No Mandatory Role for the Spleen in the Exercise-Induced Leucocytosis in Man

1994 ◽  
Vol 86 (5) ◽  
pp. 505-510 ◽  
Author(s):  
P. O. Iversen ◽  
B. L. Arvesen ◽  
H. B. Benestad

1. Short-lasting strenuous physical exercise leads to a marked increase in the blood concentration of leucocytes in healthy humans. The cell sources of this leucocytosis have not been definitely identified, neither has the contribution made by the various subtypes of leucocytes. 2. We have compared the exercise-induced leucocytosis in six splenectomized and six intact subjects. The blood concentrations of leucocytes as well as of most subtypes, except monocytes and eosinophilic granulocytes, increased substantially at the end of a 5 min exercise (200 W) bout. 3. The increases were similar in the splenectomized subjects and in the control subjects. Thirty minutes after completion of the exercise the various leucocyte blood concentrations had returned to pre-exercise levels. 4. The plasma concentrations of several cytokines (interleukins-1α and −6; tumour necrosis factor-α and granulocyte colony-stimulating factor) known to affect leucocyte kinetics did not change appreciably with exercise in either group. 5. We conclude that exercise-induced leucocytosis can take place in the absence of the spleen. There was no evidence that cytokines known to affect leucocyte formation, mobilization and activity are involved in this leucocytosis.

2002 ◽  
Vol 30 (3) ◽  
pp. 269-274 ◽  
Author(s):  
A. A. Dahaba ◽  
G. A. Elawady ◽  
P. H. Rehak ◽  
W. F. List

Procalcitonin (PCT), interleukin-6 (IL-6), tumour necrosis factor α (TNFα), and interleukin-1β (IL-1β) are important clinical prognostic markers in ICU septic patients. The goal of the study was to determine whether continuous venovenous haemofiltration (CVVH), using an AN69 haemofilter, leads to elimination of PCT, TNFα, IL-6 and IL-1βin 13 septic patients with multi-organ failure. At the start of haemofiltration (0), 6 and 12 hours the mean afferent plasma concentration ±SD of PCT (10.1±9.1, 7±6, 5.9±5.7 ng/ml), IL-6 (804.6±847.6, 611.7±528.4, 575.2±539.2 pg/ml), and that of TNFα (4.5±2.6, 4±3.1, 3.8±2.9 pg/ml) significantly declined during CVVH. The efferent plasma concentrations were significantly lower than the corresponding afferent concentrations. PCT, IL-6 and TNFαwere detectable in the ultra-filtrate of all patients. IL-1βwas only detectable in the plasma of eight patients and the ultrafiltrate of five patients. The plasma clearance of PCT, IL-6 and TNFαsignificantly decreased after 12 hours as a result of a decline in the adsorptive elimination of the mediators due to progressive membrane saturation. We demonstrated that if PCT, IL-6 and TNFα are used as clinical prognostic markers in septic patients who are treated with CVVH using an AN69 membrane, one should be aware that their plasma level could be modified by the therapy. In addition CVVH could represent an appropriate tool to remove a broad spectrum of proinflammatory mediators, if such removal is required in septic patients.


2013 ◽  
Vol 3 (1) ◽  
pp. 6 ◽  
Author(s):  
Ted H. Elsasser ◽  
Stanislaw Kahl ◽  
Katie M. Lebold ◽  
Maret G. Traber ◽  
Jessica Shaffer ◽  
...  

While vitamin E has been used for decades in cattle diets, the principle form used traditionally is the synthetic α-isoform acetate or succinate and largely no data exist on the biological partitioning or functionality of the major naturally occurring γ- and δ-isoforms in cattle. Using tyrosine 3’-nitrated protein (pNT) as a biomarker of nitrosative cell stress, we sought to evaluate the effectiveness of short-term feeding supplementation of high content natural α-tocopherol (<em>α-T</em>, 96% α-isomer) compared to high content γ- and δ-enriched low α-content mixed tocopherol oils (<em>γ-T</em>, ~70% <em>γ-</em>, 20% δ-, &lt;5% α-isoform) to mitigate systemic and hepatic aspects of the proinflammatory response to endotoxin (LPS). Calves fed diets supplemented with <em>α-T</em>, <em>γ-T</em> for five days or no tocopherol supplement (<em>T0E</em>) were challenged with a low-level of LPS (0.25 μg/kg, iv, <em>E. coli </em>055:B5) sufficient to effect a liver nitration response. As fed,<em> α-T</em> or <em>γ-T</em> increased plasma and liver content of the respective tocopherols reflecting their relative abundance in the respective diets. Plasma or tissue mediators and biomarkers of the proinflammatory response [plasma concentrations of tumor necrosis factor-α (TNF-α, P&lt;0.001), nitrate+nitrite (NOx, P&lt;0.01), and serum amyloid A (SAA, P&lt;0.001)], and general liver content of pNT (P&lt;0.005) increased after LPS. LPS-mediated increases in TNF-α were not dif- ferent between diet treatments; both plasma NOx (P&lt;0.05) and generalized liver pNT (P&lt;0.03) responses were attenuated significantly in <em>α-T </em>and <em>γ-T versus T0E calves</em>. Plasma SAA was significantly decreased in γ-T calves at 24 h post-LPS relative to responses in <em>α-T</em> or <em>T0E </em>calves. The nitration of the mitochondrial proteins 24 h post-LPS was not only attenuated in <em>α-T</em> and <em>γ-T vs T0E</em>, but also the mitigating effect of <em>γ-T</em> on these specific nitration events was greater than that of <em>α-T </em>(P&lt;0.01). Results are consistent with the concept that short-term <em>α-T</em> or <em>γ-T</em> supplementation can effectively decrease proinflammatory liver pNT after LPS; some mitochondrial nitration targets may be better protected with prophylactic supplementation with γ-,δ-tocopherol enriched oil.


2017 ◽  
Vol 138 (1) ◽  
pp. 14-23 ◽  
Author(s):  
Yanan Cai ◽  
Zhangzhen Shi ◽  
Yuansong Bai

Rosai-Dorfman disease (RDD) is a rare histiocytosis typically with bilateral painless cervical lymphadenopathy. Laboratory data are nonspecific, and the presence of emperipolesis in large foamy S-100+ CD1a- histiocytes is the prominent histologic feature. The pathogenesis of RDD still remains elusive. According to published studies, we propose that RDD cells might represent intermediate recruiting monocytes with differentiation blockade. Both disturbance of homoeostasis and inherent genomic alterations could contribute to initiation of the disorder through signal transduction. Several inflammatory molecules such as macrophage colony-stimulating factor, IL-1β, IL-6, and tumor necrosis factor-α also play a pivotal role in the development of this rare entity. Additional studies are needed to further elucidate the essence of the disease.


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