IL-10 Plasma Levels are Elevated After LPS Injection in Splenectomized A/J Mice1

Torres, Manuel B.; Vega, Virginia L.; Bedri, Mazen I.; Saad, Daniel F.; Trentzsch, Heiko; Reeves, Roger H.; Maio, Antonio De

doi:10.1016/j.jss.2005.06.008

Cited by 10 publications

(9 citation statements)

References 23 publications

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“…IL-10 levels detected in our assay were much higher compared with the values observed by others (42). It has been reported that antiinflammatory strategies applied early in patients with a hyperinflammatory immune response may prove to be lifesaving (43).…”

Section: Antiinflammatory Cytokine Profilescontrasting

confidence: 60%

Plasma Cytokine Profiles in Preprotachykinin-A Knockout Mice Subjected to Polymicrobial Sepsis

Hegde

Uttamchandani

Moochhala

et al. 2009

Mol Med

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During the course of polymicrobial sepsis, a range of pro-and antiinflammatory cytokines are produced by the host immune system. Successful recovery from sepsis involves striking a balance between these counteracting cytokines. We herein investigated the circulating cytokine profiles in preprotachykinin-A knockout (PPTA -/-) mice, which have been found to be protected significantly against microbial sepsis, by employing multiplexed bead-based suspension arrays for the measurement of 18 plasma cytokines. Four sets of PPTA -/-and wild-type mice, each with six mice, were subjected to cecal ligation and puncture-induced sepsis or a sham procedure and were killed at 1, 5, 8 and 24 h post surgery. The cytokine profiles revealed, rather interestingly, that both pro-and antiinflammatory cytokines were elevated in the knockout group in response to a septic challenge. The higher systemic levels of both pro-and antiinflammatory cytokines in PPTA -/-septic mice was similar to the increase that we observed earlier in lung tissue of PPTA -/-mice after induction of sepsis. Thus, elevated levels of both pro-and antiinflammatory mediators may act simultaneously and help to resolve the infectious assault at the early stages of sepsis without excessively damaging the host tissue in PPTA -/-mice. In addition, our results underline the importance of comprehensive clinical analysis of multiple biomarkers to provide a better prognostic tool.

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Section: Antiinflammatory Cytokine Profilescontrasting

confidence: 60%

Plasma Cytokine Profiles in Preprotachykinin-A Knockout Mice Subjected to Polymicrobial Sepsis

Hegde

Uttamchandani

Moochhala

et al. 2009

Mol Med

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“…Pilot studies were performed before the actual concentration of IL-10 was selected; 30 ng/ml IL-10 showed no effect on the improvement of the endothelium-dependent ACh-induced relaxation. Hence, supraphysiological levels of IL-10 (300 ng/ml) were selected for this study, although previous studies have suggested that the plasma level of IL-10 is ϳ4 -6 ng/ml (41).…”

Section: Methodsmentioning

confidence: 99%

Interleukin-10 counteracts impaired endothelium-dependent relaxation induced by ANG II in murine aortic rings

Zemse

Hilgers

Webb³

2007

American Journal of Physiology-Heart and Circulatory Physiology

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ANG II stimulates the production of reactive oxygen species and activates proinflammatory cytokines leading to endothelial dysfunction. We hypothesized that the anti-inflammatory cytokine IL-10 counteracts the impairment in endothelium-dependent ACh relaxation caused by ANG II. Aortic rings of C57BL/6 mice were incubated in DMEM in the presence of vehicle (deionized H(2)O), ANG II (100 nmol/l), recombinant mouse IL-10 (300 ng/ml), or both ANG II and IL-10 for 22 h at 37 degrees C. After incubation, rings were mounted in a wire myograph to assess endothelium-dependent vasorelaxation to cumulative concentrations of ACh. Overnight exposure of aortic rings to ANG II resulted in blunted ACh-induced vasorelaxation compared with that shown in untreated rings (maximal response = 44 +/- 3% vs. 64 +/- 3%, respectively; P<0.05). IL-10 treatment significantly restored this impairment in relaxation (63 +/- 2%). In addition, the NADPH oxidase inhibitor apocynin restored the impairment in relaxation (maximal response = 76 +/- 3%). Western blotting showed increased gp91(phox) expression (a subunit of NADPH oxidase) in response to ANG II. Vessels treated with a combination of ANG II and IL-10 showed decreased expression of gp91(phox). Immunohistochemical analysis showed increased gp91(phox) expression in ANG II-treated vessels compared with those treated with combined ANG II and IL-10. We found that the anti-inflammatory cytokine IL-10 prevents impairment in endothelium-dependent vasorelaxation in response to long-term incubation with ANG II via decreasing NADPH oxidase expression.

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“…The literature on leukocytes’ inflammatory responses upon AR engagement or catecholamine stimulation is largely variable such that catecholamines induce both pro- (e.g., Flierl et al, 2008; Kavelaars et al, 1997; Torres et al, 2005) and anti-inflammatory (e.g., Hu et al, 1991; van der Poll et al, 1994) responses by immune cells. These seemingly contradictory effects of catecholamines on inflammatory responses appear to depend on a number of factors (see Padro & Sanders, 2014 for review), including AR subtype (Hanke et al, 2012; Heijnen et al, 1996), AR agonist concentrations (e.g., Szelenyi et al, 2000), and the timing of AR engagement in relation to antigen stimulation (Sanders, 2012).…”

Section: Introductionmentioning

confidence: 99%

Beta-adrenergic receptor mediated inflammation control by monocytes is associated with blood pressure and risk factors for cardiovascular disease

Hong

Dimitrov

Cheng

et al. 2015

Brain, Behavior, and Immunity

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Overwhelming data indicate that individuals with even mildly elevated blood pressure (BP) are at great risk for developing clinical hypertension and future cardiovascular disease (CVD). There remains a lack of consensus regarding treatment strategies for mildly elevated BP, termed prehypertension, and the knowledge of pathophysiology and mechanisms of its clinical outcomes remains limited. Our primary aim was to investigate βAR-mediated inflammation control (BARIC) responses of blood monocytes to isoproterenol (Iso) in relation to BP and CVD risk factors, including obesity, depressive mood, fasting glucose, triglycerides, and cholesterol levels in the 64 prehypertensive compared to 84 individuals with normal BP. BARIC was determined by measuring the degree of inhibition in lipopolysaccharides-stimulated monocytic intracellular TNF production by ex vivo Iso treatment (10−8 M). Depressive mood was assessed by Beck Depression Inventory (BDI). Fasting metabolic and lipid panels were assessed, and plasma levels of inflammatory cytokines TNF, IL-1β, IL-6 were measured in a subset to confirm proinflammatory state of prehypertensive participants. Prehypertensive participants were older, heavier, included more men, and presented higher levels of fasting glucose, triglycerides, cholesterol, and plasma TNF compared to normotensive participants (p’s< .05). BARIC was significantly attenuated in the prehypertensive compared to normotensive group (p< .05). BARIC was negatively associated with systolic BP, diastolic BP, age, BMI, fasting glucose, triglycerides, total and low density cholesterol levels, and somatic depressive symptoms in all participants (p’s< .0001 to .05). However, among the prehypertensive individuals BARIC was positively associated with SBP even after controlling for the covariates (age, gender, race, BMI, glucose and lipid panel, somatic BDI scores) (p< .05). This differing nature of the BARIC-SBP relationship between the two BP groups may be attributed to moderating factors such as cardiorespiratory fitness or depressive symptoms that could not be clearly deciphered in this current study. Nonetheless, our findings indicate the associations between inflammation dysregulation mediated by sympathoadrenal activation and BP that is observable even among individuals with normal to mildly elevated BP. BARIC may be a useful and sensitive indicator of elevated risk for vascular inflammatory disease that can be detected even at lower BP levels, especially given its associations with traditional CVD risk factors and the critical role of monocytes in atherogenic processes.

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IL-10 Plasma Levels are Elevated After LPS Injection in Splenectomized A/J Mice1

Cited by 10 publications

References 23 publications

Plasma Cytokine Profiles in Preprotachykinin-A Knockout Mice Subjected to Polymicrobial Sepsis

Plasma Cytokine Profiles in Preprotachykinin-A Knockout Mice Subjected to Polymicrobial Sepsis

Interleukin-10 counteracts impaired endothelium-dependent relaxation induced by ANG II in murine aortic rings

Beta-adrenergic receptor mediated inflammation control by monocytes is associated with blood pressure and risk factors for cardiovascular disease

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