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2013 ; 8
(1
): e53043
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Inhibitory influence of Enterococcus faecium on the propagation of swine
influenza A virus in vitro
#MMPMID23308134
Wang Z
; Chai W
; Burwinkel M
; Twardziok S
; Wrede P
; Palissa C
; Esch B
; Schmidt MF
PLoS One
2013[]; 8
(1
): e53043
PMID23308134
show ga
The control of infectious diseases such as swine influenza viruses (SwIV) plays
an important role in food production both from the animal health and from the
public health point of view. Probiotic microorganisms and other health improving
food supplements have been given increasing attention in recent years, but, no
information on the effects of probiotics on swine influenza virus is available.
Here we address this question by assessing the inhibitory potential of the
probiotic Enterococcus faecium NCIMB 10415 (E. faecium) on the replication of two
porcine strains of influenza virus (H1N1 and H3N2 strain) in a continuous porcine
macrophage cell line (3D4/21) and in MDBK cells. Cell cultures were treated with
E. faecium at the non-toxic concentration of 1×10(6) CFU/ml in growth medium for
60 to 90 min before, during and after SwIV infection. After further incubation of
cultures in probiotic-free growth medium, cell viability and virus propagation
were determined at 48 h or 96 h post infection. The results obtained reveal an
almost complete recovery of viability of SwIV infected cells and an inhibition of
virus multiplication by up to four log units in the E. faecium treated cells. In
both 3D4/21- and MDBK-cells a 60 min treatment with E. faecium stimulated nitric
oxide (NO) release which is in line with published evidence for an antiviral
function of NO. Furthermore, E. faecium caused a modified cellular expression of
selected mediators of defence in 3D4-cells: while the expression of TNF-?, TLR-3
and IL-6 were decreased in the SwIV-infected and probiotic treated cells, IL-10
was found to be increased. Since we obtained experimental evidence for the direct
adsorptive trapping of SwIV through E. faecium, this probiotic microorganism
inhibits influenza viruses by at least two mechanisms, direct physical
interaction and strengthening of innate defence at the cellular level.
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