scholarly journals Enhanced levels of leukotriene B4in synovial fluid in Lyme disease

1993 ◽  
Vol 2 (3) ◽  
pp. 225-228 ◽  
Author(s):  
E. Mayatepek ◽  
D. Hassler ◽  
M. Maiwald
Keyword(s):  
Lyme Disease ◽  
Synovial Fluid ◽  
Healthy Subjects ◽  
Polymorphonuclear Leukocytes ◽  
Statistical Difference ◽  
Potential Role ◽  
Lyme Arthritis ◽  
Control Groups ◽  
Cysteinyl Leukotrienes

The purpose of this study was to evaluate the potential role of LTB4and cysteinyl leukotrienes in Lyme disease (LD). Therefore, a total number of 34 patients divided into four groups was studied. The patients were classified as having Lyme arthritis (n = 7) or Lyme meningitis (n = 10), and as control groups patients with a noninflammatory arthropathy (NIA) (n = 7) and healthy subjects (n = 10). LTB4as well as LTC4secretion from stimulated polymorphonuclear leukocytes (PMNL) from all groups of patients showed no statistical differences. LTB4levels in synovial fluid were significantly increased in patients with Lyme arthritis (median 142 ng/ml, range 88–296) when compared to the control subjects with NIA (median 46 ng/ml, range 28–72) (p < 0.05). No statistical difference of urinary LTE4levels between all the different groups of patients was observed. These results show that cysteinyl leukotrienes do not play an important role in the pathogenesis of LD. In contrast to previous findings in rheumatoid arthritis, LTB4production from stimulated PMNL was not found to be increased in LD. However, the significantly elevated levels of LTB4in synovial fluid of patients with Lyme arthritis underline the involvement of LTB4in the pathogenesis of this disease.

scholarly journals The role of oxidative and nitrosative stress in the pathology of osteoarthritis: Novel candidate biomarkers for quantification of degenerative changes in the knee joint

2018 ◽  
Vol 10 (2) ◽  
Author(s):  
Alexander Franz ◽  
Laura Joseph ◽  
Constantin Mayer ◽  
Jan-Frieder Harmsen ◽  
Holger Schrumpf ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Synovial Fluid ◽  
Knee Joint ◽  
Human Serum ◽  
Synovial Membrane ◽  
Nitrosative Stress ◽  
Control Groups ◽  
Oxidative And Nitrosative Stress ◽  
And Oxidative Stress

Osteoarthritis (OA) is the most frequently diagnosed joint disorder worldwide with increasing prevalence and crucial impact on the quality of life of affected patients through chronic pain, decreasing mobility and invalidity. Although some risk factors, such as age, obesity and previous joint injury are well established, the exact pathogenesis of OA on a cellular and molecular level remains less understood. Today, the role of nitrosative and oxidative stress has not been investigated conclusively in the pathogenesis of OA yet. Therefore, the objective of this study was to identify biological substances for oxidative and nitrosative stress, which mirror the degenerative processes in an osteoarthritic joint. 69 patients suffering from a diagnosed knee pain participated in this study. Based on the orthopedic diagnosis, patients were classified into an osteoarthritis group (OAG, n=24) or in one of two control groups (meniscopathy, CG1, n=11; anterior cruciate ligament rupture, CG2, n=34). Independently from the study protocol, all patients underwent an invasive surgical intervention which was used to collect samples from the synovial membrane, synovial fluid and human serum. Synovial biopsies were analyzed histopathologically for synovitis (Krenn-Score) and immunohistochemically for detection of end products of oxidative (8-isoprostane F2α) and nitrosative (3-nitrotyrosine) stress. Additionally, the fluid samples were analyzed for 8-isoprostane F2α and 3-nitrotyrosine by competitive ELISA method. The analyzation of inflammation in synovial biopsies revealed a slight synovitis in all three investigated groups. Detectable concentrations of 3-nitrotyrosine were reported in all three investigated groups without showing any significant differences between the synovial biopsies, fluid or human serum. In contrast, significant increased concentrations of 8-isoprostane F2α were detected in OAG compared to both control groups. Furthermore, our data showed a significant correlation between the histopathological synovitis and oxidative stress in OAG (r=0.728, P<0.01). There were no significant differences between the concentrations of 8-isoprostane F2α in synovial fluid and human serum. The findings of the current study support the hypothesis that oxidative and nitrosative stress are components of the multi-factory pathophysiological formation of OA. It seems reasonable that an inflammatory process in the synovial membrane triggers the generation of oxidative and nitrosative acting substances which can lead to a further degradation of the articular cartilage. Based on correlations between the observed degree of inflammation and investigated biomarkers, especially 8-isoprostane F2α seems to be a novel candidate biomarker for OA. However, due to the finding that also both control groups showed increased concentrations of selected biomarkers, future studies have to validate the diagnostic potential of these biomarkers in OA and in related conditions of the knee joint.

Differential diagnosis between rheumatoid arthritis and psoriatic arthritis: the value of ultrasound findings at metacarpophalangeal joints level

2011 ◽  
Vol 70 (6) ◽  
pp. 1111-1114 ◽  
Author(s):  
Marwin Gutierrez ◽  
Emilio Filippucci ◽  
Fausto Salaffi ◽  
Luca Di Geso ◽  
Walter Grassi
Keyword(s):  
Rheumatoid Arthritis ◽  
Differential Diagnosis ◽  
Psoriatic Arthritis ◽  
Synovial Fluid ◽  
Potential Role ◽  
Power Doppler ◽  
Extensor Tendon ◽  
Synovial Hypertrophy ◽  
Ultrasound Findings

ObjectiveTo investigate the potential of ultrasound (US) in the differential diagnosis between rheumatoid arthritis (RA) and psoriatic arthritis (PsA) at metacarpophalangeal (MCP) joints level.Methods18 RA patients and 20 PsA patients with clinical involvement of MCP joints were included. All US examinations were performed by two rheumatologists investigating: presence of joint cavity widening (JCW), synovial fluid and/or synovial hypertrophy, peritenon extensor tendon inflammation (PTI) and intra-articular or peri-tendinous power Doppler (PD) signal.ResultsA total of 83 MCP joints in 18 RA patients were assessed. In all of these the authors found different degrees of JCW. 15 of 83 (18%) MCP joints showed synovial fluid, whereas 68 of 83 (82%) MCP joints showed synovial hypertrophy. In 72 of 83 (86.7%) MCP joints intra-articular PD was detected. No PTI pattern was found in these patients.In PsA patients, a total of 82 MCP joints in 20 patients were assessed. 54 of 82 (65.8%) MCP joints showed PTI pattern (p = 0.001). In 50 of these 54 (92.5%) MCP joints extra-articular PD signal was detected (p = 0.001). 28 of 82 (34.1%) MCP joints showed different degrees of JCW. 6 of 28 (21.4%) MCP joints presented synovial fluid, whereas 22 of 28 (78.5%) MCP joints showed synovial hypertrophy. In 8 of 82 (9.7%) MCP joints the JCW and PTI patterns were found contemporaneously.ConclusionsPreliminary results demonstrate that PTI pattern is a higher characteristic of PsA, which suggests a potential role of US in the differential diagnosis between RA and PsA at MCP joints level.

scholarly journals Hip Osteonecrosis Is Associated with Increased Plasma IL-33 Level

2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
Jinhui Ma ◽  
Wanshou Guo ◽  
Zirong Li ◽  
Bailiang Wang ◽  
Shirui Li ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Femoral Head ◽  
Prospective Study ◽  
Family Member ◽  
Healthy Subjects ◽  
Potential Role ◽  
Osteonecrosis Of Femoral Head ◽  
Elisa Kit ◽  
L1 And L2

The recently discovered IL-33 as an IL-1 cytokine family member has been proved to be specifically released from osteonecrotic bones. We aimed to investigate the potential role of IL-33 in the development of osteonecrosis of femoral head (ONFH). Forty patients diagnosed with ONFH and forty age-, sex-, and body mass index- (BMI-) matched healthy subjects were included in this prospective study between March 2016 and September 2016. A commercially available ELISA kit was used to test the level of plasma IL-33. The IL-33 levels were compared among different ARCO stages, CJFH types, and etiology groups. Plasma IL-33 levels were significantly higher in the ONFH patients than that in the control subjects. The levels of IL-33 did not differ significantly among the ONFH patients with different ARCO stages. The IL-33 levels of patients with CJFH type L3 were significantly higher than that of patients with types L1 and L2. No significant differences were observed in IL-33 levels between steroid-induced, alcohol-induced, and idiopathic patients. Our findings seem to indicate that IL-33 effects may be detrimental during ONFH, which appeared to be associated with the prognosis of ONFH. The IL-33 deserves particular attention in the pathogenesis of ONFH.

scholarly journals mPGES-1 deletion potentiates urine concentrating capability after water deprivation

2012 ◽  
Vol 302 (8) ◽  
pp. F1005-F1012 ◽  
Author(s):  
Zhanjun Jia ◽  
Gang Liu ◽  
Maicy Downton ◽  
Zheng Dong ◽  
Aihua Zhang ◽  
...  
Keyword(s):  
Water Deprivation ◽  
Potential Role ◽  
Urine Volume ◽  
Renal Medulla ◽  
Urine Osmolality ◽  
Protein Abundance ◽  
Wild Type ◽  
Control Groups ◽  
Urine Concentrating Ability

PGE2 plays an important role in the regulation of fluid metabolism chiefly via antagonizing vasopressin-induced osmotic permeability in the distal nephron, but its enzymatic sources remain uncertain. The present study was undertaken to investigate the potential role of microsomal PGE synthase (mPGES)-1 in the regulation of urine concentrating ability after water deprivation (WD). Following 24-h WD, wild-type (WT) mice exhibited a significant reduction in urine volume, accompanied by a significant elevation in urine osmolality compared with control groups. In contrast, in response to WD, mPGES-1 knockout (KO) mice had much less urine volume and higher urine osmolality. Analysis of plasma volume by measurement of hematocrit and by using a nanoparticle-based method consistently demonstrated that dehydrated WT mice were volume depleted, which was significantly improved in the KO mice. WD induced a twofold increase in urinary PGE2 output in WT mice, which was completely blocked by mPGES-1 deletion. At baseline, the KO mice had a 20% increase in V2 receptor mRNA expression in the renal medulla but not the cortex compared with WT controls; the expression was unaffected by WD irrespective of the genotype. In response to WD, renal medullary aquaporin-2 (AQP2) mRNA exhibited a 60% increase in WT mice, and this increase was greater in the KO mice. Immunoblotting demonstrated increased renal medullary AQP2 protein abundance in both genotypes following WD, with a greater increase in the KO mice. Similar results were obtained by using immunohistochemistry. Paradoxically, plasma AVP response to WD seen in WT mice was absent in the KO mice. Taken together, these results suggest that mPGES-1-derived PGE2 reduces urine concentrating ability through suppression of renal medullary expression of V2 receptors and AQP2 but may enhance it by mediating the central AVP response.

scholarly journals RNase A Inhibits Formation of Neutrophil Extracellular Traps in Subarachnoid Hemorrhage

2021 ◽  
Vol 12 ◽  
Author(s):  
Anton Früh ◽  
Katharina Tielking ◽  
Felix Schoknecht ◽  
Shuheng Liu ◽  
Ulf C. Schneider ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Potential Role ◽  
Neutrophil Extracellular Traps ◽  
Brain Parenchyma ◽  
Rnase A ◽  
Innate Immune ◽  
Control Groups ◽  
Extracellular Traps ◽  
Over Time

Background: Subarachnoid hemorrhage (SAH) caused by rupture of an intracranial aneurysm, is a life-threatening emergency that is associated with substantial morbidity and mortality. Emerging evidence suggests involvement of the innate immune response in secondary brain injury, and a potential role of neutrophil extracellular traps (NETs) for SAH-associated neuroinflammation. In this study, we investigated the spatiotemporal patterns of NETs in SAH and the potential role of the RNase A (the bovine equivalent to human RNase 1) application on NET burden.Methods: A total number of n=81 male C57Bl/6 mice were operated utilizing a filament perforation model to induce SAH, and Sham operation was performed for the corresponding control groups. To confirm the bleeding and exclude stroke and intracerebral hemorrhage, the animals received MRI after 24h. Mice were treated with intravenous injection of RNase A (42μg/kg body weight) or saline solution for the control groups, respectively. Quadruple-immunofluorescence (IF) staining for cell nuclei (DAPI), F-actin (phalloidin), citrullinated H3, and neurons (NeuN) was analyzed by confocal imaging and used to quantify NET abundance in the subarachnoid space (SAS) and brain parenchyma. To quantify NETs in human SAH patients, cerebrospinal spinal fluid (CSF) and blood samples from day 1, 2, 7, and 14 after bleeding onset were analyzed for double-stranded DNA (dsDNA) via Sytox Green.Results: Neutrophil extracellular traps are released upon subarachnoid hemorrhage in the SAS on the ipsilateral bleeding site 24h after ictus. Over time, NETs showed progressive increase in the parenchyma on both ipsi- and contralateral site, peaking on day 14 in periventricular localization. In CSF and blood samples of patients with aneurysmal SAH, NETs also increased gradually over time with a peak on day 7. RNase application significantly reduced NET accumulation in basal, cortical, and periventricular areas.Conclusion: Neutrophil extracellular trap formation following SAH originates in the ipsilateral SAS of the bleeding site and spreads gradually over time to basal, cortical, and periventricular areas in the parenchyma within 14days. Intravenous RNase application abrogates NET burden significantly in the brain parenchyma, underpinning a potential role in modulation of the innate immune activation after SAH.

scholarly journals Borrelia burgdorferipeptidoglycan is a persistent antigen in patients with Lyme arthritis

2019 ◽  
Vol 116 (27) ◽  
pp. 13498-13507 ◽  
Author(s):  
Brandon L. Jutras ◽  
Robert B. Lochhead ◽  
Zachary A. Kloos ◽  
Jacob Biboy ◽  
Klemen Strle ◽  
...  
Keyword(s):  
Lyme Disease ◽  
Synovial Fluid ◽  
Antibiotic Treatment ◽  
Mononuclear Cells ◽  
Inflammatory Responses ◽  
Human Peripheral Blood ◽  
Cell Envelope ◽  
Lyme Arthritis ◽  
Multisystem Disorder ◽  
Peripheral Blood Mononuclear

Lyme disease is a multisystem disorder caused by the spirocheteBorrelia burgdorferi. A common late-stage complication of this disease is oligoarticular arthritis, often involving the knee. In ∼10% of cases, arthritis persists after appropriate antibiotic treatment, leading to a proliferative synovitis typical of chronic inflammatory arthritides. Here, we provide evidence that peptidoglycan (PG), a major component of theB. burgdorfericell envelope, may contribute to the development and persistence of Lyme arthritis (LA). We show thatB. burgdorferihas a chemically atypical PG (PGBb) that is not recycled during cell-wall turnover. Instead, this pathogen sheds PGBbfragments into its environment during growth. Patients with LA mount a specific immunoglobulin G response against PGBb, which is significantly higher in the synovial fluid than in the serum of the same patient. We also detect PGBbin 94% of synovial fluid samples (32 of 34) from patients with LA, many of whom had undergone oral and intravenous antibiotic treatment. These same synovial fluid samples contain proinflammatory cytokines, similar to those produced by human peripheral blood mononuclear cells stimulated with PGBb. In addition, systemic administration of PGBbin BALB/c mice elicits acute arthritis. Altogether, our study identifies PGBbas a likely contributor to inflammatory responses in LA. Persistence of this antigen in the joint may contribute to synovitis after antibiotics eradicate the pathogen. Furthermore, our finding thatB. burgdorferisheds immunogenic PGBbfragments during growth suggests a potential role for PGBbin the immunopathogenesis of other Lyme disease manifestations.

POTENTIAL ROLE OF WHOLE-BODY HYPERTHERMIA TO TREAT LYME DISEASE

1995 ◽  
Vol 88 ◽  
pp. S142
Author(s):  
L. M. Shecterle ◽  
P. Gasper ◽  
J. A. St. Cyr. Jacqmar
Keyword(s):  
Lyme Disease ◽  
Potential Role ◽  
Whole Body ◽  
Whole Body Hyperthermia

Biomarkers in the serum, synovial fluid and articular cartilage show promising utility in patients with femoroacetabular impingement: a systematic review

2017 ◽  
Vol 3 (3) ◽  
pp. 167-176 ◽  
Author(s):  
Jeffrey Kay ◽  
Muzammil Memon ◽  
Vito Z Zou ◽  
Andrew Duong ◽  
Nicole Simunovic ◽  
...  
Keyword(s):  
Systematic Review ◽  
Articular Cartilage ◽  
Synovial Fluid ◽  
Femoroacetabular Impingement ◽  
Matrix Protein ◽  
Potential Role ◽  
Cartilage Damage ◽  
Cost Effective ◽  
Level Of Evidence

ImportanceBiomarkers have promising potential to provide a cost-effective tool to identify patients with femoroacetabular impingement (FAI) who are most at risk and who may benefit most from early joint preservation surgery.ObjectiveTo assess the potential role of biomarkers in the diagnosis and prognosis of FAI.Evidence reviewThree databases (PubMed, Ovid (MEDLINE) and Embase) were searched on 20 August 2017 from database inception, and two reviewers independently and in duplicate screened the resulting literature. Methodological quality of all included papers was assessed using the Methodological Index for Non-Randomized Studies criteria. The results are presented in a narrative summary fashion using descriptive statistics including means, proportions and ranges.FindingsSeven studies (one retrospective laboratory series and six controlled laboratory studies) were identified including a total of 227 patients. The mean age of the patients was 41.6 years (range: 13–80), with a mean follow-up period of 29.9 months (SD=3.2). Markers of articular cartilage breakdown, including cartilage oligomeric matrix protein (COMP) and fibronectin–aggrecan complex (FAC), were identified in high concentrations in the serum and synovial fluid of patients with FAI, respectively. Moreover, mRNA expression of catabolic cytokines in the articular cartilage of patients with FAI has been reported.Conclusions and relevanceAlthough not yet used in clinical settings, several biomarkers of articular cartilage damage have been identified in the serum, synovial fluid and articular cartilage of patients with FAI. These findings provide promising insight into the potential role of biomarkers in guiding clinical practice and assisting with patient selection and preoperative counselling in patients with FAI and should be evaluated further.Level of evidenceIV, systematic review of level III and IV studies.

Sign in / Sign up

Export Citation Format

Share Document