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Lactoferrin supplementation and Bifidobacteria infantis administration in a piglet model of systemic Staphylococcus aureus infection (623.17)
Author(s) -
Reznikov Elizabeth,
Hoeflinger Jennifer,
Miller Michael,
Donovan Sharon
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.623.17
Subject(s) - staphylococcus aureus , lactoferrin , colostrum , antibiotics , medicine , immune system , microbiology and biotechnology , immunology , biology , bacteria , antibody , genetics
Infections in infants caused by antibiotic resistant S. aureus have limited treatment options. In a clinical trial, premature infants fed formula with bovine lactoferrin (bLf) had decreased blood‐borne staphylococcal infections, but the mechanism was not known. Additionally, Lf promotes the growth of B. infantis , a predominant species in the breast‐fed infant intestine. Herein, the effect of bLf alone or in combination with B. infantis on the course of S. aureus infection was assessed. Colostrum‐deprived pigs had umbilical catheters placed at birth and were fed formula with 4g/L bLf (LF) or whey protein (CON); half of the piglets in each group were further randomized to receive B. infantis (10 9 CFU/day, ATCC 15697). On d7, piglets were infected intravenously with S. aureus (10 5 CFU/kg BW, S54F9) and euthanized on d12. Piglets had elevated (p<0.05) rectal temperature beginning at 36 h post‐infection. Piglets fed B. infantis alone or with bLF had higher (p<0.05) total WBC. No differences in weight gain or tissue weights were observed. Importantly, LF piglets had decreased (p<0.05) staphylococcal load at the kidney and lung compared to CON, with no effect of B. infantis . Thus, bLf decreases translocation of S. aureus to tissues, which could potentially reduce organ dysfunction. On‐going investigations are defining the potential mechanism by which bLf and B. infantis regulate the immune response to S. aureus infection.