Stunting is characterized by chronic inflammation in zimbabwean infants

Andrew J. Prendergast, Sandra Rukobo, Bernard Chasekwa, Kuda Mutasa, Robert Ntozini, Mduduzi N N Mbuya, Andrew Jones, Lawrence Hale Moulton, Rebecca J. Stoltzfus, Jean Hawes Humphrey

Research output: Contribution to journalArticle

Abstract

Background: Stunting affects one-third of children in developing countries, but the causes remain unclear. We hypothesized that enteropathy leads to low-grade inflammation, which suppresses the growth hormone-IGF axis and mediates stunting. Methods: We conducted a case-control study of 202 HIV-unexposed Zimbabwean infants who were stunted (height-for-age Z-score (HAZ) -0.5; controls) at 18 months. We measured biomarkers of intestinal damage (I-FABP), inflammation (CRP, AGP, IL-6) and growth hormone-IGF axis (IGF-1, IGFBP3) in infant plasma at 6 weeks and 3, 6, 12 and 18 months, and in paired maternal-infant plasma at birth. Adjusted mean differences between biomarkers were estimated using regression models. Multivariate odds ratios of stunting were estimated by logistic regression. Results: At birth, cases were shorter (median (IQR) HAZ -1.00 (-1.53, -0.08) vs 0.03 (-0.57, 0.62,); P10 levels of CRP (aOR 3.06 (95%CI 1.34, 6.99); P = 0.008) and AGP (aOR 7.87 (95%CI 0.74, 83.74); P = 0.087) during infancy were associated with stunting. There were no associations between levels of I-FABP, IL-6, sCD14 or EndoCAb and stunting. Conclusions: Stunting began in utero and was associated with low maternal IGF-1 levels at birth. Inflammatory markers were higher in cases than controls from 6 weeks of age and were associated with lower levels of IGF-1 throughout infancy. Higher levels of CRP and AGP during infancy were associated with stunting. These findings suggest that an extensive enteropathy occurs during infancy and that low-grade chronic inflammation may impair infant growth.

Original languageEnglish (US)
Article numbere86928
JournalPLoS One
Volume9
Issue number2
DOIs
StatePublished - Feb 18 2014

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Growth Disorders
Insulin-Like Growth Factor I
growth retardation
inflammation
Biomarkers
Inflammation
infancy
Growth Hormone
Interleukin-6
Plasmas
Developing countries
Parturition
Logistics
digestive system diseases
interleukin-6
somatotropin
biomarkers
Mothers
infant growth
case-control studies

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Medicine(all)

Cite this

Prendergast, A. J., Rukobo, S., Chasekwa, B., Mutasa, K., Ntozini, R., Mbuya, M. N. N., ... Humphrey, J. H. (2014). Stunting is characterized by chronic inflammation in zimbabwean infants. PLoS One, 9(2), [e86928]. https://doi.org/10.1371/journal.pone.0086928

Stunting is characterized by chronic inflammation in zimbabwean infants. / Prendergast, Andrew J.; Rukobo, Sandra; Chasekwa, Bernard; Mutasa, Kuda; Ntozini, Robert; Mbuya, Mduduzi N N; Jones, Andrew; Moulton, Lawrence Hale; Stoltzfus, Rebecca J.; Humphrey, Jean Hawes.

In: PLoS One, Vol. 9, No. 2, e86928, 18.02.2014.

Research output: Contribution to journalArticle

Prendergast, AJ, Rukobo, S, Chasekwa, B, Mutasa, K, Ntozini, R, Mbuya, MNN, Jones, A, Moulton, LH, Stoltzfus, RJ & Humphrey, JH 2014, 'Stunting is characterized by chronic inflammation in zimbabwean infants', PLoS One, vol. 9, no. 2, e86928. https://doi.org/10.1371/journal.pone.0086928
Prendergast AJ, Rukobo S, Chasekwa B, Mutasa K, Ntozini R, Mbuya MNN et al. Stunting is characterized by chronic inflammation in zimbabwean infants. PLoS One. 2014 Feb 18;9(2). e86928. https://doi.org/10.1371/journal.pone.0086928
Prendergast, Andrew J. ; Rukobo, Sandra ; Chasekwa, Bernard ; Mutasa, Kuda ; Ntozini, Robert ; Mbuya, Mduduzi N N ; Jones, Andrew ; Moulton, Lawrence Hale ; Stoltzfus, Rebecca J. ; Humphrey, Jean Hawes. / Stunting is characterized by chronic inflammation in zimbabwean infants. In: PLoS One. 2014 ; Vol. 9, No. 2.
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abstract = "Background: Stunting affects one-third of children in developing countries, but the causes remain unclear. We hypothesized that enteropathy leads to low-grade inflammation, which suppresses the growth hormone-IGF axis and mediates stunting. Methods: We conducted a case-control study of 202 HIV-unexposed Zimbabwean infants who were stunted (height-for-age Z-score (HAZ) -0.5; controls) at 18 months. We measured biomarkers of intestinal damage (I-FABP), inflammation (CRP, AGP, IL-6) and growth hormone-IGF axis (IGF-1, IGFBP3) in infant plasma at 6 weeks and 3, 6, 12 and 18 months, and in paired maternal-infant plasma at birth. Adjusted mean differences between biomarkers were estimated using regression models. Multivariate odds ratios of stunting were estimated by logistic regression. Results: At birth, cases were shorter (median (IQR) HAZ -1.00 (-1.53, -0.08) vs 0.03 (-0.57, 0.62,); P10 levels of CRP (aOR 3.06 (95{\%}CI 1.34, 6.99); P = 0.008) and AGP (aOR 7.87 (95{\%}CI 0.74, 83.74); P = 0.087) during infancy were associated with stunting. There were no associations between levels of I-FABP, IL-6, sCD14 or EndoCAb and stunting. Conclusions: Stunting began in utero and was associated with low maternal IGF-1 levels at birth. Inflammatory markers were higher in cases than controls from 6 weeks of age and were associated with lower levels of IGF-1 throughout infancy. Higher levels of CRP and AGP during infancy were associated with stunting. These findings suggest that an extensive enteropathy occurs during infancy and that low-grade chronic inflammation may impair infant growth.",
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AU - Mbuya, Mduduzi N N

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