scholarly journals Time-Dependent Changes in Local and Serum Levels of Inflammatory Cytokines as Markers for Incised Wound Aging of Skeletal Muscles

2018 ◽  
Vol 245 (1) ◽  
pp. 29-35 ◽  
Author(s):  
Mohammed Hassan Gaballah ◽  
Tetsuya Horita ◽  
Masataka Takamiya ◽  
Keisuke Yokoji ◽  
Mamiko Fukuta ◽  
...  
2020 ◽  
Vol 16 (4) ◽  
pp. 470-480
Author(s):  
Cristina T. Roth-Stefanski ◽  
Carla Dolenga ◽  
Lia S. Nakao ◽  
Roberto Pecoits-Filho ◽  
Thyago P. de Moraes ◽  
...  

Background: Bacterial metabolism contributes to the generation of uremic toxins in patients with chronic kidney disease (CKD). It has been investigated the use of probiotics in the reduction of uremic toxins intestinal production. Objective: The aim of this pilot study was to evaluate the effect of probiotic supplementation on reducing the production of uremic toxins and the inflammatory profile of CKD patients. Methods: We performed a randomized, blind, placebo-controlled, crossover study on patients with CKD stages 3 and 4. The intervention was a probiotic formulation composed of Lactobacillus acidophilus strains given orally three times a day for 3 months. Changes in uremic toxins (p-Cresylsulfate and Indoxyl Sulfate) and serum inflammatory cytokines were the primary endpoints. Results: Of the 44 patients randomized, 25 completed the study (mean age 51 ± 9.34, 64% female, mean eGFR 36 ± 14.26 mL/min/1.73m², mean BMI 28.5 ± 5.75 kg/m²). At 3 months, there were no significant changes in any of the studied biomarkers including p-cresylsulfate (p = 0.57), Indoxyl sulfate (p = 0.08) and interleukin-6 (p = 0.55). Conclusion: Lactobacillus acidophilus strains given as probiotic were not able to reduce serum levels of uremic toxins and biomarkers of inflammation in CKD patients in stage 3 and 4.


Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1686
Author(s):  
Adelaida M. Celaya ◽  
Lourdes Rodríguez-de la Rosa ◽  
Jose M. Bermúdez-Muñoz ◽  
José M. Zubeldia ◽  
Carlos Romá-Mateo ◽  
...  

Insulin-like growth factor 1 (IGF-1) deficiency is an ultrarare syndromic human sensorineural deafness. Accordingly, IGF-1 is essential for the postnatal maturation of the cochlea and the correct wiring of hearing in mice. Less severe decreases in human IGF-1 levels have been associated with other hearing loss rare genetic syndromes, as well as with age-related hearing loss (ARHL). However, the underlying mechanisms linking IGF-1 haploinsufficiency with auditory pathology and ARHL have not been studied. Igf1-heterozygous mice express less Igf1 transcription and have 40% lower IGF-1 serum levels than wild-type mice. Along with ageing, IGF-1 levels decreased concomitantly with the increased expression of inflammatory cytokines, Tgfb1 and Il1b, but there was no associated hearing loss. However, noise exposure of these mice caused increased injury to sensory hair cells and irreversible hearing loss. Concomitantly, there was a significant alteration in the expression ratio of pro- and anti-inflammatory cytokines in Igf1+/− mice. Unbalanced inflammation led to the activation of the stress kinase JNK and the failure to activate AKT. Our data show that IGF-1 haploinsufficiency causes a chronic subclinical proinflammatory age-associated state and, consequently, greater susceptibility to stressors. This work provides the molecular bases to further understand hearing disorders linked to IGF-1 deficiency.


Author(s):  
Bhagirath Ramawat ◽  
Alvee Saluja ◽  
Jayashree Bhatacharjee ◽  
Anshuman Srivastava ◽  
Rajinder K. Dhamija

Blood ◽  
2009 ◽  
Vol 113 (15) ◽  
pp. 3512-3519 ◽  
Author(s):  
Roberta Caruso ◽  
Carmine Stolfi ◽  
Massimiliano Sarra ◽  
Angelamaria Rizzo ◽  
Massimo C. Fantini ◽  
...  

Abstract IL-25, a member of the IL-17 cytokine family, is known to enhance Th2-like responses associated with increased serum levels of IgE, IgG1, IgA, blood eosinophilia, and eosinophilic infiltrates in various tissues. However, IL-25 also abrogates inflammatory responses driven by Th17 cells. However, the cell types that respond to IL-25 and the mechanisms by which IL-25 differentially regulates immune reactions are not well explored. To identify potential targets of IL-25, we initially examined IL-25 receptor (IL-25R) in human peripheral blood cells. IL-25R was predominantly expressed by CD14+ cells. We next assessed the functional role of IL-25 in modulating the response of CD14+ cells to various inflammatory signals. CD14+ cells responded to IL-25 by down-regulating the synthesis of inflammatory cytokines induced by toll-like receptor (TLR) ligands and inflammatory cytokines. Inhibition of cytokine response by IL-25 occurred via a p38 Map kinase–driven Socs-3–dependent mechanism. In vivo, IL-25 inhibited monocyte-derived cytokines and protected against LPS-induced lethal endotoxemia in mice. These data indicate that IL-25 is a negative regulator of monocyte proinflammatory cytokine responses, which may have therapeutic implications.


2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 410.3-410
Author(s):  
S. Oreska ◽  
M. Špiritović ◽  
P. Česák ◽  
O. Marecek ◽  
H. Štorkánová ◽  
...  

Background:Skeletal muscle, pulmonary and articular involvement in idiopathic inflammatory myopathies (IIM) limit the mobility/self-sufficiency of patients, and can have a negative impact on body composition.Objectives:The aim was to assess body composition and physical activity of IIM patients and healthy controls (HC) and the association with selected inflammatory cytokines/chemokines and laboratory markers of nutrition and lipid metabolism.Methods:54 patients with IIM (45 females; mean age 57.7; disease duration 5.8 years; polymyositis (PM, 22) / dermatomyositis (DM, 25) / necrotizing myopathy (IMNM, 7)) and 54 age-/sex-matched HC (45 females, mean age 57.7) without rheumatic/tumor diseases were included. PM/DM patients fulfilled Bohan/Peter criteria for PM/DM. We assessed body composition (densitometry: iDXA Lunar, bioelectric impedance: BIA2000-M), physical activity (Human Activity Profile, HAP questionnaire), serum levels of 27 cytokines/chemokines (commercial multiplex ELISA kit, Bio-Rad Laboratories) and serum levels of selected parameters of nutrition and lipidogram. Disease activity (MITAX and MYOACT activity score) and muscle involvement (manual muscle testing, MMT-8, and functional index 2, FI2) were evaluated. Data are presented as mean±SD.Results:Compared to HC, patients with IIM had a trend towards significantly increased body fat % (BF%; iDXA: 39.9±7.1 vs. 42.4±7.1 %, p=0.077), but significantly decreased lean body mass (LBM; iDXA: 45.6±8.1 vs. 40.6±7.2 kg, p=0.001; BIA: 52.6±8.8 vs. 48.7±9.0 kg, p=0.023), increased extracellular mass/body cell mass (ECM/BCM) ratio (1.06±0.15 vs. 1.44±0.42, p<0.001), reflecting deteriorated nutritional status and predisposition for physical activity, and significantly lower bone mineral density (BMD: 1.2±0.1 vs. 1.1±0.1 g/cm2, p<0.001). Disease duration negatively correlated with BMD and LBM-BIA. Disease activity (MITAX, MYOACT) positively correlated with LBM (by BIA and DXA), similarly as with basal metabolic rate (BMR), and fat free mass (FFM). CRP was positively associated with BF% (BIA and DXA). Higher BF%-DEXA was associated with worse physical endurance (FI2) and worse ability to perform physical activity (HAP). MMT-8 score negatively correlated with ECM/BCM ratio. Serum levels of several inflammatory cytokines/chemokines (specifically IL-1ra, MCP, IL-10) and markers of nutrition (specifically albumin, C3-, C4-complement, cholinesterase, amylase, insulin and C-peptide, vitamin-D, orosomucoid), and lipid metabolism (specifically triglycerides, high-density lipoprotein, apolipoprotein A and B, atherogenic index of plasma) were significantly associated with alterations of body composition in IIM patients. (p<0.05 for all correlations)Conclusion:Compared to healthy age-/sex-matched individuals we found significant negative changes in body composition of our IIM patients associated with their disease activity and duration, inflammatory status, skeletal muscle involvement, and physical activity. These data could reflect their impaired nutritional status and predispositions for physical exercise, aerobic fitness and performance.Serum levels of certain inflammatory cytokines/chemokines and markers of nutrition and lipid metabolism were associated with alterations of body composition in IIM patients. This might further support the role of systemic inflammation and nutritional status on the negative changes in body composition of IIM patients.Acknowledgments:Supported by AZV NV18-01-00161A, MHCR 023728, SVV 260373 and GAUK 312218Disclosure of Interests:Sabina Oreska: None declared, Maja Špiritović: None declared, Petr Česák: None declared, Ondrej Marecek: None declared, Hana Štorkánová: None declared, Barbora Heřmánková: None declared, Kateřina Kubinova: None declared, Martin Klein: None declared, Lucia Vernerová: None declared, Olga Růžičková: None declared, Karel Pavelka Consultant of: Abbvie, MSD, BMS, Egis, Roche, UCB, Medac, Pfizer, Biogen, Speakers bureau: Abbvie, MSD, BMS, Egis, Roche, UCB, Medac, Pfizer, Biogen, Ladislav Šenolt: None declared, Heřman Mann: None declared, Jiří Vencovský: None declared, Michal Tomčík: None declared


2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Radu Albulescu ◽  
Elena Codrici ◽  
Ionela Daniela Popescu ◽  
Simona Mihai ◽  
Laura Georgiana Necula ◽  
...  

Inflammation represents the immune system response to external or internal aggressors such as injury or infection in certain tissues. The body’s response to cancer has many parallels with inflammation and repair; the inflammatory cells and cytokines present in tumours are more likely to contribute to tumour growth, progression, and immunosuppression, rather than in building an effective antitumour defence. Using new proteomic technology, we have investigated serum profile of pro- (IL-1β, IL-6, IL-8, IL-12, GM-CSF, and TNF-α) and anti-inflammatory cytokines (IL-4, IL-10), along with angiogenic factors (VEGF, bFGF) in order to assess tumoural aggressiveness. Our results indicate significant dysregulation in serum levels of cytokines and angiogenic factors, with over threefold upregulation of IL-6, IL-1β, TNF-α, and IL-10 and up to twofold upregulation of VEGF, FGF-2, IL-8, IL-2, and GM-CSF. These molecules are involved in tumour progression and aggressiveness, and are also involved in a generation of disease associated pain.


2020 ◽  
Author(s):  
Alejandra Palomino-Antolin ◽  
Paloma Narros-Fernández ◽  
Víctor Farré-Alins ◽  
Javier Sevilla-Montero ◽  
Celine Decouty-Pérez ◽  
...  

AbstractBackground and purposePost-ischemic inflammation contributes to worsening of ischemic brain injury and in this process, the inflammasomes play a key role. Inflammasomes are cytosolic multiprotein complexes which upon assembly activate the maturation and secretion of the inflammatory cytokines IL-1β and IL-18. However, participation of the NLRP3 inflammasome in ischemic stroke remains controversial. Our aims were to determine the role of NLRP3 in ischemia and to explore the mechanism involved in the potential protective effect of the neurovascular unit.MethodsWT and NLRP3 knock-out mice were subjected to ischemia by middle cerebral artery occlusion (60 minutes) with or without treatment with MCC950 at different time points post-stroke. Brain injury was measured histologically with 2,3,5-triphenyltetrazolium chloride (TTC) staining.ResultsWe identified a time-dependent dual effect of NLRP3. While neither the pre-treatment with MCC950 nor the genetic approach (NLRP3 KO) proved to be neuroprotective, post-reperfusion treatment with MCC950 significantly reduced the infarct volume in a dose-dependent manner. Importantly, MCC950 improved the neuro-motor function and reduced the expression of different pro-inflammatory cytokines (IL-1β, TNF-α), NLRP3 inflammasome components (NLRP3, pro-caspase-1), protease expression (MMP9) and endothelial adhesion molecules (ICAM, VCAM). We observed a marked protection of the blood-brain barrier (BBB), which was also reflected in the recovery of the tight junctions proteins (ZO-1, Claudin-5). Additionally, MCC950 produced a reduction of the CCL2 chemokine in blood serum and in brain tissue, which lead to a reduction in the immune cell infiltration.ConclusionsThese findings suggest that post-reperfusion NLRP3 inhibition may be an effective acute therapy for protecting the blood-brain barrier in cerebral ischemia with potential clinical translation.


2015 ◽  
Vol 7 (3) ◽  
pp. 163
Author(s):  
Abdul Qadar Punagi ◽  
Sutji Pratiwi Rahardjo

BACKGROUND: Rhinosinusitis occurs when the lining of the nasal and sinuses gets inflamed, infected or irritated, become swollen, and create extra mucus, the swollen lining may also interfere with drainage of mucus. Chronic rhinosinusitis (CRS) is a more persistent problem that requires a specific treatment approach. Aim of this study was to determine changes in interleukin (IL)-10 as an anti-inflammatory cytokines in allergic and non-allergic CRS at Makassar. METHODS: A prospective cohort study was designed to assess the level of IL-10 for three times during two weeks of therapy. Medication of Cefadroxil 500 mg 2x1, Pseudoephedrine 30 mg 2x1, Terfenadine 40 mg 2x1 and Methylprednisolone 4 mg 3x1, was conducted during two weeks for 13 subjects in allergic CRS group and 12 subjects in non-allergic CRS group. Results were statistically analyzed with student t-test and paired t-test.RESULTS: The changes in levels of IL-10 in allergic CRS group were increased, but not significant (5.293 to 5.769, p=0.058), and in non-allergic CRS group were decreased, but not significant (6.125 to 5.475, p=0.103). CONCLUSION: The serum levels of IL-10 were not significant increased in allergic CRS group and not significant decreased in non-allergic CRS group. KEYWORDS: interleukin-10, chronic rhinosinusitis, allergy, cefadroxil, pseudoephedrine, terfenadine, methylprednisolone


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