Vitamin A supplementation reduces the monocyte chemoattractant protein-1 intestinal immune response of Mexican children.
The impact of vitamin A supplementation on childhood diarrhea may be determined by the regulatory effect supplementation has on the mucosal immune response in the gut. Previous studies have not addressed the impact of vitamin A supplementation on the production of monocyte chemoattractant protein 1 (MCP-1), an essential chemokine involved in pathogen-specific mucosal immune response. Fecal MCP-1 concentrations, determined by an enzyme-linked immuno absorption assay, were compared among 127 Mexican children 5-15 mo of age randomized to receive a vitamin A supplement (<12 mo of age, 20,000 IU of retinol; > or =12 mo, 45,000 iu) every 2 mo or a placebo as part of a larger vitamin A supplementation trial. Stools collected during the summer months were screened for MCP-1 and gastrointestinal pathogens. Values of MCP-1 were categorized into 3 levels (nondetectable, <median, > or =median). Multinomial logistic regression models were used to determine whether vitamin A-supplemented children had different categorical values of MCP-1 compared with children in the placebo group. Differences in categorical values were also analyzed stratified by gastrointestinal pathogen infections and by diarrheal symptoms. Overall, children who received the vitamin A supplement had reduced fecal concentrations of MCP-1 compared with children in the placebo group (median pg/mg protein +/- interquartile range: 284.88 +/- 885.35 vs. 403.39 +/- 913.16; odds ratio 0.64, 95% CI 0.42-97, P = 0.03). Vitamin A supplemented children infected with enteropathogenic Escherichia coli (EPEC) had reduced MCP-1 levels (odds ratio = 0.38, 95% CI 0.18-0.80) compared with children in the placebo group. Among children not infected with Ascaris lumbricoides vitamin A supplemented children had reduced MCP-1 levels (OR = 0.62, 95% CI 0.41-0.94). These findings suggest that vitamin A has an anti-inflammatory effect in the gastrointestinal tract by reducing MCP-1 concentrations.
Long
Kurt Z
KZ
Department of Nutrition, Harvard School of Public Health, Boston, MA, USA. klong@hsph.harvard.edu
Santos
Jose Ignacio
JI
Estrada Garcia
Teresa
T
Haas
Meredith
M
Firestone
Mathew
M
Bhagwat
Jui
J
Dupont
Herbert L
HL
Hertzmark
Ellen
E
Rosado
Jorge L
JL
Nanthakumar
Nanda N
NN
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage; D001196:Ascariasis / Q000276:immunology; D017164:Ascaris lumbricoides; D018932:Chemokine CCL2 / Q000032:analysis* / Q000096:biosynthesis / Q000276:immunology*; D003967:Diarrhea / Q000276:immunology* / Q000382:microbiology / Q000469:parasitology; D019587:Dietary Supplements; D004797:Enzyme-Linked Immunosorbent Assay; D004927:Escherichia coli Infections / Q000276:immunology; D005243:Feces / Q000737:chemistry / Q000382:microbiology / Q000469:parasitology; D016829:Giardia lamblia; D005873:Giardiasis / Q000276:immunology; D006801:Humans; D007223:Infant; D007422:Intestines / Q000737:chemistry / Q000276:immunology*; D016015:Logistic Models; D008800:Mexico; D010919:Placebos; D014801:Vitamin A / Q000008:administration & dosage*
D000893:Anti-Inflammatory Agents; C111835:CCL2 protein, human; D018932:Chemokine CCL2; D010919:Placebos; D014801:Vitamin A