte/endothelial cell proinflammatory/prothrombotic mediators, which may help ameliorate secondary brain injury after TBI.</p> <p>Trial registration</p> <p>NCT00878631.</p

Hemorrhagic shock primes for increased expression of cytokine-induced neutrophil chemoattractant in the lung: role in pulmonary inflammation following lipopolysaccharide

Q2Q1440-447Recent studies have suggested that hemorrhagic shock followed by resuscitation renders patients more susceptible to lung injury by priming for an exaggerated response to a second stimulus, the so-called "two-hit" hypothesis. We investigated the role of C-X-C chemokines in mediating the augmented lung inflammation in response to LPS following resuscitated shock. In a rodent model, animals exposed to antecedent shock exhibited enhanced lung neutrophil sequestration and transpulmonary albumin flux in response to intratracheal LPS. This effect correlated with an exaggerated expression of cytokine-induced neutrophil chemoattractant (CINC) protein and mRNA, but not macrophage-inflammatory protein 2. Strategies designed to inhibit CINC, both anti-CINC Ab and supplementation with the antioxidant N-acetyl-cysteine, prevented the enhanced neutrophil sequestration, suggesting that CINC played a central role in the enhanced leukocyte accumulation following shock plus LPS treatment. Shock alone increased lung nuclear factor-kappaB expression and augmented the response to LPS. Prevention of this effect by N-acetylcysteine supplementation of the resuscitation fluid implicates a role for oxidant stress in the priming for lung inflammation following shock. Finally, alveolar macrophages recovered from shock-resuscitated animals released more CINC protein in vitro in response to LPS than macrophages from sham animals. Considered together, these findings show that augmented release of CINC, in part from primed alveolar macrophages, contributes significantly to the enhanced lung leukosequestration and transpulmonary albumin flux in response to LPS following resuscitated shock

The Cytokine response to physical activity and training

The mechanical properties of hydrogels are commonly modified by changing the concentration of the molecular components. This approach, however, does not only change hydrogel mechanics, but also the microstructure, which in turn alters the macroscopic properties of the gel. Here, the Hofmeister effect is used to change the thermoresponsiveness of polyisocyanide hydrogels. In contrast to previous Hofmeister studies, the effect is used to change the phase transition temperatures and to tailor the mechanics of the thermoresponsive (semiflexible) polymer gels. It is demonstrated that the gel stiffness can be manipulated over more than two orders of magnitude by the addition of salts. Surprisingly, the microstructure of the gels does not change upon salt addition, demonstrating that the Hofmeister effect provides an excellent route to change the mechanical properties without distorting other influential parameters of the gel. Salts are known to change the interactions between water and polymers and consequently change transition temperatures, an effect known as the Hofmeister effect. It is shown that beyond phase transition temperatures, ions can be used to tailor the linear and nonlinear mechanical behavior of hydrogels. A hundredfold stiffness increase is realized with gels of identical morphology

Temporal-spatial neural activation patterns linked to perceptual encoding of emotional salience.

It is well known that we continuously filter incoming sensory information, selectively allocating attention to what is important while suppressing distracting or irrelevant information. Yet questions remain about spatiotemporal patterns of neural processes underlying attentional biases toward emotionally significant aspects of the world. One index of affectively biased attention is an emotional variant of an attentional blink (AB) paradigm, which reveals enhanced perceptual encoding for emotionally salient over neutral stimuli under conditions of limited executive attention. The present study took advantage of the high spatial and temporal resolution of magnetoencephalography (MEG) to investigate neural activation related to emotional and neutral targets in an AB task. MEG data were collected while participants performed a rapid stimulus visual presentation task in which two target stimuli were embedded in a stream of distractor words. The first target (T1) was a number and the second (T2) either an emotionally salient or neutral word. Behavioural results replicated previous findings of greater accuracy for emotionally salient than neutral T2 words. MEG source analyses showed that activation in orbitofrontal cortex, characterized by greater power in the theta and alpha bands, and dorsolateral prefrontal activation were associated with successful perceptual encoding of emotionally salient relative to neutral words. These effects were observed between 250 and 550 ms, latencies associated with discrimination of perceived from unperceived stimuli. These data suggest that important nodes of both emotional salience and frontoparietal executive systems are associated with the emotional modulation of the attentional blink