Effects of age and comorbidities on inflammatory markers in community-acquired pneumonia

Abstract Background: Studies have suggested that an inappropriate inflammatory response is a major cause of treatment failure and mortality in patients with community-acquired pneumonia (CAP). We aimed to determine the effect of comorbidities and age on serum inflammatory markers in CAP.Methods: We performed a prospective cohort study of adults hospitalized with CAP. For the purposes of this study, we compared patients according to comorbidities and age. Inflammatory markers were measured at hospital admission, focusing on acute phase proteins, cytokines, and monocyte human leukocyte antigen DR (mHLA-DR) expression.Results: In patients with chronic pulmonary disease (COPD), serum cytokines had significantly decreased levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and mHLA-DR expression, as well as the C-reactive protein (CRP), compared with patients who had no comorbidities. Similarly, patients with chronic heart disease had a significantly reduced CRP levels and mHLA-DR expression, whereas patients with chronic kidney disease had significantly higher serum levels of procalcitonin and TNF-α. Lower procalcitonin, IL-6, and IL-10 levels, as well as mHLA-DR expression, were documented in older patients, but with no significant differences compared to younger patients. Multimorbidity in older patients was associated with significant lower levels of CRP and mHLA-DR expression.Conclusions: The circulating inflammatory markers to CAP have profiles that differ with age and underlying comorbidities. Multimorbidity in the elderly is also associated with lower serum levels of some inflammatory markers. These findings suggest that age and comorbidities have much more of an impact than to simply reduce physiological reserve and can cause variations in the inflammatory response in CAP.

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Effects of age and comorbidities on serum levels of inflammatory markers in community‐acquired pneumonia

European Journal of Clinical Investigation ◽

10.1111/eci.13480 ◽

2021 ◽

Author(s):

Diego Viasus ◽

Antonella F. Simonetti ◽

Andrés F. Estupiñan‐Bohórquez ◽

Jordi Carratalà

Keyword(s):

Inflammatory Markers ◽

Serum Levels ◽

Community Acquired Pneumonia

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Anti-Inflammatory Effects of Exercise on Metabolic Syndrome Patients: A Systematic Review and Meta-Analysis

Biological Research For Nursing ◽

10.1177/1099800420958068 ◽

2020 ◽

pp. 109980042095806 ◽

Cited By ~ 1

Author(s):

Heidar Alizaei Yousefabadi ◽

Arghavan Niyazi ◽

Sahar Alaee ◽

Mehrdad Fathi ◽

Gholam Rasul Mohammad Rahimi

Keyword(s):

Metabolic Syndrome ◽

Exercise Training ◽

Inflammatory Markers ◽

Meta Analysis ◽

Serum Levels ◽

Future Research ◽

The Metabolic Syndrome ◽

Inflammatory Status ◽

Tnf Α ◽

Training Impact

Background: Increments in inflammatory indicators and low levels of physical activity are correlated to the expansion of the metabolic syndrome (MetS). Objective: The purpose of this study was to establish if exercise training ameliorates inflammatory status in MetS patients. Data sources: PubMed, CINAHL, and Medline, Google Scholar, and Scopus databases and reference lists of included studies were searched. Study selection: Twenty randomized controlled trials (RCTs) of exercise-training impact on inflammatory markers (tumor necrosis factor (TNF) α, C-reactive protein (CRP), interleukin (IL) 6, IL-8, IL-10, and IL-18) with concurrent control groups were included in this analysis. Results: Results demonstrated an overall significant decrease in serum levels of TNF-α (mean difference (MD): −1.21 pg/ml; 95% confidence interval (CI): −1.77, −0.66), CRP (MD: −0.52 mg/l; 95% CI: −0.79, −0.25), IL-8 (MD: −1.31 pg/ml; 95% CI: −2.57, −0.06), and a significant increase in IL-10 (MD: 0.48 pg/ml; 95% CI: 0.10, 0.86). But exercise training did not change the level of IL-6 (MD: −0.69 pg/ml; 95% CI: −1.53, 0.14) and IL-18 (MD: −53.01 pg/ml; 95% CI: −166.64, 60.62). Conclusion: Exercise training improves TNF-α, CRP, IL-8, and IL-10 levels in patients with MetS. For some variables, isolated aerobic exercise, and combined aerobic and resistance exercise appears to be optimal. Future research is needed to clarify the mechanisms underlying exercise training’s effect on this population’s inflammatory markers. More studies are required to confirm these findings.

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Effects of Metformin on Life Span, Cognitive Ability, and Inflammatory Response in a Short-Lived Fish

The Journals of Gerontology Series A ◽

10.1093/gerona/glaa109 ◽

2020 ◽

Vol 75 (11) ◽

pp. 2042-2050 ◽

Cited By ~ 1

Author(s):

Juntong Wei ◽

He Qi ◽

Keke Liu ◽

Changsheng Zhao ◽

Yan Bian ◽

...

Keyword(s):

Inflammatory Response ◽

Life Span ◽

Cognitive Ability ◽

Healthy Aging ◽

Natural Aging ◽

Serum Levels ◽

Annual Fish ◽

Tnf Α ◽

Accelerated Growth ◽

Nothobranchius Guentheri

Abstract Metformin, an oral antidiabetic drug, prolongs the life span in nematode, silkworm, and other transgenic rodents, but its effects on longevity and aging-related cognitive ability using natural aging vertebrate models remain poorly understood. The genus of annual fish Nothobranchius show accelerated growth and expression of aging biomarkers. Here, using the short-lived fish Nothobranchius guentheri, we investigated effects of metformin on life span and aging-related cognitive ability and inflammation. Total of 145 fish, 72 fish were fed with metformin in the concentration of 2 mg/g food and 73 fish without metformin from 16 weeks of age until the end of their lives. The chronic feeding with metformin prolonged the life span of the fish and delayed aging with retarded accumulation of lipofuscin in liver, senescence-associated beta-galactosidase (SA-β-gal) activity in skin and serum levels of cholesterol and triglyceride significantly in the 10-month-old fish. Furthermore, metformin improved motor, learning, and memory skills by behavior tests accompanying with reduction of SA-β-gal activity and neurofibrillary degeneration and inhibition of inflammatory response including downregulated NF-κB and proinflammatory cytokines IL-8, TNF-α, and IL-1β expression and enhanced anti-inflammatory cytokine IL-10 level in brain. These findings demonstrate that metformin prolongs the life span and exerts neuroprotective and anti-inflammation function to improve cognitive ability in annual fish. It might be an effective strategy by using metformin to raise the possibility of promoting healthy aging of old population in aging process.

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Inflammatory and immunogenetic markers in correlation with pulmonary tuberculosis

Jornal Brasileiro de Pneumologia ◽

10.1590/s1806-37132013000600011 ◽

2013 ◽

Vol 39 (6) ◽

pp. 719-727 ◽

Cited By ~ 3

Author(s):

Beatriz Lima Alezio Muller ◽

Daniela Maria de Paula Ramalho ◽

Paula Fernanda Gonçalves dos Santos ◽

Eliene Denites Duarte Mesquita ◽

Afranio Lineu Kritski ◽

...

Keyword(s):

Inflammatory Response ◽

Pulmonary Tuberculosis ◽

Gene Polymorphisms ◽

Serum Levels ◽

Acute Inflammatory Response ◽

Reactive Protein ◽

Antituberculosis Treatment ◽

Tnf Α ◽

Referral Hospitals ◽

Ifn Γ

OBJECTIVE: To describe serum levels of the cytokines IL-10, TNF-α, and IFN-γ, as well as polymorphisms in the genes involved in their transcription, and their association with markers of the acute inflammatory response in patients with pulmonary tuberculosis.METHODS: This was a descriptive, longitudinal study involving 81 patients with pulmonary tuberculosis treated at two referral hospitals. We collected data on sociodemographic variables and evaluated bacteriological conversion at the eighth week of antituberculosis treatment, gene polymorphisms related to the cytokines studied, and serum levels of those cytokines, as well as those of C-reactive protein (CRP). We also determined the ESR and CD4+ counts.RESULTS: The median age of the patients was 43 years; 67 patients (82.7%) were male; and 8 patients (9.9%) were infected with HIV. The ESR was highest in the patients with high IFN-γ levels and low IL-10 levels. IFN-γ and TNF-α gene polymorphisms at positions +874 and −238, respectively, showed no correlations with the corresponding cytokine serum levels. Low IL-10 levels were associated with IL-10 gene polymorphisms at positions −592 and −819 (but not −1082). There was a negative association between bacteriological conversion at the eighth week of treatment and CRP levels.CONCLUSIONS: Our results suggest that genetic markers and markers of acute inflammatory response are useful in predicting the response to antituberculosis treatment.

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Molecular Inflammatory Responses Measured in Blood of Patients with Severe Community-Acquired Pneumonia

Clinical and Diagnostic Laboratory Immunology ◽

10.1128/cdli.10.5.813-820.2003 ◽

2003 ◽

Vol 10 (5) ◽

pp. 813-820 ◽

Cited By ~ 72

Author(s):

Silvia Fernández-Serrano ◽

Jordi Dorca ◽

Mercè Coromines ◽

Jordi Carratalà ◽

Francesc Gudiol ◽

...

Keyword(s):

Inflammatory Response ◽

Inflammatory Responses ◽

Community Acquired Pneumonia ◽

Causative Organism ◽

Time Interval ◽

Necrosis Factor Alpha ◽

Arterial Blood ◽

Tnf Α ◽

Intensive Care Unit Admittance ◽

Severe Community Acquired Pneumonia

ABSTRACT In order to analyze the characteristics of the inflammatory response occurring in blood during pneumonia, we studied 38 patients with severe community-acquired pneumonia. Venous and arterial blood samples were collected at study entry and on days 1, 2, 3, 5, and 7 after inclusion. The concentrations of proinflammatory (tumor necrosis factor alpha [TNF-α], interleukin 1β [IL-1β], IL-6, and IL-8) and anti-inflammatory (IL-10) cytokines were determined in order to detect differences related to the origin of the sample, the causative organism, the clinical variables, and the final outcome of the episode. Legionella pneumonia infections showed higher concentrations of TNF-α, IL-6, IL-8, and IL-10. After 24 h, plasma IL-6, IL-8, and IL-10 concentrations in pneumococcal episodes increased, whereas in the same time interval, cytokine concentrations in Legionella episodes markedly decreased. The characteristics of the inflammatory response in bacteremic pneumococcal episodes were different from those in nonbacteremic episodes, as indicated by the higher plasma cytokine concentrations in the former group. Finally, our analysis of cytokine concentrations with regard to the outcome—in terms of the need for intensive care unit admittance and/or mechanical ventilation as well as mortality—suggests that there is a direct relationship between the intensity of the inflammatory response measured in blood and the severity of the episode.

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CLINICAL AND IMMUNOLOGICAL INFLAMMATORY PATTERNS OF BRONCHIAL ASTHMA IN OBESE PATIENTS

Journal of microbiology epidemiology immunobiology ◽

10.36233/0372-9311-2019-1-59-63 ◽

2019 ◽

Vol 1 (1) ◽

pp. 59-63

Author(s):

A. Yu. Konischeva ◽

V. B. Gervazieva ◽

S. A. Mazurina

Keyword(s):

Bronchial Asthma ◽

Acute Phase ◽

Acute Phase Proteins ◽

Serum Levels ◽

Asthma Severity ◽

The Body ◽

Excess Body Weight ◽

Biochemical Tests ◽

Chronic Inflammatory Condition ◽

Tnf Α

We aimed to investigate immunological patterns of inflammation and autoimmunity, in bronchial asthma (BA) associated with obesity. Materials and methods. 109 people aged from 17 to 58 years with various body weights have been examined in total, including 64 individuals with allergic diseases as bronchial asthma (BA) and allergic rhinitis (AR). We performed the measurement of the body mass index according to WHO criteria, and evaluation of the asthma severity and comorbid conditions. In the samples of peripheral blood we measured biochemical tests (cholesterol and its fractions), spontaneous and PHA-induced production of cytokines: IL-4, IL-10, IL-17, TNF-, and serum levels of C-reactive protein (CRP), leptin, total IgE and IgE-autoAT, specific for a number of tissue AH (epithelial keratin, collagen 3 and 6 types, elastin and myosin). Results. Our study showed that in both groups of adults, the obesity was associated with increasing of acute phase proteins, CRP, leptin and TNF-α in serum, being most enhanced in asthma group. Individuals with excess body weight are characterized by significantly an increased level of acute phase proteins (Westergren ESR, CRP) and pro-inflammatory cytokines (TNF-α) in serum, thereby confirming the involvement of systemic inflammation in the obesity pathogenesis. The phenotype of BA with obesity is characterized by overproduction of CRP and leptin, along with increased spontaneous production of IL-4 and TNF-α, and also revealed sIgE to self-antigen as keratin, that in total could indicate more prominent inflammatory pathways with the impairment of immune regulation in this endotype of patients. Conclusion. The revealed associations confirm the link between obesity, as a chronic inflammatory condition, with atopy and development of asthma with further immune-mediated inflammation of the conduction airways.

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Variation in the Level of Thyroid Markers in Association with Inflammation in Patients with Type 2 Diabetes

Endocrine Metabolic & Immune Disorders - Drug Targets ◽

10.2174/1871530319666191125150929 ◽

2020 ◽

Vol 20 (6) ◽

pp. 924-929

Author(s):

Khalid Siddiqui ◽

Teena P. George ◽

Salini Scaria Joy ◽

Muhammad Mujammami

Keyword(s):

Type 2 Diabetes ◽

Glucose Metabolism ◽

Thyroid Hormones ◽

Inflammatory Markers ◽

Inflammatory Marker ◽

Serum Levels ◽

Cross Sectional Study ◽

Cross Sectional ◽

Tnf Α

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.

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Statins Attenuate the Increase in P-Selectin Produced by Prolonged Exercise

Journal of Sports Medicine ◽

10.1155/2013/487567 ◽

2013 ◽

Vol 2013 ◽

pp. 1-5 ◽

Cited By ~ 5

Author(s):

Amanda Zaleski ◽

Jeffrey Capizzi ◽

Kevin D. Ballard ◽

Christopher Troyanos ◽

Aaron Baggish ◽

...

Keyword(s):

Cardiovascular Risk ◽

Inflammatory Response ◽

Inflammatory Markers ◽

Prolonged Exercise ◽

Venous Blood ◽

Serum Levels ◽

Blood Samples ◽

Boston Marathon ◽

Exercise Induced ◽

Response To Exercise

Strenuous endurance exercise increases inflammatory markers and acutely increases cardiovascular risk; however, statins may mitigate this response. We measured serum levels of p-selectin in 37 runners treated with statins and in 43 nonstatin treated controls running the 2011 Boston Marathon. Venous blood samples were obtained the day before (PRE) as well as within 1 hour after (FINISH) and 24 hours after (POST) the race. The increase in p-selectin immediately after exercise was lower in statin users (PRE to FINISH: 20.5 ± 19.4 ng/mL) than controls (PRE to FINISH: 30.9 ± 27.1 ng/mL;P<0.001). The increase in p-selectin 24 hours after exercise was also lower in statin users (PRE to POST: 21.5 ± 26.6 ng/mL) than controls (PRE to POST: 29.3 ± 31.9 ng/mL;P<0.001). Furthermore, LDL-C was positively correlated with p-selectin at FINISH and POST (P<0.01andP<0.05, resp.), irrespective of drug treatment, suggesting that lower levels of LDL-C are associated with a reduced inflammatory response to exercise. We conclude that statins blunt the exercise-induced increase in p-selectin following a marathon and that the inflammatory response to a marathon varies directly with LDL-C levels.

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