Early-life enteric infections: relation between chronic systemic inflammation and poor cognition in children

Oriá, Reinaldo B.; Murray‐Kolb, Laura E.; Scharf, Rebecca J.; Pendergast, Laura L.; Lang, Dennis; Kolling, Glynis L.; Guerrant, Richard L.

doi:10.1093/nutrit/nuw008

Cited by 76 publications

(58 citation statements)

References 179 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Studies on the impact of chronic inflammation on early stages of disease development, as well as the impact of early life nutrition on the adult inflammatory status, greatly extended the knowledge in the field (reviewed in [ 5 ]). Emergence of inflammation in childhood has been associated with obesity [ 6 ], diet [ 7 ], enteral infections [ 8 ], and even social stress [ 9 ]. Gene polymorphisms of inflammatory markers [ 4 , 10 ] and/or inflammasome components [ 11 ] are also determinants of the inflammatory response of patients in the face of chronic injuries.…”

Section: Introductionmentioning

confidence: 99%

Inflammation-Related Mechanisms in Chronic Kidney Disease Prediction, Progression, and Outcome

Mihai

Codrici

Popescu

et al. 2018

Journal of Immunology Research

375

254

View full text Add to dashboard Cite

Persistent, low-grade inflammation is now considered a hallmark feature of chronic kidney disease (CKD), being involved in the development of all-cause mortality of these patients. Although substantial improvements have been made in clinical care, CKD remains a major public health burden, affecting 10–15% of the population, and its prevalence is constantly growing. Due to its insidious nature, CKD is rarely diagnosed in early stages, and once developed, its progression is unfortunately irreversible. There are many factors that contribute to the setting of the inflammatory status in CKD, including increased production of proinflammatory cytokines, oxidative stress and acidosis, chronic and recurrent infections, altered metabolism of adipose tissue, and last but not least, gut microbiota dysbiosis, an underestimated source of microinflammation. In this scenario, a huge step forward was made by the increasing progression of omics approaches, specially designed for identification of biomarkers useful for early diagnostic and follow-up. Recent omics advances could provide novel insights in deciphering the disease pathophysiology; thus, identification of circulating biomarker panels using state-of-the-art proteomic technologies could improve CKD early diagnosis, monitoring, and prognostics. This review aims to summarize the recent knowledge regarding the relationship between inflammation and CKD, highlighting the current proteomic approaches, as well as the inflammasomes and gut microbiota dysbiosis involvement in the setting of CKD, culminating with the troubling bidirectional connection between CKD and renal malignancy, raised on the background of an inflammatory condition.

show abstract

Section: Introductionmentioning

confidence: 99%

Inflammation-Related Mechanisms in Chronic Kidney Disease Prediction, Progression, and Outcome

Mihai

Codrici

Popescu

et al. 2018

Journal of Immunology Research

375

254

View full text Add to dashboard Cite

show abstract

“…CSI is believed to be one of the most important causes and playing an important role in the onset and development of diabetes, atherosclerosis and glycolipid disorders [3][4][5][6]. It is also reported to be associated with aging, obesity, disorder of lipid metabolism, poor cognition in children and a lot of major chronic, progressive and preventable diseases including cardiovascular diseases (CVD), diabetes mellitus (DM), cancers and others [7][8][9][10][11]. Since these major non-communicable chronic diseases (NCDs) can be managed upon early diagnosis, it enhances the necessity for a comprehensive approach in identifying the onset of CSI and related functional impairments in time.…”

Section: Introductionmentioning

confidence: 99%

Individual and joint association of bioavailable testosterone and aging with neutrophil-to-lymphocyte ratio in Chinese middle-aged and elderly men

et al. 2019

View full text Add to dashboard Cite

Background and objectives Accumulating evidences suggest that chronic systemic inflammation (CSI) is independently associated with large number of major non-communicable chronic diseases (NCDs) ranging from metabolic disorders to cancers, and neutrophil-to-lymphocyte ratio (NLR) has been accepted as a novel, convenient marker for CSI response. Testosterone deficiency in men is linked to high risk of NCDs. This cross-sectional study aimed to investigate the individual and joint association of bioavailable testosterone (BIOT) and aging with NLR. Methods A total of 132 male adults were enrolled during Jan. 2011 and Oct. 2017 in the first affiliated hospital of University of Science and Technology of China. Local weighted regression (LOESS) and multivariable generalized linear regression models were utilized to comprehensively examine the individual and joint association between BIOT and age with NLR. Results Obvious linear relationships between NLR and BIOT or age were observed with the LOESS models. NLR was negatively correlated to BIOT after adjusting for some potential confounding factors (P = 0.034). As compared to the lowest quartile of BIOT, the adjusted decrease of NLR for the 2nd, 3rd and 4th quartiles were 0.40, 0.64 and 0.72, respectively. Meanwhile, NLR was observed to be independently correlated to elevated age (P = 0.043). Furthermore, as compared to the counterparts, men over 70 years combined with plasma BIOT less than 4.7 nmol/L had the highest NLR level, which suggested that low BIOT and aging jointly correlated to the level of NLR (P = 0.005). Conclusion BIOT deficiency and aging were individually and jointly correlated to CSI. Men over 70 years combined with BIOT < 4.7 nmol/L were more like to have higher grade of CSI than others.

show abstract

“…Chronic diarrheal illness is associated with a combination of blunted villi, intestinal barrier dysfunction, and submucosal inflammation (45). In addition, early life enteric infections that impair intestinal barrier function have been proposed to cause a shift in the gut microbiota, promoting chronic systemic inflammation and consequently impaired cognitive development (3). In our studies neonatal EPEC infection resulted in intestinal pathophysiology, with increased ileal and colonic ion secretion persisting until adulthood.…”

mentioning

confidence: 59%

“…Despite advances in sanitation and access to clean drinking water, enteric infections remain a global public health issue, with diarrheal diseases a leading cause of death in children under age five worldwide (1). While treatment of diarrhea with oral rehydration solution has significantly decreased childhood mortality, repeated exposures to diarrheal pathogens have been correlated with impaired growth and cognitive deficits into adulthood (2)(3)(4). Malnutrition caused by enteric bacterial pathogens may support ongoing dysbiosis, resulting in gastrointestinal (GI) barrier dysfunction and systemic translocation of bacterial products (3,5).…”

Section: Introductionmentioning

confidence: 99%

Neonatal enteropathogenic Escherichia coli infection disrupts microbiota-gut-brain axis signaling

Hennessey

Barboza

Brust‐Mascher

et al. 2020

Preprint

View full text Add to dashboard Cite

BackgroundDiarrheal diseases are a leading cause of death in children under age five worldwide. Repeated early life exposures to diarrheal pathogens can result in co-morbidities including stunted growth and cognitive deficits suggesting an impairment in the microbiota-gut-brain (MGB) axis.MethodsNeonatal C57BL/6 mice were infected with EPEC (strain e2348/69; ΔescV [T3SS mutant]), or vehicle (LB broth) via orogastric gavage (105 CFU) at post-natal day (P7). Behavior (novel object recognition [NOR] task, light/dark [L/D] box, and open field test [OFT]), intestinal physiology (Ussing chambers), and the microbiota (16S Illumina sequencing) were assessed in adulthood (6-8 weeks).ResultsNeonatal infection of mice with EPEC impaired recognition memory (NOR task), coupled with increased neurogenesis (Ki67 and doublecortin immunostaining) and neuroinflammation (increased microglia activation [Iba1]) in adulthood. Intestinal pathophysiology was characterized by increased secretory state (short circuit current; Isc) and permeability (conductance; FITC-dextran flux) in the ileum and colon of neonatally EPEC-infected mice, along with increased expression of pro-inflammatory cytokines (Tnfα, Il12, Il6) and pattern recognition receptors (Nlr, Tlr). Finally, neonatal EPEC infection caused significant dysbiosis of the gut microbiota, including decreased Firmicutes, in adulthood.ConclusionsTogether these findings demonstrate that infection in early life can significantly impair the MGB axis in adulthood.

show abstract

Early-life enteric infections: relation between chronic systemic inflammation and poor cognition in children

Cited by 76 publications

References 179 publications

Inflammation-Related Mechanisms in Chronic Kidney Disease Prediction, Progression, and Outcome

Inflammation-Related Mechanisms in Chronic Kidney Disease Prediction, Progression, and Outcome

Individual and joint association of bioavailable testosterone and aging with neutrophil-to-lymphocyte ratio in Chinese middle-aged and elderly men

Neonatal enteropathogenic Escherichia coli infection disrupts microbiota-gut-brain axis signaling

Contact Info

Product

Resources

About