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Abstract
Environmental Enteric Dysfunction (EED) is an acquired small intestinal inflammatory condition underlying high rates of stunting in children <5 years of age in low- and middle-income countries. Children with EED are known to have repeated exposures to enteropathogens and environmental toxins that leads to malabsorptive syndrome. We aimed to characterize association of linear growth faltering with enteropathogen burden and subsequent changes in EED biomarkers. In a longitudinal birth cohort (n = 272), monthly anthropometric measurements (Length for Age Z score- LAZ) of asymptomatic children were obtained up to 18 months. Biological samples were collected at 6 and 9 months for the assessment of biomarkers. A customized TaqMan array card was used to target 40 enteropathogens in fecal samples. Linear regression was applied to study the effect of specific enteropathogen infection on change in linear growth (ΔLAZ). Presence of any pathogen in fecal sample correlated with serum flagellin IgA (6 mo, r = 0.19, p = 0.002), fecal Reg 1b (6 mo, r = 0.16, p = 0.01; 9mo, r = 0.16, p = 0.008) and serum Reg 1b (6 mo, r = 0.26, p<0.0001; 9 mo, r = 0.15, p = 0.008). At 6 months, presence of Campylobacter [β (SE) 7751.2 (2608.5), p = 0.003] and ETEC LT [β (SE) 7089.2 (3015.04), p = 0.019] was associated with increase in MPO. Giardia was associated with increase in Reg1b [β (SE) 72.189 (26.394), p = 0.006] and anti-flic IgA[β (SE) 0.054 (0.021), p = 0.0091]. Multiple enteropathogen infections in early life negatively correlated with ΔLAZ, and simultaneous changes in gut inflammatory and permeability markers. A combination vaccine targeting enteropathogens in early life could help in the prevention of future stunting.
Highlights
Environmental Enteric dysfunction (EED) is a subclinical inflammatory disease of the small intestine characterized histologically by blunted villi, elongated crypts and increased lymphocytic infiltration of the lamina propria [1, 2]
Our study is limited with a) censoring of data at 18 months of age, limiting follow-up beyond 18 months to be able to ascertain the persistence of infection and outcome on long term growth and cognition; b) we evaluated growth faltering as changes in the linear slope of z scores, and were limited in using growth faltering at the first 18 months of life as a clinical proxy of EED; and lastly c) we were unable to collect dietary information in this cohort to correlate these important findings and d) multiple comparison of pathogens and biomarker data in regression model lost some of the significance after correction for false discovery rate (FDR)
Childhood infection with increasing numbers of pathogens is associated with an increase in biomarkers of inflammation and intestinal permeability with a decrease in linear growth
Summary
Environmental Enteric dysfunction (EED) is a subclinical inflammatory disease of the small intestine characterized histologically by blunted villi, elongated crypts and increased lymphocytic infiltration of the lamina propria [1, 2]. These histological changes are associated with subsequent malabsorption, impaired cognitive development [3, 4], reduced responsiveness to nutritional intervention [5], and reduced immunogenicity of oral vaccine [6, 7] in apparently healthy children [8, 9]. It is known that in the absence of diarrhea, 15% of children under five years are infected with ETEC as asymptomatic carriers [14]
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