scholarly journals Massage Therapy Modulates Inflammatory Mediators Following Sprint Exercise in Healthy Male Athletes

2020 ◽  
Vol 5 (1) ◽  
pp. 9
Author(s):  
Gillian E. White ◽  
Sarah L. West ◽  
Jessica E. Caterini ◽  
Alex P. Di Battista ◽  
Shawn G. Rhind ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Inflammatory Marker ◽  
Massage Therapy ◽  
Muscle Performance ◽  
Drop Jump ◽  
Healthy Male ◽  
Necrosis Factor Alpha ◽  
Male Athletes ◽  
Jump Performance ◽  
Baseline Levels

Massage therapy is a common postexercise muscle recovery modality; however, its mechanisms of efficacy are uncertain. We evaluated the effects of massage on systemic inflammatory responses to exercise and postexercise muscle performance and soreness. In this crossover study, nine healthy male athletes completed a high-intensity intermittent sprint protocol, followed by massage therapy or control condition. Inflammatory markers were assessed pre-exercise; postexercise; and at 1, 2, and 24 h postexercise. Muscle performance was measured by squat and drop jump, and muscle soreness on a Likert scale. Significant time effects were observed for monocyte chemoattractant protein-1 (MCP-1), interleukin-8 (IL-8), interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor alpha (TNFα), drop jump performance, squat jump performance, and soreness. No significant effects for condition were observed. However, compared with control, inflammatory marker concentrations (IL-8, TNFα, and MCP-1) returned to baseline levels earlier following the massage therapy condition (p < 0.05 for all). IL-6 returned to baseline levels earlier following the control versus massage therapy condition (p < 0.05). No differences were observed for performance or soreness variables. MCP-1 area under the curve (AUC) was negatively associated with squat and drop jump performance, while IL-10 AUC was positively associated with drop jump performance (p < 0.05 for all). In conclusion, massage therapy promotes resolution of systemic inflammatory signaling following exercise but does not appear to improve performance or soreness measurements.

Tumor Necrosis Factor Alpha Converting Enzyme (TACE) as Possible Therapeutic Target in SARS-CoV-2 Induced Acute Respiratory Distress Syndrome (ARDS)

2020 ◽  
Author(s):  
Joao Batista Junior
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Inflammatory Responses ◽  
Converting Enzyme ◽  
Necrosis Factor Alpha ◽  
Tace Inhibitors ◽  
Factor Alpha ◽  
Activity State ◽  
Necrosis Factor

<div>This study reveals, for the first time, that rosiglitazone and pioglitazone, two thiazolidinedione drugs already approved as therapeutic agents to treat type II diabetes, were found to bind favorably to tumor necrosis factor alpha converting enzyme catalytic site with highlighted binding features.</div><div><br></div>This study suggests that rosiglitazone and pioglitazone, acting as TACE inhibitors agents might avoid or attenuate the hyperexcitability proteolytic activity state of TACE, represent a new potential therapeutic approach to treat SARS-CoV-2 infection-associated severe systemic inflammatory responses observed among severely or critically ill SARS-CoV-2 patients and, consequently, to diminish severe inflammatory‐induced lung injury, ARDS development and death rates.<br><br>

scholarly journals Cardioprotective Effect of Linalool against Isoproterenol-Induced Myocardial Infarction

Life ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 120
Author(s):  
Maged E. Mohamed ◽  
Mohamed S. Abduldaium ◽  
Nancy S. Younis
Keyword(s):  
Myocardial Infarction ◽  
Molecular Mechanisms ◽  
Inflammatory Responses ◽  
Antioxidant Activities ◽  
Interleukin 1 ◽  
Cardioprotective Effect ◽  
Cardiac Enzymes ◽  
Necrosis Factor Alpha ◽  
Group Iii ◽  
Apoptotic Markers

Background: Myocardial infarction (MI), a life-threatening disorder, arises from the imbalance between oxygen supply and myocardial demand. Linalool is a naturally occurring monoterpenes with proved numerous pharmacological actions. This study investigated the cardioprotective effect of Linalool on isoproterenol (ISO)-induced MI in rat models and explored part of the underlying molecular mechanisms. Methods: Rats were divided into five groups; groups I and II served as normal and linalool control groups, Group III administered ISO alone; groups V and VI received two different doses of Linalool and were challenged by ISO. Different biochemical parameters were determined, including hemodynamic, infarction size, cardiac enzymes, apoptotic markers, and inflammatory mediators. Results: Linalool limited the infarcted area size and diminished the elevated cardiac enzymes. Linalool escalated HO-1 and Nrf2, both nuclear and cytosol fractions, and reduced Keap 1. Linalool enhanced cardiac antioxidant activities, reduced inflammatory cytokines (tumor necrosis factor-alpha (TNF-α), nuclear factor-κ-B (NF-κB), interleukin 1 beta (IL-1β), interleukin 6 (IL-6)), apoptotic markers (Caspase-3, Caspase-9, and Bax), and elevated Bcl2. Conclusion: Linalool could act as an effective cardioprotective agent in the MI model through improving the oxidative condition, probably via the Nrf2/HO-1 pathway and by abolishing both apoptotic and inflammatory responses.

scholarly journals Scutellaria baicalensis Alleviates Insulin Resistance in Diet-Induced Obese Mice by Modulating Inflammation

2019 ◽  
Vol 20 (3) ◽  
pp. 727 ◽  
Author(s):  
Hyun-Young Na ◽  
Byung-Cheol Lee
Keyword(s):  
Insulin Resistance ◽  
Inflammatory Responses ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Postprandial Glucose ◽  
Scutellaria Baicalensis ◽  
Necrosis Factor Alpha ◽  
Insulin Resistant ◽  
The Metabolic Syndrome ◽  
Epididymal Fat

Insulin resistance is strongly associated with the metabolic syndrome, and chronic inflammation is known to be a major mechanism of insulin resistance and is a therapeutic target. This study was designed to evaluate the effect of Scutellaria baicalensis (SB) in high-fat diet (HFD)-induced insulin-resistant mice and to investigate its mechanism based on inflammatory responses. Mice were fed a HFD to induce insulin resistance and then administered SB for nine weeks. Body weight, glucose, lipid, insulin, epididymal fat pad and liver weights, and histologic characteristics were evaluated to determine the effect on insulin resistance. In order to evaluate the effects on the inflammatory process, we analyzed the proportions of macrophages in liver and epididymal fat and measured inflammatory gene expression. Fasting and postprandial glucose, fasting insulin, HOMA-IR, triglycerides, and low density lipoprotein cholesterol levels were significantly decreased by SB administration. The epididymal fat and liver showed significant weight decreases and histological improvements. Total adipose tissue macrophages (ATMs) decreased (27.71 ± 3.47% vs. 45.26 ± 7.26%, p < 0.05), M2 ATMs increased (47.02 ± 6.63% vs. 24.28 ± 8.00%, p < 0.05), and CD11b+ Kupffer cells decreased. The expression levels of tumor necrosis factor alpha and F4/80 in the liver were significantly decreased (12.03 ± 1.47% vs. 25.88 ± 4.57%, p < 0.05) compared to HFD group. These results suggest that SB improved insulin resistance through inhibition of macrophage-mediated inflammation.

scholarly journals CD4+ CD25+ Foxp3+ Regulatory T Cells, Dendritic Cells, and Circulating Cytokines in Uncomplicated Malaria: Do Different Parasite Species Elicit Similar Host Responses?

2010 ◽  
Vol 78 (11) ◽  
pp. 4763-4772 ◽  
Author(s):  
Raquel M. Gonçalves ◽  
Karina C. Salmazi ◽  
Bianca A. N. Santos ◽  
Melissa S. Bastos ◽  
Sandra C. Rocha ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Parasite Species ◽  
Inflammatory Responses ◽  
Clinical Symptoms ◽  
Clinical Manifestations ◽  
Surface Expression ◽  
Interleukin 10 ◽  
Treg Cells ◽  
Experimental Models ◽  
Necrosis Factor Alpha

ABSTRACT Clearing blood-stage malaria parasites without inducing major host pathology requires a finely tuned balance between pro- and anti-inflammatory responses. The interplay between regulatory T (Treg) cells and dendritic cells (DCs) is one of the key determinants of this balance. Although experimental models have revealed various patterns of Treg cell expansion, DC maturation, and cytokine production according to the infecting malaria parasite species, no studies have compared all of these parameters in human infections with Plasmodium falciparum and P. vivax in the same setting of endemicity. Here we show that during uncomplicated acute malaria, both species induced a significant expansion of CD4+ CD25+ Foxp3+ Treg cells expressing the key immunomodulatory molecule CTLA-4 and a significant increase in the proportion of DCs that were plasmacytoid (CD123+), with a decrease in the myeloid/plasmacytoid DC ratio. These changes were proportional to parasite loads but correlated neither with the intensity of clinical symptoms nor with circulating cytokine levels. One-third of P. vivax-infected patients, but no P. falciparum-infected subjects, showed impaired maturation of circulating DCs, with low surface expression of CD86. Although vivax malaria patients overall had a less inflammatory cytokine response, with a higher interleukin-10 (IL-10)/tumor necrosis factor alpha (TNF-α) ratio, this finding did not translate to milder clinical manifestations than those of falciparum malaria patients. We discuss the potential implications of these findings for species-specific pathogenesis and long-lasting protective immunity to malaria.

scholarly journals Toxoplasma gondii Cyclophilin 18-Mediated Production of Nitric Oxide Induces Bradyzoite Conversion in a CCR5-Dependent Manner

2009 ◽  
Vol 77 (9) ◽  
pp. 3686-3695 ◽  
Author(s):  
Hany M. Ibrahim ◽  
Hiroshi Bannai ◽  
Xuenan Xuan ◽  
Yoshifumi Nishikawa
Keyword(s):  
Nitric Oxide ◽  
Toxoplasma Gondii ◽  
Inflammatory Responses ◽  
Interleukin 12 ◽  
Dependent Manner ◽  
Independent Manner ◽  
Necrosis Factor Alpha ◽  
Parasite Multiplication ◽  
Factor Alpha

ABSTRACT Toxoplasma gondii modulates pro- and anti-inflammatory responses to regulate parasite multiplication and host survival. Pressure from the immune response causes the conversion of tachyzoites into slowly dividing bradyzoites. The regulatory mechanisms involved in this switch are poorly understood. The aim of this study was to investigate the immunomodulatory role of T. gondii cyclophilin 18 (TgCyp18) in macrophages and the consequences of the cellular responses on the conversion machinery. Recombinant TgCyp18 induced the production of nitric oxide (NO), interleukin-12 (IL-12), and tumor necrosis factor alpha through its binding with cysteine-cysteine chemokine receptor 5 (CCR5) and the production of gamma interferon and IL-6 in a CCR5-independent manner. Interestingly, the treatment of macrophages with TgCyp18 resulted in the inhibition of parasite growth and an enhancement of the conversion into bradyzoites via NO in a CCR5-dependent manner. In conclusion, T. gondii possesses sophisticated mechanisms to manipulate host cell responses in a TgCyp18-mediated process.

scholarly journals Oral Mucosal Endotoxin Tolerance Induction in Chronic Periodontitis

2005 ◽  
Vol 73 (2) ◽  
pp. 687-694 ◽  
Author(s):  
Manoj Muthukuru ◽  
Ravi Jotwani ◽  
Christopher W. Cutler
Keyword(s):  
Immune Response ◽  
Oral Mucosa ◽  
Chronic Periodontitis ◽  
Intracellular Signaling ◽  
Inflammatory Responses ◽  
Endotoxin Tolerance ◽  
Necrosis Factor Alpha ◽  
Initial Stimulus ◽  
Tlr4 Mrna ◽  
Tnf Α

ABSTRACT The oral mucosa is exposed to a high density and diversity of gram-positive and gram-negative bacteria, but very little is known about how immune homeostasis is maintained in this environment, particularly in the inflammatory disease chronic periodontitis (CP). The cells of the innate immune response recognize bacterial structures via the Toll-like receptors (TLR). This activates intracellular signaling and transcription of proteins essential for the induction of an adaptive immune response; however, if unregulated, it can lead to destructive inflammatory responses. Using single-immunoenzyme labeling, we show that the human oral mucosa (gingiva) is infiltrated by large numbers of TLR2+ and TLR4+ cells and that their numbers increase significantly in CP, relative to health (P < 0.05, Student's t test). We also show that the numbers of TLR2+ but not TLR4+ cells increase linearly with inflammation (r 2 = 0.33, P < 0.05). Double-immunofluorescence analysis confirms that TLR2 is coexpressed by monocytes (MC)/macrophages (mφ) in situ. Further analysis of gingival tissues by quantitative real-time PCR, however, indicates that despite a threefold increase in the expression of interleukin-1β (IL-1β) mRNA during CP, there is significant (30-fold) downregulation of TLR2 mRNA (P < 0.05, Student's t test). Also showing similar trends are the levels of TLR4 (ninefold reduction), TLR5 (twofold reduction), and MD-2 (sevenfold reduction) mRNA in CP patients compared to healthy persons, while the level of CD14 was unchanged. In vitro studies with human MC indicate that MC respond to an initial stimulus of lipopolysaccharide (LPS) from Porphyromonas gingivalis (PgLPS) or Escherichia coli (EcLPS) by upregulation of TLR2 and TLR4 mRNA and protein; moreover, IL-1β mRNA is induced and tumor necrosis factor alpha (TNF-α), IL-10, IL-6, and IL-8 proteins are secreted. However, restimulation of MC with either PgLPS or EcLPS downregulates TLR2 and TLR4 mRNA and protein and IL-1β mRNA and induces a ca. 10-fold reduction in TNF-α secretion, suggesting the induction of endotoxin tolerance by either LPS. Less susceptible to tolerance than TNF-α were IL-6, IL-10, and IL-8. These studies suggest that certain components of the innate oral mucosal immune response, most notably TLRs and inflammatory cytokines, may become tolerized during sustained exposure to bacterial structures such as LPS and that this may be one mechanism used in the oral mucosa to attempt to regulate local immune responses.

scholarly journals Inflammatory Biomarkers Predictive of Metabolic Syndrome in a Nigerian Population: A Case-Control Study

2020 ◽  
Vol 6 (4) ◽  
pp. 382-390
Author(s):  
EN Adejumo ◽  
OA Adejumo ◽  
OA Ogundahunsi
Keyword(s):  
Metabolic Syndrome ◽  
Case Control Study ◽  
Inflammatory Marker ◽  
Characteristic Curve ◽  
Area Under The Curve ◽  
Case Control ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Hs Crp ◽  
Control Study

Background: Inflammation is linked to the aetiopathogenesis of Metabolic syndrome (MetS). Objective: To assess the ability of high sensitivity C-Reactive Protein (hs-CRP), Tumour Necrosis Factor-alpha (TNFα) and Interleukin-6 (IL-6) to predict MetS. Methods: A case-control study involving 123 subjects with MetS (cases) and age-matched 123 subjects. without MetS (controls) was conducted. The levels of TNFα, IL-6, and hs-CRP between independent groups were compared. The Receiver Operative Characteristic Curve was used to assess the ability of inflammatory markers to discriminately identify MetS. Results: The mean age of the case and control groups was 49.9±0.9 years and 48.1±1.1 years (p = 0.274) respectively. The median levels of TNFα, IL-6 and hS-CRP were significantly higher among the cases than the control group in both genders (p <0.001). There was a significant increase in the serum values of the markers with increasing components of MetS (p <0.001). The Area Under the Curve of TNFα, IL-6 and hs-CRP was > 0.9 in both males and females. Conclusion: TNFα, IL-6, and hs-CRP identified MetS. There is a need for further studies to determine the inflammatory marker most predictive of MetS.

scholarly journals Toll-Like Receptor Signaling in Airborne Burkholderia thailandensis Infection

2009 ◽  
Vol 77 (12) ◽  
pp. 5612-5622 ◽  
Author(s):  
T. Eoin West ◽  
Thomas R. Hawn ◽  
Shawn J. Skerrett
Keyword(s):  
Low Dose ◽  
Inflammatory Responses ◽  
High Dose ◽  
Tlr Signaling ◽  
Necrosis Factor Alpha ◽  
Airborne Infection ◽  
Essential Components ◽  
High Doses

ABSTRACT Melioidosis is a tropical disease endemic in southeast Asia and northern Australia caused by the gram-negative soil saprophyte Burkholderia pseudomallei. Although infection is often systemic, the lung is frequently involved. B. thailandensis is a closely related organism that at high doses causes lethal pneumonia in mice. We examined the role of Toll-like receptors (TLRs), essential components of innate immunity, in vitro and in vivo during murine B. thailandensis pneumonia. TLR2, TLR4, and TLR5 mediate NF-κB activation by B. thailandensis in transfected HEK293 or CHO cells. In macrophages, TLR4 and the adaptor molecule MyD88, but not TLR2 or TLR5, are required for tumor necrosis factor alpha production induced by B. thailandensis. In low-dose airborne infection, TLR4 is needed for early, but not late, bacterial containment, and MyD88 is essential for control of infection and host survival. TLR2 and TLR5 are not necessary to contain low-dose infection. In high-dose airborne infection, TLR2 deficiency confers a slight survival advantage. Lung and systemic inflammatory responses are induced by low-dose inhaled B. thailandensis independently of individual TLRs or MyD88. These findings suggest that redundancy in TLR signaling or other MyD88-dependent pathways may be important in pneumonic B. thailandensis infection but that MyD88-independent mechanisms of inflammation are also activated. TLR signaling in B. thailandensis infection is substantially comparable to signaling induced by virulent B. pseudomallei. These studies provide additional insights into the host-pathogen interaction in pneumonic Burkholderia infection.

Changes of Whole-Body Power, Muscle Function, and Jump Performance With Prolonged Cycling to Exhaustion

2012 ◽  
Vol 7 (4) ◽  
pp. 332-339 ◽  
Author(s):  
Jordan P.R. McIntyre ◽  
Grant A. Mawston ◽  
Simeon P. Cairns
Keyword(s):  
Performance Measures ◽  
Muscle Function ◽  
Perceived Exertion ◽  
Rest Period ◽  
Whole Body ◽  
Peak Power Output ◽  
Time To Exhaustion ◽  
Drop Jump ◽  
Jump Performance ◽  
Isokinetic Torque

Purpose:To quantify how whole-body power, muscle-function, and jump-performance measures change during prolonged cycling and recovery and determine whether there are relationships between the different fatigue measures.Methods:Ten competitive or recreationally active male cyclists underwent repeated 20-min stages of prolonged cycling at 70% VO2peak until exhaustion. Whole-body peak power output (PPO) was assessed using an all-out 30-s sprint 17 min into each cycle stage. Ratings of perceived exertion (RPE) were recorded throughout. Isometric and isokinetic muscle-function tests were made between cycle stages, over ~6 min, and during 30-min recovery. Drop-jump measures were tested at exhaustion and during recovery.Results:PPO initially increased or was maintained in some subjects but fell to 81% of maximum at exhaustion. RPE was near maximal (18.7) at exhaustion, with the time to exhaustion related to the rate of rise of RPE. PPO first started to decline only when RPE exceeded 16 (ie, hard). Peak isometric and concentric isokinetic torque (180°/s) for the quadriceps fell to 86% and 83% of pretest at exhaustion, respectively. In contrast, the peak concentric isokinetic torque (180°/s) of the hamstrings increased by 10% before declining to 93% of maximum. Jump height fell to 92% of pretest at exhaustion and was correlated with the decline in PPO (r = .79). Muscle-function and jump-performance measures did not recover over the 30-min postexercise rest period.Conclusions:At exhaustion, whole-body power, muscle-function, and jump-performance measures had all fallen by 7–19%. PPO and drop-jump decrements were linearly correlated and are appropriate measures of maximal performance.

Effects of Individualized Versus Traditional Power Training on Strength, Power, Jump Performances, and Body Composition in Young Male Nordic Athletes

2021 ◽  
pp. 1-8
Author(s):  
Olaf Prieske ◽  
Helmi Chaabene ◽  
Niclas Kullmann ◽  
Urs Granacher
Keyword(s):  
Body Composition ◽  
Muscle Strength ◽  
Young Male ◽  
Drop Jump ◽  
Power Training ◽  
Strength Index ◽  
Jump Performance ◽  
Back Squat ◽  
Main Effects ◽  
Regular Training

Purpose: This study aimed to examine the effects of individualized-load power training (IPT) versus traditional moderate-load power training (TPT) on strength, power, jump performance, and body composition in elite young Nordic athletes. Methods: In a randomized crossover design, 10 young male athletes (ski jumpers, Nordic combined athletes) age 17.5 (0.6) years (biological maturity status: +3.5 y postpeak height velocity) who competed on a national or international level performed 5 weeks of IPT (4 × 5 repetitions at 49%–72% 1-repetiton maximum [RM]) and TPT (5 × 5 repetitions at 50%–60% 1-RM) in addition to their regular training. Testing before, between, and after both training blocks comprised the assessment of muscle strength (loaded back squat 3-RM), power (maximal loaded back squat power), jump performance (eg, drop-jump height, reactive strength index), and body composition (eg, skeletal muscle mass). Results: Significant, large-size main effects for time were found for muscle strength (P < .01; g = 2.7), reactive strength index (P = .03; g = 1.6), and drop-jump height (P = .02; g = 1.9) irrespective of the training condition (IPT, TPT). No significant time-by-condition interactions were observed. For measures of body composition, no significant main effects of condition and time or time-by-condition interactions were found. Conclusions: Our findings demonstrate that short-term IPT and TPT at moderate loads in addition to regular training were equally effective in improving measures of muscle strength (loaded back squat 3-RM) and vertical-jump performance (reactive strength index, drop jump, and height) in young Nordic athletes.

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