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Pathobiome driven gut inflammation in Pakistani children with Environmental Enteric Dysfunction
Najeeha T Iqbal1,2, Sana Syed1,3, Furqan Kabir1
1Department of Pediatrics and Child Health, Aga Khan University, Karachi, Pakistan.
Insights
Environmental Enteric Dysfunction (EED) in children is linked to enteropathogen infections, causing growth faltering. Targeting these pathogens with vaccines may prevent stunting.
Area of Science:
- Pediatrics
- Infectious Diseases
- Gastroenterology
Background:
- Environmental Enteric Dysfunction (EED) is a significant cause of stunting in children under five in low- and middle-income countries.
- EED results from repeated exposure to enteropathogens and toxins, leading to malabsorption and impaired linear growth.
- Understanding the link between pathogen burden and EED biomarkers is crucial for developing effective interventions.
Purpose of the Study:
- To investigate the association between enteropathogen infections and linear growth faltering in a birth cohort.
- To analyze the correlation between pathogen burden and specific biomarkers of EED.
- To identify key enteropathogens contributing to growth impairment in early childhood.
Main Methods:
- A longitudinal birth cohort study with 272 children, tracking monthly anthropometric measurements (Length for Age Z score - LAZ) up to 18 months.
- Fecal samples analyzed using a customized TaqMan array card to detect 40 enteropathogens at 6 and 9 months.
- Linear regression models used to assess the impact of specific enteropathogen infections on changes in linear growth (ΔLAZ) and EED biomarkers (MPO, Reg1b, flagellin IgA).
Main Results:
- Presence of any enteropathogen correlated with increased levels of serum flagellin IgA and fecal/serum Reg1b.
- Specific pathogens like Campylobacter and ETEC LT were associated with increased MPO levels at 6 months.
- Giardia infection correlated with elevated Reg1b and anti-flic IgA.
- Multiple enteropathogen infections in early life showed a negative correlation with ΔLAZ and altered gut inflammatory/permeability markers.
Conclusions:
- Early-life enteropathogen infections are associated with impaired linear growth and EED biomarkers.
- The findings highlight the detrimental impact of pathogen burden on child development.
- A combination vaccine targeting common enteropathogens could be a viable strategy for preventing stunting.
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.
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