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. 2018 Feb 14;8:2966. doi: 10.1038/s41598-018-21319-8

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Framework of EED showing gut/systemic inflammation influencing growth in children. This figure describes the hypothetical pathway of EED through the gut (A) and systemic inflammation (B). Factors driving the inflammatory pathway include respiratory illnesses, enteropathogen infection (measured by TaqMan Array), translocation of bacteria from the gut (IgG/IgA against LPS and Flagellin) due to repeated diarrheal episodes. The two distinct pathways regulating growth hormone, are being measured by gut-specific and systemic biomarkers shown in boxes (A) & (B). The negative association of biomarkers with IGF results in growth failure in children as shown by the black arrow. The dotted arrows show a weak relationship between the gut and systemic inflammatory biomarkers. *Information collected through weekly morbidity data. ^≠Estimated through TaqMan array card for bacterial, viral and protozoal targets at 6 and 9 month fecal samples. ±IgG/IgA antibodies against LPS and Flagellin was measured in serum samples at 6 and 9 months.