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Lipid metabolism and inflammation contribute to cardiovascular disease development. This study investigated whether the consumption of cranberry (CR; Vaccinium macrocarpon) can alter high-density lipoprotein (HDL) metabolism and prevent inflammation in mice expressing human apolipoprotein A-I transgene (hApoAITg), which have similar HDL profiles to those of humans. Male hApoAITg mice were fed a modified American Institute of Nutrition-93M high-fat/high-cholesterol diet (16% fat, 0.25% cholesterol, w/w; n=15) or high-fat/high-cholesterol diet containing CR (5 % dried CR powder, w/w, n=16) for 8 weeks. There were no significant differences in body weight between the groups. Serum total cholesterol, non-HDL cholesterol and triglyceride concentrations were significantly lower in control than CR group with no significant differences in serum HDL-C and apoA-I. Mice fed CR showed significantly higher serum lecithin-cholesterol acyltransferase activity than the control. Liver weight and steatosis were not significantly different between the groups, but hepatic expression of genes involved in cholesterol metabolism was significantly lower in the CR group. In the epididymal white adipose tissue (eWAT), the CR group showed higher weights with decreased expression of genes for lipogenesis and fatty acid oxidation. The mRNA abundance of F4/80, a macrophage marker, and the numbers of crown-like structures were less in the CR group. In the soleus muscle, the CR group also demonstrated higher expression of genes for fatty acid β-oxidation and mitochondrial biogenesis than those of the control. In conclusion, although CR consumption elicited minor effects on HDL metabolism, it prevented obesity-induced inflammation in eWAT with concomitant alterations in soleus muscle energy metabolism.
This study aimed to evaluate the inflammatory response, oxidative status, and fatty acid deposition in reproductive tissues of cats supplemented with the dried microalgae Schizochytrium spp. (Thraustochytriaceae) as docosahexaenoic acid (DHA) source. Thirty-seven cats (males, n= 21; females, n= 16; 11.5±0.5 months of age) were divided by sex into five groups. Treatment diets contained algae biomass at 4.0, 8.0, 12.0, or 16.0 g/kg replacing poultry fat (omega-6 source). Cats were fed the respective diet for 62 d and neutered on day 58. Blood samples were collected at the beginning of the experiment (day 1), before neutering (day 58), and four days after surgery (day 62) for analysis of inflammation and oxidative markers. Acute-phase protein levels were altered (P < 0•01) in the postoperative period, without any treatment effect (P > 0•05). Prostaglandin E2 (PGE2) concentrations after surgery was reduced linearly (R2 = 0.8706; P = 0•002) with microalgal inclusion. Blood platelet count was reduced (P = 0•001) after the surgery regardless treatment but, it was higher in the DHA group compared to Control (P < 0•001). The DHA deposition (testicles, R2 = 0.846; ovaries, R2 = 0.869), and the omega-6/omega-3 ratio (testicles, R2 = 0.859; ovaries, R2 = 0.955) in gonads had a pattern which fitted a quadratic model. DHA from Schizochytrium spp. modifies PGE2 response after the surgery in cats. The physiological roles of the DHA in the reproduction of cats were not investigated, but its gonadal deposition after supplementation was observed.
Hair cortisol concentration (HCC) can be used to periodically assess hypothalamo-pituitary-adrenal axis function, and appears correlated with prolonged exposure to stress.
Serial assessment (at Baseline, Week 6 and Week 12) of participants (n=35) with anxiety disorders by psychopathological rating scales, with assays of HCC and levels of peripheral anti- and pro- inflammatory cytokines. Patients underwent antidepressant treatment for an initial six weeks, followed by COX-2 inhibitor (celecoxib) augmentation or ‘treatment as usual’ for a further six weeks.
At Baseline (n=35), HCC was elevated in patients with single-episode but not recurrent-episode anxiety disorders, mean IL-12p70 levels were low, and mean TNF-α levels were elevated. Following 6 weeks of antidepressant treatment (n=33), mean HCC was within the normal range but mean IL-2 level was low. Celecoxib augmentation (n=18) was associated with reduction in anxiety symptoms and normalisation of mean IL-2 levels.
Small sample size. Not all participants were assessed at all time points.
Serial assessment of hair cortisol concentration is practicable in patients with anxiety disorders. These preliminary findings warrant further investigation in larger samples.
As COVID-19 continues to spread worldwide, severe disease and mortality have been observed in obese patients. We discuss how obesity and obesity-associated factors such as ‘meta-flammation’, dietary fat intake and paradoxical suppression of the innate immune response within the pulmonary compartment may be crucial determinants in the host response to a novel viral pathogen. Modulation of immune cell bioenergetics and metabolic potential plays a central role in the innate immune response to infection, and as we strive to combat this new global health threat, immunometabolism of the innate immune system warrants attention.
Air pollution is linked to mortality and morbidity. Since humans spend nearly all their time indoors, improving indoor air quality (IAQ) is a compelling approach to mitigate air pollutant exposure. To assess interventions, relying on clinical outcomes may require prolonged follow-up, which hinders feasibility. Thus, identifying biomarkers that respond to changes in IAQ may be useful to assess the effectiveness of interventions.
We conducted a narrative review by searching several databases to identify studies published over the last decade that measured the response of blood, urine, and/or salivary biomarkers to variations (natural and intervention-induced) of changes in indoor air pollutant exposure.
Numerous studies reported on associations between IAQ exposures and biomarkers with heterogeneity across study designs and methods. This review summarizes the responses of 113 biomarkers described in 30 articles. The biomarkers which most frequently responded to variations in indoor air pollutant exposures were high sensitivity C-reactive protein (hsCRP), von Willebrand Factor (vWF), 8-hydroxy-2′-deoxyguanosine (8-OHdG), and 1-hydroxypyrene (1-OHP).
This review will guide the selection of biomarkers for translational studies evaluating the impact of indoor air pollutants on human health.
Depression is a major cause of disability in adolescents. Higher dietary fibre intake has been associated with lower depressive symptoms in adults, but there is a lack of research in adolescents. We examined the association between dietary fibre intake (Commonwealth Scientific and Industrial Research Organisation (CSIRO) FFQ) and depressive symptoms (Beck Depression Inventory for Youth) in adolescents with prospective data from the Raine Study Gen2 14- and 17-year follow-ups (n 1260 and 653). Odds of moderate/extreme (clinically relevant) depressive symptoms by quartile of fibre intake were calculated using mixed-effects logistic regression for all participants, in a paired sample without moderate/extreme depressive symptoms at 14 years and in a sub-sample of participants with available inflammatory data at the ages of 14 and 17 years (n 718 and 547). Odds of moderate/extreme depressive symptoms were lower in the fourth (highest) quartile of overall fibre intake (OR 0·273, 95 % CI 0·09, 0·81) compared with the first (lowest) quartile, adjusting for sex, age, energy intake, adiposity, and family and lifestyle factors. However, further adjustment for dietary patterns attenuated the results. Associations of depressive symptoms with cereal or fruit and vegetable fibre intake were not significant in the final model. Adjustment for inflammation had no effect on OR. The association between a higher dietary fibre intake and lower odds of clinically relevant depressive symptoms may be more reflective of a high-fibre diet with all its accompanying nutrients than of an independent effect of fibre.
To compare the effects of a typical Food Distribution Program on Indian Reservations (FDPIR) diet with an FDPIR diet that meets Dietary Guidelines for Americans (DGA) on inflammation response, appetite and energy intake on a combination of American Indian (AI) and non-AI individuals.
A within-subjects, randomised, crossover design was used to compare two dietary conditions: (1) a FDPIR diet that met DGA and (2) a FDPIR diet that did not meet DGA. Each participant served as their own control and was exposed to both dietary conditions. Repeated-measures ANOVA and t tests assessed significance between the two dietary conditions.
This took place in the Montana State University Nutrition Research Laboratory in the USA.
Female and male participants (n 13) aged 18–55 years from the university and local community.
There were no significant differences in inflammatory response and appetite sensations between the two dietary conditions. Findings indicated that participants ate 14 % more (P < 0·01) kcal on a typical FDPIR diet compared with a FDPIR diet that met DGA.
Higher energy intake during a typical FDPIR diet compared with a FDPIR diet that meets DGA may increase risk for obesity and nutrition-related diseases, including type 2 diabetes and other chronic inflammatory conditions.
COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), was recognised by the WHO as a pandemic in 2020. Host preparation to combat the virus is an important strategy to avoid COVID-19 severity. Thus, the relationship between eating habits, nutritional status and their effects on the immune response and further implications in viral respiratory infections is an important topic discussed in this review. Malnutrition causes the most diverse alterations in the immune system, suppressing of the immune response and increasing the susceptibility to infections such as SARS-CoV-2. On the other hand, obesity induces low-grade chronic inflammation caused by excess adiposity, which increases angiotensin-converting enzyme 2. It decreases the immune response favouring SARS-CoV-2 virulence and promoting respiratory distress syndrome. The present review highlights the importance of food choices considering their inflammatory effects, consequently increasing the viral susceptibility observed in malnutrition and obesity. Healthy eating habits, micronutrients, bioactive compounds and probiotics are strategies for COVID-19 prevention. Therefore, a diversified and balanced diet can contribute to the improvement of the immune response to viral infections such as COVID-19.
Inflammation is a major cause of chronic diseases. Several studies have investigated the effects of soya intake on inflammatory biomarkers; however, the results are equivocal. The aim of this study was to conduct a systematic review and meta-analysis of clinical trials that evaluated the effect of soya consumption on inflammatory biomarkers. Medline, Scopus, ISI Web of Science and Google Scholar were systematically searched, up to and including May 2020, for clinical trials that evaluated the effects of soya and soya products on TNF-α, IL-6, IL-2, IL-1β and interferon γ (IFN-γ) in adults. A random effects method was used to calculate overall effects, and subgroup analyses were performed to discern probable sources of inter-study heterogeneity. A total of twenty-eight clinical trials were included. Although soya consumption reduced TNF-α (Hedges’ g = –0·28; 95 % CI –0·49, –0·07), it had no significant effect on IL-6 (Hedges’ g = 0·07, 95 % CI –0·14, 0·28), IL-2 (mean difference (MD) = –1·38 pg/ml; 95 % CI –3·07, 0·31), IL-1β (MD = –0·02 pg/ml; 95 % CI –0·08, 0·03) and IFN-γ (MD = 1685·82 pg/ml; 95 % CI –1604·86, 4976·50). Subgroup analysis illustrated a reduction in TNF-α in parallel designed studies, at dosages ≥100 mg of isoflavones, and in unhealthy subjects. The present study showed that high doses of isoflavones in unhealthy subjects may yield beneficial effects on TNF-α.
The present study was conducted to determine the effects of dietary terrestrial oils (TO) supplemented with l-carnitine on growth performance, biochemical and antioxidant response, lipid metabolism and inflammation in large yellow croaker (Larimichthys crocea). Three iso-nitrogenous and iso-lipidic experimental diets were formulated with FO (fish oil, the control group), 75 % TO (75 % FO was substituted by the oil mixture with equal amounts of soyabean oil, linseed oil and pork lard) and 75 % TOC (75 % TO supplemented with 800 mg/kg l-carnitine). Compared with the control group, feed efficiency ratio and specific growth rate were significantly increased in fish fed diets with 75 % TO and 75 % TOC. Hepatic lipid content, serum TAG level, LDL-cholesterol level and the mRNA expression of pro-inflammatory genes (tnfα and ifnγ) were significantly increased in fish fed the diet with 75 % TO compared with the control group. However, the supplementation of 800 mg/kg l-carnitine in the 75 % TO diet repressed hepatic lipid content, serum LDL-cholesterol level and the mRNA expression of tnfα and ifnγ in fish compared with fish fed the diet with 75 % TO. Total antioxidant capacity, the activity of superoxide dismutase, the mRNA expression of cpt-I and the activity of CPT-I were significantly increased in fish fed the diet with 75 % TOC compared with 75 % TO. In conclusion, these results suggested that the supplementation of 800 mg/kg l-carnitine in the diet with TO mixture could increase growth, antioxidant capacity and fatty acid oxidation and decrease the expression of inflammatory genes in large yellow croaker.
Evidence from animal models demonstrate that intrauterine growth restriction (IUGR) alters airway structure and function which may affect susceptibility to disease. Airway inflammation and dysregulated epithelial barrier properties are features of asthma which have not been examined in the context of IUGR. This study used a maternal hypoxia-induced IUGR mouse model to assess lung-specific and systemic inflammation and airway epithelial tight junctions (TJs) protein expression. Pregnant BALB/c mice were housed under hypoxic conditions (10.5% O2) from gestational day (GD) 11 to 17.5 (IUGR group; term, GD 21). Following hypoxic exposure, mice were returned to a normoxic environment (21% O2). A Control group was housed under normoxic conditions throughout pregnancy. Offspring weights were recorded at 2 and 8 weeks of age and euthanized for bronchoalveolar lavage (BAL) and peritoneal cavity fluid collection for inflammatory cells counts. From a separate group of mice, right lungs were collected for Western blotting of TJs proteins. IUGR offspring had greater inflammatory cells in the BAL fluid but not in peritoneal fluid compared with Controls. At 8 weeks of age, interleukin (IL)-2, IL-13, and eotaxin concentrations were higher in male IUGR compared with male Control offspring but not in females. IUGR had no effect on TJs protein expression. Maternal hypoxia-induced IUGR increases inflammatory cells in the BAL fluid of IUGR offspring with no difference in TJs protein expression. Increased cytokine release, specific to the lungs of IUGR male offspring, indicates that both IUGR and sex can influence susceptibility to airway disease.
Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome. Recent evidence has suggested the protective effects of honey consumption against the metabolic syndrome, but the association between honey intake and NAFLD is still unclear. We investigated how the consumption frequency of honey was associated with NAFLD in the general population. This was a cross-sectional study of 21 979 adults aged 20–90 years. NAFLD was diagnosed based on the ultrasound-diagnosed fatty liver without significant alcohol intake and other liver diseases. Diet information, including consumption frequency of honey, was assessed by a validated 100-item FFQ. OR with 95 % CI were calculated by the binary logistic regression model, adjusting for confounding factors identified by the directed acyclic graph. Overall, 6513 adults (29·6 %) had NAFLD. Compared with participants consuming ≤1 time/week of honey, the multivariable OR of NAFLD were 0·86 (95 % CI 0·77, 0·97) for 2–6 times/week and 1·10 (95 % CI 0·95, 1·27) for ≥1 times/d (Pfor trend = 0·90). The results were generally similar in subgroups of BMI at a cut-point of 24·0 kg/m2 (Pfor interaction = 0·10). In this large-scale study, consuming honey 2–6 times/week was inversely associated with NAFLD, whereas consuming honey ≥1 times/d had no association with NAFLD. These results need replication in other large-scale prospective studies.
Polycystic ovary syndrome (PCOS) is defined as a reproductive endocrine disease that results in a low-grade inflammatory and pro-oxidant state. Dietary factors, including n-3 fatty acids, may have a key role in improving metabolic disorders in PCOS patients. The present study aimed to investigate the influence of n-3 fatty acid supplementation on inflammatory and oxidative stress (OS) markers in patients with PCOS. A systematic literature search of Medline/PubMed, Cochrane Central Register of Controlled Trials, Scopus and Lilacs, until November 2019, was conducted. Randomised clinical trials that reported inflammatory and OS markers as endpoints in women with PCOS receiving n-3 fatty acid supplementation were included. The pooled estimates of the weighted mean differences (WMD) and the standard mean differences (SMD) were calculated. Random effects models were adopted to measure the pooled outcomes. Among the 323 studies retrieved, ten fulfilled the inclusion criteria for a meta-analysis. We founded a significant decrease in high-sensitivity C-reactive protein (hs-CRP) (SMD –0·29 (95 % CI –0·56, –0·02) mg/l) and an increase in adiponectin (WMD 1·42 (95 % CI 1·09, 1·76) ng/ml) concentrations in the intervention group when compared with the placebo group. No statistically significant results were found in the meta-analysis for visfatin, nitric oxide, GSH or malondialdehyde levels or total antioxidant capacity. The data suggest that supplementation of n-3 fatty acids could reduce the inflammatory state in women with PCOS, through a decrease in hs-CRP and an increase in adiponectin levels.
Se is a micronutrient essential for human health. Sub-optimal Se status is common, occurring in a significant proportion of the population across the world including parts of Europe and China. Human and animal studies have shown that Se status is a key determinant of the host response to viral infections. In this review, we address the question whether Se intake is a factor in determining the severity of response to coronavirus disease 2019 (COVID-19). Emphasis is placed on epidemiological and animal studies which suggest that Se affects host response to RNA viruses and on the molecular mechanisms by which Se and selenoproteins modulate the inter-linked redox homeostasis, stress response and inflammatory response. Together these studies indicate that Se status is an important factor in determining the host response to viral infections. Therefore, we conclude that Se status is likely to influence human response to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and that Se status is one (of several) risk factors which may impact on the outcome of SARS-CoV-2 infection, particularly in populations where Se intake is sub-optimal or low. We suggest the use of appropriate markers to assess the Se status of COVID-19 patients and possible supplementation may be beneficial in limiting the severity of symptoms, especially in countries where Se status is regarded as sub-optimal.
Sarcopenic obesity is characterised by the double burden of diminished skeletal muscle mass and the presence of excess adiposity. From a mechanistic perspective, both obesity and sarcopenia are associated with sub-acute, chronic pro-inflammatory states that impede metabolic processes, disrupting adipose and skeletal functionality, which may potentiate disease. Recent evidence suggests that there is an important cross-talk between metabolism and inflammation, which has shifted focus upon metabolic-inflammation as a key emerging biological interaction. Dietary intake, physical activity and nutritional status are important environmental factors that may modulate metabolic-inflammation. This paradigm will be discussed within the context of sarcopenic obesity risk. There is a paucity of data in relation to the nature and the extent to which nutritional status affects metabolic-inflammation in sarcopenic obesity. Research suggests that there may be scope for the modulation of sarcopenic obesity with alterations in diet. The potential impact of increasing protein consumption and reconfiguration of dietary fat composition in human dietary interventions are evaluated. This review will explore emerging data with respect to if and how different dietary components may modulate metabolic-inflammation, particularly with respect to adiposity, within the context of sarcopenic obesity.
Coeliac disease (CD) is a chronic, immune-mediated condition caused by exposure to dietary gluten in genetically susceptible individuals. The prevalence of CD in the general population is estimated at 1%. A gluten-free diet (GFD) is an effective treatment for the vast majority of individuals with CD. Despite advances in serological testing, the duodenal biopsy remains essential for the diagnosis of CD.
The morphological features of established CD have been well described. However, early changes in the duodenum, e.g. an increase in intraepithelial lymphocytes, are not specific for CD. Architectural changes in the duodenal biopsy are more specific for CD, but the pathologist should be aware of other conditions that can cause villous atrophy.
Some patients with CD do not respond to a GFD, and may have refractory CD (RCD), a condition believed to represent a cryptic form of the most common malignancy in CD: enteropathy-associated T-cell lymphoma. Early detection of RCD is essential in guiding more aggressive management.
The aims of this chapter are to describe the histological features of CD and its variations and complications, and to discuss the key differential diagnoses, with particular emphasis on features that help to distinguish CD from other conditions.
Inflammation and metabolic dysregulation are age-related physiological changes and are associated with depressive disorder. We tried to identify subgroups of depressed older patients based on their metabolic-inflammatory profile and examined the course of depression for these subgroups.
This clinical cohort study was conducted in a sample of 364 depressed older (⩾60 years) patients according to DSM-IV criteria. Severity of depressive symptoms was monitored every 6 months and a formal diagnostic interview repeated at 2-year follow-up. Latent class analyses based on baseline metabolic and inflammatory biomarkers were performed. Adjusted for confounders, we compared remission of depression at 2-year follow-up between the metabolic-inflammatory subgroups with logistic regression and the course of depression severity over 2-years by linear mixed models.
We identified a ‘healthy’ subgroup (n = 181, 49.7%) and five subgroups characterized by different profiles of metabolic-inflammatory dysregulation. Compared to the healthy subgroup, patients in the subgroup with mild ‘metabolic and inflammatory dysregulation’ (n = 137, 37.6%) had higher depressive symptom scores, a lower rate of improvement in the first year, and were less likely to be remitted after 2-years [OR 0.49 (95% CI 0.26–0.91)]. The four smaller subgroups characterized by a more specific immune-inflammatory dysregulation profile did not differ from the two main subgroups regarding the course of depression.
Nearly half of the patients with late-life depressions suffer from metabolic-inflammatory dysregulation, which is also associated with more severe depression and a worse prognosis. Future studies should examine whether these depressed older patients benefit from a metabolic-inflammatory targeted treatment.
Less than 40% of depressed older adults treated with an antidepressant achieve remission. Incomplete response to treatment is common. Current augmentation strategies have limited efficacy, and many have side effects that restrict their utilization in older adults. We conducted the first open pilot trial of minocycline augmentation in older adults who had failed to achieve remission after adequate psychopharmacologic treatment. Subjects older than 55 years of age with major depression and failure to achieve substantial improvement of depressive symptoms after at least 6 weeks of antidepressant treatment were given augmentation with minocycline 100 mg twice daily over an 8-week period. At the end of 8 weeks of augmentation with minocycline, 31% (4/13) patients achieved remission. Remitters had higher baseline ratings of hopelessness and apathy. Minocycline was well tolerated with no reported adverse events or discontinuation due to intolerance. Larger placebo-controlled studies are needed to evaluate the effects of minocycline augmentation in older adults who had failed to achieve remission after adequate treatment with antidepressants.
The aims of this study were to evaluate changes in inflammatory and oxidative stress levels following treatment with N-acetylcysteine (NAC) or mitochondrial-enhancing agents (CT), and to assess the how these changes may predict and/or moderate clinical outcomes primarily the Montgomery-Åsberg Depression Rating Scale (MADRS).
This study involved secondary analysis of a placebo-controlled randomised trial (n = 163). Serum samples were collected at baseline and week 16 of the clinical trial to determine changes in Interleukin-6 (IL-6) and total antioxidant capacity (TAC) following adjunctive CT and/or NAC treatment, and to explore the predictability of the outcome or moderator effects of these markers.
In the NAC-treated group, no difference was observed in serum IL-6 and TAC levels after 16 weeks of treatment with NAC or CT. However, results from a moderator analysis showed that in the CT group, lower IL-6 levels at baseline was a significant moderator of MADRS χ2 (df) = 4.90, p = 0.027) and Clinical Global Impression-Improvement (CGI-I, χ2 (df) = 6.28 p = 0.012). In addition, IL-6 was a non-specific but significant predictor of functioning (based on the Social and Occupational Functioning Assessment Scale (SOFAS)), indicating that individuals with higher IL-6 levels at baseline had a greater improvement on SOFAS regardless of their treatment (p = 0.023).
Participants with lower IL-6 levels at baseline had a better response to the adjunctive treatment with the mitochondrial-enhancing agents in terms of improvements in MADRS and CGI-I outcomes.
Whole-grain wheat, in particular coloured varieties, may have health benefits in adults with chronic metabolic disease risk factors. Twenty-nine overweight and obese adults with chronic inflammation (high-sensitivity C-reactive protein) > 1·0 mg/l) replaced four daily servings of refined grain food products with bran-enriched purple or regular whole-wheat convenience bars (approximately 41–45 g fibre, daily) for 8 weeks in a randomised, single-blind parallel-arm study where body weight was maintained. Anthropometrics, blood markers of inflammation, oxidative stress, and lipaemia and metabolites of anthocyanins and phenolic acids were compared at days 1, 29 and 57 using repeated-measures ANOVA within groups and ANCOVA between groups at day 57, with day 1 as a covariate. A significant reduction in IL-6 and increase in adiponectin were observed within the purple wheat (PW) group. TNF-α was lowered in both groups and ferulic acid concentration increased in the regular wheat (RW) group. Comparing between wheats, only plasma TNF-α and glucose differed significantly (P < 0·05), that is, TNF-α and glucose decreased with RW and PW, respectively. Consumption of PW or RW products showed potential to improve plasma markers of inflammation and oxidative stress in participants with evidence of chronic inflammation, with modest differences observed based on type of wheat.