Modulating intestinal immune responses by lipoteichoic acid-deficient Lactobacillus acidophilus

To investigate the mechanism(s) by which the intestinal commensal microbe Lactobacillus acidophilus can affect host immunity, we studied the role of a component of the cell wall, lipoteichoic acid, in colitis. Colitis was induced by the intraperitoneal injection of pathogenic CD4(+)CD25(-)CD45RB(hi)...

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Published inImmunotherapy Vol. 4; no. 2; pp. 151 - 161
Main Authors Khan, Mohammad W, Zadeh, Mojgan, Bere, Praveen, Gounaris, Elias, Owen, Jennifer, Klaenhammer, Todd, Mohamadzadeh, Mansour
Format Journal Article
LanguageEnglish
Published England Future Medicine Ltd 01.02.2012
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Summary:To investigate the mechanism(s) by which the intestinal commensal microbe Lactobacillus acidophilus can affect host immunity, we studied the role of a component of the cell wall, lipoteichoic acid, in colitis. Colitis was induced by the intraperitoneal injection of pathogenic CD4(+)CD25(-)CD45RB(hi) T cells into Rag1(-/-) mice. The parental strain, NCK56, or the lipoteichoic acid-deficient strain, NCK2025, was then administered orally. Fluorescent microscopy was employed to examine resulting cell populations and their cytokine production in the colon. NCK2025 enhanced IL-10 production by dendritic cells and macrophages. Increased numbers of regulatory dendritic cells coincided with the induction of activated FoxP3(+) Tregs. These results suggest that the oral administration of the genetically modified strain NCK2025 may be an effective immunotherapeutic approach that reprograms the immune response in colonic inflammatory conditions.
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ISSN:1750-743X
1750-7448
DOI:10.2217/imt.11.163