scholarly journals Analysis of inflammatory markers in apparently healthy automobile vehicle drivers in response to exposure to traffic pollution fumes

2020 ◽  
Vol 36 (4) ◽  
Author(s):  
Hina Riaz Ahmed ◽  
Binafsha Manzoor Syed ◽  
Zulfiqar Laghari ◽  
Suleman Pirzada

Objective: This study aimed to evaluate pattern of markers of inflammation in apparently healthy drivers who exposed to traffic fumes. Methods: This cross-sectional study was conducted from June 2016 to January 2017 at Liaquat University of Medical & Health Sciences (LUMHS), Jamshoro. It looked into the effects of traffic pollutants on markers of inflammation including CRP, Leukocytes count, IL-6, TNF-α, TNF-β of healthy human volunteers. Eighty-seven, apparently healthy, non-smoking automobile vehicle drivers, having daily contact of traffic exhaust for at least six hours, aged between 18-40 years recruited for this study. Levels of traffic-generated pollutants P.M2.5, P.M10, NOx were recorded in different areas of Hyderabad City. Results: P.M2.5 found to be positively correlated with markers of inflammation including IL-6 (rs = 0.99), TNF-α (rs = 0.41), CRP mg/dl (rs = 0.99) , neutrophils (rs = 0.29), lymphocytes (rs = 0.31), eosinophils (rs = 0.20), monocytes (rs = 0.42) and basophils (rs = 0.16). Positive correlation present among IL-6 (rs = 0.21), TNF-α (rs = 0.49) and CRP mg/dl (rs = 0.22) (rs = -0.31), Leukocytes (rs = 0.14) neutrophils (rs = 0.31), lymphocytes (rs = 0.21), monocytes (rs = 0.50), basophils (rs = 0.17) with P.M10. NOx showed positive correlation with IL-6 (rs = 0.22), TNF-α (rs = 0.48), CRP (rs = 0.22), neutrophils (rs = 0.31), lymphocytes (rs = 0.13), basophils (rs = 0.17) and monocytes (rs = 0.48). Conclusion: Findings of our study suggest that almost all markers of inflammation are positively correlated with traffic pollutants and this condition might raise the risk of systemic diseases. doi: https://doi.org/10.12669/pjms.36.4.2025 How to cite this:Riaz H, Syed BM, Laghari Z, Pirzada S. Analysis of inflammatory markers in apparently healthy automobile vehicle drivers in response to exposure to traffic pollution fumes. Pak J Med Sci. 2020;36(4):---------. doi: https://doi.org/10.12669/pjms.36.4.2025 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

2017 ◽  
Vol 19 (4) ◽  
pp. 419-427 ◽  
Author(s):  
Emilio González-Jiménez ◽  
Jacqueline Schmidt-RioValle ◽  
Laura Sinausía ◽  
Javier S. Perona

Background: Breastfeeding duration has been associated with less low-grade inflammation in healthy adolescents, but there is scarce information regarding obese subjects. This study aimed to evaluate whether exclusive breastfeeding is related to serum concentrations of inflammatory markers in a population of Spanish adolescents. Method: A cross-sectional study was performed on 1,001 adolescents (13.2 ± 1.2 years) randomly recruited from schools in southeast Spain. Data on breastfeeding duration were collected via a parental questionnaire. Interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) were determined by enzyme-linked immunosorbent assay. C-reactive protein (CRP) was determined by solid-phase chemiluminescent immunometric assay. Results: Nonadjusted and adjusted multivariate correlation analyses confirmed a strong association ( p < .001, 95% confidence interval) between the three markers of inflammation and exclusive breastfeeding duration. No significant differences were observed for IL-6, TNF-α, and CRP serum concentrations among normal weight, overweight, and obese adolescents, except for IL-6 between normal weight and obese subjects. Likewise, no significant association was found between these markers of inflammation and body mass index (BMI) z-score. Conclusions: We found a possible association between inflammatory markers and exclusive breastfeeding duration in adolescents, regardless of their BMI. This finding suggests that increased body weight or obesity might not mediate the association between breastfeeding and inflammation. These results contribute to the understanding of the relationship between breastfeeding and inflammatory markers in adolescents.


Author(s):  
Fatih Öner Kaya ◽  
Yeşim Ceylaner ◽  
Belkız Öngen İpek ◽  
Zeynep Güneş Özünal ◽  
Gülbüz Sezgin ◽  
...  

Aims: The etiopathogenesis of Rheumatoid Arthritis (RA) is not clearly understood. However, the role of the cytokines takes an important part in this mechanism. We aimed to bring a new approach to the concept of 'remission' in patients with RA. Background: RA is a chronic, autoimmune, inflammatory disease that involves small joints in the form of symmetrical polyarthritis and progresses with exacerbations and remissions. Pain, swelling, tenderness and morning stiffness are typical of the joints involved. Although it is approached as a primary joint disease, a wide variety of extra-articular involvements may also occur. It is an interesting pathophysiological process, the exact cause of which is still unknown, with many environmental, genetic and potentially undiscovered possible factors in a chaotic manner. Objective: In this cross-sectional study, sedimentation rate (ESR), C- Reactive protein (CRP), Tumor necrosis factor (TNF)-α, soluble-TNF-α receptor (TNF-R), Interleukin (IL)-1B and IL-10 were measured in three groups which were healthy volunteers, patients with RA in the active period, and patients with RA in remission. Disease activity score-28 (DAS-28) was calculated in active RA and RA in remission. Methods: This study included 20 healthy volunteers, 20 remission patients with RA and 20 active RA patients. Venous blood samples were collected from patients in both healthy and RA groups. Results: RA group consisted 43 (71.6%) female and 17 (28.4%) male. Control group consisted 11 (55%) female and 9 (45%) male. TNF-R was significantly high only in the active group according to the healthy group (p=0.002). IL-10 was significantly high in active RA according to RA in remission (p=0.03). DAS-28 was significantly high in active RA according to RA in remission (p=0.001). In the active RA group, ESR and TNF-R had a positive correlation (r:0.442; p=0.048). In the active RA group, there was also a positive correlation between TNF-R and CRP (r:0.621; p=0,003). Both healthy and active RA group had significant positive correlation between ESR and CRP (r: 0.481; p=0.032 and r: 0,697; p=0,001 respectively). Conclusion: TNF-R can be the main pathophysiological factor and a marker showing activation. TNF-R can be very important in revealing the effect of TNF on the disease and the value of this effect in the treatment and ensuring the follow-up of the disease with CRP instead of ESR in activation.


2007 ◽  
Vol 157 (4) ◽  
pp. 419-426 ◽  
Author(s):  
David H St-Pierre ◽  
Jean-Philippe Bastard ◽  
Lise Coderre ◽  
Martin Brochu ◽  
Antony D Karelis ◽  
...  

Objective: Recent reports have suggested that the existence of associations between hormonal dysregulation and chronic upregulation of inflammatory markers, which may cause obesity-related disturbances. Thus, we examined whether acylated ghrelin (AcylG) and total ghrelin (TotG) levels could be associated with the following inflammatory markers: C-reactive protein (CRP), tumor necrosis factor α (TNF-α), and soluble TNF receptor 1 (sTNF-R1). Design: Cross-sectional study consisting of 50 overweight and obese postmenopausal women. Methods: AcylG and TotG levels were assessed at 0, 60, 160, 170, and 180 min of the euglycemic/hyperinsulinemic clamp (EHC). We evaluated insulin sensitivity, body composition, and blood lipid profiles as well as fasting concentrations of CRP, TNF-α, and sTNF-R1. Results: In fasting conditions, sTNF-R1 was negatively correlated with AcylG (r = −0.48, P < 0.001) levels. In addition, AcylG/TotG was associated negatively with sTNF-R1 (r = −0.44, P = 0.002) and positively with TNF-α (r = 0.38, P = 0.009) values. During the EHC, TotG (at all time points) and AcylG (at 60 and 160 min) values were significantly decreased from fasting concentrations. AcylG maximal reduction and area under the curve (AUC) values were correlated to sTNF-R1 (r = −0.35, P = 0.02 and r = −0.34, P = 0.02, respectively). Meanwhile, the AcylG/TotG AUC ratio was associated negatively with sTNF-R1 (r = −0.29, P < 0.05) and positively with TNF-α (r = 0.36, P = 0.02). Following adjustments for total adiposity, sTNF-R1 remained correlated with fasting and maximal reduction AcylG values. Similarly, AcylG/TotG ratios remained significantly correlated with sTNF-R1 and TNF-α. Importantly, 23% of the variation in sTNF-R1 was independently predicted by fasting AcylG. Conclusion: These results are the first to suggest that both fasting and EHC-induced AcylG profiles are correlated with fasting values of sTNF-R1, a component of the TNF-α system. Thus, AcylG may act, at least in part, as one mediator of chronic inflammatory activity in human obesity.


2020 ◽  
Vol 20 (6) ◽  
pp. 924-929
Author(s):  
Khalid Siddiqui ◽  
Teena P. George ◽  
Salini Scaria Joy ◽  
Muhammad Mujammami

Background: A possible relationship between thyroid hormones and glucose metabolism in diabetes has already been established. Objectives: We aimed to evaluate the thyroid function markers and their relationship with inflammation, which is considered as a pathogenic condition of diabetes. Methods: This cross-sectional study included 276 patients with type 2 diabetes. Serum levels of thyroid (TSH, FT4, and FT3) and inflammatory markers (CRP, IL-6, and TNF-α) were measured. Results: The mean age of the subjects was 55.2 years and mean diabetes duration of 16.8 years. The inflammatory markers showed significant differences with the tertiles of TSH and thyroid hormones. TSH was significantly correlated with inflammatory markers, IL-6 (r = 0.13, P = 0.020) and TNF-α (r = 0.17, P = 0.003), while FT4 had a correlation only with TNF-α (r = 0.25, P = <0.001). FT3 was negatively correlated with inflammatory marker IL-6 (r = -0.14, P = 0.020), HbA1c (r = -0.12, P = 0 .040), and HOMA-IR (r = -0.17, P = 0.010). Conclusion: Abnormalities in the thyroid hormone metabolism are related to the increased inflammatory activity as well as insulin resistance, and are associated with the disorders of glucose metabolism.


Cartilage ◽  
2020 ◽  
pp. 194760352090477 ◽  
Author(s):  
Cristóbal Orellana ◽  
Joan Calvet ◽  
Antoni Berenguer-Llergo ◽  
Néstor Albiñana ◽  
María García Manrique ◽  
...  

Objective Different adipokines have been reported to play a role in the development, progression, and severity of knee osteoarthritis, but this association may be mediated by obesity. The aim of this study was to evaluate separately the associations of leptin and adiponectin with clinical severity and inflammatory markers in nonobese and obese women with knee osteoarthritis. Design Cross-sectional study with systematic inclusion of 115 women with symptomatic primary knee osteoarthritis. Age, physical exercise, symptoms duration, and body mass index were collected. Radiographic severity was evaluated according to Kellgren-Lawrence scale. Pain and disability were assessed by WOMAC-total, -pain, -function subscales. Two adipokines (leptin and adiponectin) and 3 inflammatory markers (TNF-α, hsCRP, and IL-6) were measured by ELISA in synovial fluid and serum. Results Synovial fluid adiponectin was associated with WOMAC pain, function, and total and with synovial fluid IL-6 in nonobese female knee osteoarthritis after controlling by confounders (partial correlation coefficient [PCC] = 0.395, 0.387, 0.427, and 0.649, respectively). Synovial fluid and serum leptin were significantly associated with IL-6 (PCC = 0.354) after controlling by confounders but associations with clinical severity and the rest of inflammatory markers were mitigated after control. Conclusions Adiponectin in synovial fluid was associated with clinical severity and local inflammatory markers in knee osteoarthritis women, while leptin relation was attenuated when controlled by confounders.


Author(s):  
RIA SANGHAVI ◽  
Tiberiu Pana ◽  
Hulkar Mamayusuppova ◽  
Ian Maidment ◽  
Chris Fox ◽  
...  

Background: Higher anticholinergic burden from medications is associated with increased risk of cardiovascular disease and cognitive function decline. A mechanistic pathway has never been established. We aimed to determine whether chronic inflammation may mediate these associations. Methods: Participants were drawn from the European Prospective Investigation into Cancer, Norfolk cohort (40-79 years at baseline). The anticholinergic cognitive burden score (ACB) was calculated at baseline/first (1HC) (1993/97) and second (2HC) (1998/2000) health checks. Plasma fibrinogen and C-reactive protein (CRP) were measured during 1HC and Tumour Necrosis Factor alpha (TNF-α) and interleukin 6 (IL-6) during 2HC. Cross-sectional associations between ACB and inflammatory markers were examined for 1HC and 2HC, respectively. The prospective association was also examined between 1HC ACB and 2HC inflammatory markers. All models adjusted for age, sex, lifestyle factors, co-morbidities and medications. Results: 17,678 and 22,051 participants were included in cross-sectional analyses for CRP, and fibrinogen, respectively. A total of 5,101 participants with available data for TNF-α and IL-6 were included in the longitudinal analyses. Cross-sectionally, a point increase in the ACB was associated with a significant increase in all inflammatory markers (beta (standard error): fibrinogen – 0.035g/l (0.006), p<0.001; CRP 0.284mg/l (0.044), p<0.001; TNF-α 0.031pg/ml (0.010), p=0.002; and IL-6 0.112pg/ml (0.033), p=0.001. Longitudinally, a unit increase in the ACB was associated with a significant increase in TNF-α 0.028pg/ml (0.011), p=0.013 and IL-6 0.076 pg/ml (0.035), p=0.029. Conclusion: Higher anticholinergic burden was significantly associated with higher inflammatory markers. Inflammation may mediate the relationship between exposure to anticholinergic medications and adverse outcomes


2020 ◽  
Vol 36 (5) ◽  
Author(s):  
Yi Sun ◽  
Liang Hong ◽  
Changbai Gao

Objective: To evaluate the correlation among 14-3-3η protein, inflammation, bone remodeling and osteoporosis in patients with rheumatoid arthritis. Methods: In this cross-sectional study, the RA patients treated in our hospital were analyzed between January 2015 and November 2019. Bone mineral density was measured using dual energy X-ray absorptiometry, and at the beginning of the study, serum samples were collected and the level of 14-3-3η, TNF-α, and IL-6 was tested using the quantitative enzyme-linked immunosorbent assay, and I-CTX and PINP were measured using automatic electrochemical luminescence immune-analyzer for all the participants. Results: In the current study, 285 patients with rheumatoid arthritis were enrolled and assigned into normal, osteopenia, and osteoporotic group respectively. The level of 14-3-3η and IL-6 presented with the highest value in the osteoporosis group, but the lowest value in the normal group, and there were significant differences in the level of 14-3-3η and IL-6 among the groups (p<0.05), and there was positive correlation between 14-3-3η and IL-6 (p<0.05). There were significant differences in PINP and I-CTX among the three groups (p<0.05), and a significantly positive correlation between I-CTX and 14-3-3η (p<0.05) and a significantly negative correlation between PINP and 14-3-3η (p<0.05) were found. Conclusion: There was a significant correlation among 14-3-3η protein, inflammation, bone remodeling and osteoporosis in patients with rheumatoid arthritis, the influence of 14-3-3η on osteoporosis may be contributed to its adjusting inflammation and bone remodeling. doi: https://doi.org/-10.12669/pjms.36.5.2403 How to cite this:Sun Y, Hong L, Gao C. The association among 14-3-3η protein, inflammation, bone remodeling and osteoporosis in patients with rheumatoid arthritis. Pak J Med Sci. 2020;36(5):---------. doi: https://doi.org/10.12669/pjms.36.5.2403 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Olga-Cecilia Vargas-Pinilla ◽  
Eliana-Isabel Rodríguez-Grande

AbstractThe protocol established for taking hand grip dynamometry measurements determines that the patient must be in a sitting position. This protocol cannot be applied due to the patient’s conditions in some cases, such as abdominal surgery, musculoskeletal spine or hip injuries. The purpose was to determine the reproducibility and level of agreement between the Handgrip dynamometry in supine position with the elbow flexed or extended, and the one measured in the sitting position, the design was a descriptive cross-sectional study. The population were young apparently healthy between 18 and 30 years of age (N = 201). Handgrip measurement was performed on both upper limbs in a sitting position with a flexed elbow, a supine position with a flexed elbow, and supine position with the elbow extended. Reproducibility was nearly perfect in all positions (ICC 0.95–0.97). Regarding the level of agreement for the comparison between sitting and supine positions with a flexed elbow, an average difference of − 0.406. For supine position with an extended elbow and supine position with a flexed elbow, the average difference was − 1.479. Considering the results, clinicians or researchers can choose any of the positions evaluated herein and obtain reliable results as long as the standardization process is followed.


Oral ◽  
2021 ◽  
Vol 1 (2) ◽  
pp. 122-138
Author(s):  
Kiranjit Kaur ◽  
Alexandria Turner ◽  
Patrice Jones ◽  
Dean Sculley ◽  
Martin Veysey ◽  
...  

(1) Background: The aetiology of oral disease is multifactorial, involving genetic and environmental factors, including dietary ones. Bitter taste genetics may be related to oral health through dietary modulation or non-gustatory roles, including modulation of inflammation. Investigations of bitter taste and oral health associations to date have been restricted to specific polymorphisms, limited outcomes (caries), and age-groups (children), and links to inflammation remain to be elucidated. (2) Methods: A cross-sectional study (n = 65) investigated the correlations between bitter taste genotypes, oral health outcomes, and oral inflammation markers. Oral examinations were conducted, including saliva testing with evaluation of flow rate, pH, and buffering and antioxidant capacity (FRAP) and IL-1β, TNF-α, IL-6 levels. DNA was collected via buccal swabs and used to evaluate the presence of multiple bitter-taste receptor gene polymorphisms. (3) Results: The major allele for TAS2R4-rs2233998, TAS2R5-rs2227264, TAS2R50-rs1376251, and TAS2R9-rs3741845 was associated with a higher mean of unstimulated salivary flow rate, FRAP, TNF-α, IL-1β, and likelihood of filled teeth. Presence of the major allele for TAS2R4-rs2234001 and TAS2R9-rs3741845 was associated with lower means FRAP, TNF-α, IL-1β, DMFT index, and likelihood of missing teeth. (4) Conclusions: These findings suggest relationships between bitter-taste genotypes, oral health outcomes, and inflammatory markers. These findings justify the need for further studies that could help identify risk groups and develop novel agents for maintaining oral health.


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