Lactobacillus rhamnosus Ingestion Promotes Innate Host Defense in an Enteric Parasitic Infection
Author(s) -
Jessica McClemens,
Janice Kim,
Huaqing Wang,
Yukang Mao,
Matthew J. Collins,
Wolfgang Kunze,
John Bienenstock,
Paul Forsythe,
Waliul I. Khan
Publication year - 2013
Publication title -
clinical and vaccine immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.649
H-Index - 77
eISSN - 1556-6811
pISSN - 1556-679X
DOI - 10.1128/cvi.00047-13
Subject(s) - lactobacillus rhamnosus , biology , goblet cell , microbiology and biotechnology , immunology , probiotic , innate immune system , mucin 2 , mucin , immune system , bacteria , epithelium , biochemistry , gene expression , genetics , gene
Enteric parasite infections around the world are a huge economic burden and decrease the quality of life for many people. The use of beneficial bacteria has attracted attention for their potential therapeutic applications in various diseases. However, the effects of beneficial bacteria in enteric parasitic infections remain largely unexplored. We investigated the effects of ingestion ofLactobacillus rhamnosus (JB-1) in a model of enteric nematode (Trichuris muris ) infection. C57BL/6 (resistant to infection), AKR (susceptible to infection), interleukin 10 (IL-10) knockout (KO), and mucin Muc2 KO mice were infected withT. muris and treated orally with probiotic JB-1 or medium. The mice were sacrificed on various days postinfection to examine goblet cells, epithelial cell proliferation, cytokines, and worm burdens. Treatment with JB-1 significantly enhanced worm expulsion in resistant C57BL/6 mice, and this was associated with increases in IL-10 levels, goblet cell numbers, and epithelial cell proliferation. Beneficial effects of JB-1 were absent in IL-10 KO and resistant mice treated with γ-irradiated bacteria. Live JB-1 treatment also expedited worm expulsion in Muc2 KO mice and, more importantly, in AKR mice (susceptible to infection). Injection of IL-10 directly into the colonic tissue of uninfected mice induced goblet cell hyperplasia. These findings demonstrate that JB-1 modulates goblet cell biology and promotes parasite expulsion via an IL-10-mediated pathway and provide novel insights into probiotic effects on innate defense in nematode infection.
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