scholarly journals Serum inflammatory biomarkers and clinical outcomes of COPD exacerbation caused by different pathogens

2017 ◽  
Vol Volume 12 ◽  
pp. 1625-1630 ◽  
Author(s):  
Theerasuk Kawamatawong ◽  
Apitch Apiwattanaporn ◽  
Warisara Siricharoonwong
2013 ◽  
Vol 131 (4) ◽  
pp. 1008-1016 ◽  
Author(s):  
Neil C. Thomson ◽  
Rekha Chaudhuri ◽  
Liam G. Heaney ◽  
Christine Bucknall ◽  
Robert M. Niven ◽  
...  

JAMA ◽  
2021 ◽  
Vol 326 (13) ◽  
pp. 1277
Author(s):  
David Jiménez ◽  
Alvar Agustí ◽  
Eva Tabernero ◽  
Luis Jara-Palomares ◽  
Ascensión Hernando ◽  
...  

2021 ◽  
Vol Volume 16 ◽  
pp. 3055-3064
Author(s):  
B Ditz ◽  
LEM Kistemaker ◽  
M van den Berge ◽  
JM Vonk ◽  
R Gosens ◽  
...  

Author(s):  
Jingrong Wang ◽  
Xingqi Dong ◽  
Boting Zhang ◽  
Xinping Yang ◽  
Zhi Li ◽  
...  

AbstractSevere COVID-19 patients showed worse clinical outcomes compared to mild and moderate patients. However, effective indicators are still lacking to predict the severity of the disease. In the present study, we retrospectively analyzed the clinical and laboratory data of 16 COVID-19 patients and found that the absolute counts of three T-cells (CD3+, CD4+, and CD8+) were significantly lower in the moderate and severe patients than those in mild patients and were significantly lower in severe patients than in moderate patients on admission. With the recovery of the COVID-19, serum levels of inflammatory biomarkers (CRP, PCT, and IL6) of moderate and severe patients gradually decreased. In contrast, the counts of lymphocytes and their subsets including CD3+, CD4+, and CD8+ T cells gradually increased in severe patients, and eventually showed comparable levels with moderate patients. ROC analysis showed that the counts of CD3+, CD4+, and CD8+ T-cells with AUC > 0.9 have potential values for predicting the severity of COVID-19 patients. In conclusion, the reduction of CD3+, CD4+, and CD8+ T-cells is related to the severity of COVID-19 and dynamic detection of these T-lymphocyte subsets may help predict the outcome of the patients.


Author(s):  
Solanka E. Ledwaba ◽  
Deiziane V. S. Costa ◽  
David T. Bolick ◽  
Natasa Giallourou ◽  
Pedro H. Q. S. Medeiros ◽  
...  

Enteropathogenic E. coli (EPEC) are recognized as one of the leading bacterial causes of infantile diarrhea worldwide. Weaned C57BL/6 mice pretreated with antibiotics were challenged orally with wild-type EPEC or escN mutant (lacking type 3 secretion system) to determine colonization, inflammatory responses and clinical outcomes during infection. Antibiotic disruption of intestinal microbiota enabled efficient colonization by wild-type EPEC resulting in growth impairment and diarrhea. Increase in inflammatory biomarkers, chemokines, cellular recruitment and pro-inflammatory cytokines were observed in intestinal tissues. Metabolomic changes were also observed in EPEC infected mice with changes in tricarboxylic acid (TCA) cycle intermediates, increased creatine excretion and shifts in gut microbial metabolite levels. In addition, by 7 days after infection, although weights were recovering, EPEC-infected mice had increased intestinal permeability and decreased colonic claudin-1 levels. The escN mutant colonized the mice with no weight loss or increased inflammatory biomarkers, showing the importance of the T3SS in EPEC virulence in this model. In conclusion, a murine infection model treated with antibiotics has been developed to mimic clinical outcomes seen in children with EPEC infection and to examine potential roles of selected virulence traits. This model can help in further understanding mechanisms involved in the pathogenesis of EPEC infections and potential outcomes and thus assist in the development of potential preventive or therapeutic interventions.


2020 ◽  
Author(s):  
Solanka E. Ledwaba ◽  
Deiziane V.S. Costa ◽  
David T. Bolick ◽  
Natasa Giallourou ◽  
Pedro H.Q.S. Medeiros ◽  
...  

ABSTRACTEnteropathogenic E. coli (EPEC) are recognized as one of the leading bacterial causes of infantile diarrhea worldwide. Weaned C57BL/6 mice pretreated with antibiotics were challenged orally with wild-type EPEC or escN mutant (lacking type 3 secretion system) to determine colonization, inflammatory responses and clinical outcomes during infection. Antibiotic disruption of intestinal microbiota enabled efficient colonization by wild-type EPEC resulting in growth impairment and diarrhea. Increase in inflammatory biomarkers, chemokines, cellular recruitment and pro-inflammatory cytokines were observed in intestinal tissues. Metabolomic changes were also observed in EPEC infected mice with changes in TCA cycle intermediates, increased creatine excretion and shifts in gut microbial metabolite levels. In addition, by 7 days after infection, although weights were recovering, EPEC-infected mice had increased intestinal permeability and decreased colonic claudin-1 levels. The escN mutant colonized the mice, but had no weight changes or increased inflammatory biomarkers, showing the importance of the T3SS in EPEC virulence in this model. In conclusion, a murine infection model treated with antibiotics has been developed to mimic many clinical outcomes seen in children with EPEC infection and to examine potential roles of selected virulence traits. This model can help in further understanding mechanisms involved in the pathogenesis of EPEC infections and potential outcomes and thus assist in the development of potential preventive or therapeutic interventions.


2019 ◽  
Vol 6 (Supplement_2) ◽  
pp. S483-S484
Author(s):  
Molly Triner ◽  
Sunita Patel ◽  
Rachael Craft ◽  
Aarthi Rajkumar ◽  
Tejas Patel

Abstract Background Chronic obstructive pulmonary disease (COPD) exacerbation and community-acquired pneumonia (CAP) are major drivers of antibiotic overuse, primarily due to challenges in pathogen identification. Procalcitonin is a serum biomarker that assists in distinguishing bacterial infection from other causes. The purpose of this study was to determine whether the use of a procalcitonin (PCT) guided algorithm in patients diagnosed with COPD exacerbation and/or CAP can reduce antibiotic exposure without negatively impacting clinical outcomes. Methods This was a quasi-experimental study conducted at Mercy Medical Center in Canton, Ohio. The patient data for the retrospective cohort (control group) was collected from the months of September 2017 through January 2018. The prospective phase (PCT group) took place during the months of September 2018 through January 2019. Physicians utilized a procalcitonin guided algorithm to determine appropriate initiation and duration of antibiotic use in patients admitted with a primary diagnosis of COPD exacerbation and/or CAP. The primary outcome was the duration of antibiotic therapy, measured in days. Secondary outcomes included all-cause hospital readmission within 30 days of discharge, respiratory-related hospital readmission within 30 days of discharge, 30-day mortality, hospital length of stay, and adverse events to antibiotics. Results A total of 76 patients were included in the study, 43 in the control group and 33 in the PCT group. Baseline characteristics were similar between groups. The use of a PCT algorithm significantly decreased duration of antibiotics by 2.7 days in comparison to the control group (2.6 [n = 33] vs. 5.3 [n = 43] days; P < 0.001; 95% CI). Secondary safety outcomes between the PCT and control group were similar, including all-cause hospital readmission within 30 days of discharge (30.3% vs. 25.6%; P = 0.648), respiratory-related hospital readmission within 30 days of discharge (80.0% [n = 10] vs. 81.8% [n = 11]; P = 0.731), and 30-day mortality (no incidence in either group). Conclusion The use of a PCT algorithm significantly reduced duration of antibiotics by 2.7 days without negatively impacting clinical outcomes in patients being treated for COPD exacerbation and/or CAP. Disclosures All authors: No reported disclosures.


Sign in / Sign up

Export Citation Format

Share Document