Association of enteric parasitic infections with intestinal inflammation and permeability in asymptomatic infants of São Tomé Island

Abstract

The cumulative effect of repeated asymptomatic enteric infections on intestinal barrier is not fully understood in infants. We aimed to evaluate the association between previous enteric parasitic infections and intestinal inflammation and permeability at 24-months of age, in asymptomatic infants of São Tomé Island. A subset of infants from a birth cohort, with intestinal parasite evaluations in at least four points of assessment, was eligible. Intestinal inflammatory response and permeability were assessed using fecal S100A12 and alpha-1-antitrypsin (A1AT), respectively. The cutoff <-1SD for weight-for-length and length-for-age was used to define wasting and stunting. Multivariable linear regression analysis explored if cumulative enteric parasitic infections explained variability of fecal biomarkers, after adjusting for potential confounders. Eighty infants were included. Giardia duodenalis and soil-transmitted helminths (STH) were the most frequent parasites. The median (interquartile range) levels were 2.87 μg/g (2.41-3.92) for S100A12 and 165.1 μg/g (66.0-275.6) for A1AT. Weak evidence of association was found between S100A12 levels and G. duodenalis (p = 0.080) and STH infections (p = 0.089), and between A1AT levels and parasitic infection of any etiology (p = 0.089), at 24-months of age. Significant associations between A1AT levels and wasting (p = 0.006) and stunting (p = 0.044) were found. Previous parasitic infections were not associated with fecal biomarkers at 24 months of age. To summarize, previous asymptomatic parasitic infections showed no association with intestinal barrier dysfunction. Notwithstanding, a tendency toward increased levels of the inflammatory biomarker was observed for current G. duodenalis and STH infections, and increased levels of the permeability biomarker were significantly associated with stunting and wasting.

Effect of selected gastrointestinal parasites and viral agents on fecal S100A12 concentrations in puppies as a potential comparative model

“…This is important for further studies evaluating fecal S100A12 concentrations in patients with suspected chronic gastrointestinal inflammation [ 27 ]. These findings are consistent with the results of a previous investigation in asymptomatic children showing fecal S100A12 concentrations to only have a tendency to be increased with concurrent Giardia duodenalis and helminth infections [ 20 ]. Also, the concentrations of fecal S100A12 measured in the study by Garzón et al [ 20 ] were comparable to those concentrations detected in our study.…”

“…Only very few studies have been published about the effect of enteric parasite infections [ 20 ] or enteropathogenic viruses [ 17 ] on fecal S100A12 concentrations in humans, and the role of S100A12 in parasite and viral infections is difficult to study using a traditional rodent animal model due to the lack of S100A12 in rodents [ 21 ]. Although the function of S100A12 may be species-specific, the existence of a homologue of this calgranulin protein in dogs [ 22 ] appears to render the dog an ideal model for studying S100A12 biology and the RAGE-S100A12 axis in human patients.…”

“…To the authors’ knowledge, the possibility of an effect of gastrointestinal pathogens on fecal S100A12 concentrations in dogs has not yet been evaluated and reported, but this information will also be important for any further evaluation of the clinical utility of fecal S100A12 as a biomarker in dogs with IBD. Based on the literature available [ 10 , 17 , 20 ], we hypothesized that infections with enteric parasites - but not enteropathogenic viruses - are associated with increased fecal canine S100A12 concentrations, and that these etiologies need to be ruled out when using fecal S100A12 as a biomarker in dogs with IBD. Thus, the aim of this study was to evaluate the effect of the presence and numbers of selected endoparasites and viral agents that are frequently encountered and known to cause gastrointestinal signs in dogs on fecal canine S100A12 concentrations in a large cohort of puppies.…”

Effects of improved water, sanitation, and hygiene and improved complementary feeding on environmental enteric dysfunction in children in rural Zimbabwe: A cluster-randomized controlled trial

“…To date, studies have failed to demonstrate reproducible changes in these markers following interventions. Nutritional supplementation with vitamin A [19], zinc [20,21], multiple micronutrients [22], alanlyl-glutamine [23][24][25] or dietary supplementation [26,27] have produced transient or inconsistent improvements. Interventions aimed at ameliorating intestinal inflammation, permeability or microbiome disruption have also been unsuccessful, including probiotics [28], antibiotics [29], long-chain polyunsaturated fatty acids [30], lactoferrin with lysozyme [31], and albendazole plus zinc [32].…”

Giardia's Epithelial Cell Interaction In Vitro: Mimicking Asymptomatic Infection?

“…In the context of this article, we define a symptomatic infection, i.e., giardiasis disease, as being characterized by acute gastrointestinal complaints, like diarrhea, abdominal pain, nausea, and vomiting (Adam, 2001 ; Ankarklev et al, 2010 ) and we like to distinguish it from asymptomatic infections defined by the absence of such acute symptoms. Asymptomatic infections according to this definition would include infections that—particularly if recurring—result in malabsorption/malnutrition phenotypes or may represent pure colonization without any pathology, which was recently shown by Garzon et al ( 2017 ) on asymptomatic children, who found no correlation between Giardia -infection and barrier dysfunction, but only of barrier dysfunction and wasting and stunting. However, infections may also trigger post-infectious syndromes such as irritable bowel disease (D'Anchino et al, 2002 ; Wensaas et al, 2012 ; Hanevik et al, 2014 ; Litleskare et al, 2015 ; Halliez et al, 2016 ; Nakao et al, 2017 ).…”