Abstract
It is well-known fact that various pathogens, including bacteria, virus, and protozoa, induce abortion in humans and animals. However the mechanisms of infectious abortion are little known. In this study, we demonstrated that Listeria monocytogenes infection in trophoblast giant cells decreased heme oxygenase (HO)-1 and B-cell lymphoma-extra large (Bcl-XL) expression, and that their overexpression inhibited cell death induced by the infection. Furthermore, HO-1 and Bcl-XL expression levels were also decreased by L. monocytogenes in pregnant mice. Treatment with cobalt protoporphyrin, which is known to induce HO-1, inhibited infectious abortion. Taken together, our study indicates that L. monocytogenes infection decreases HO-1 and Bcl-XL expression and induces cell death in placenta, leading to infectious abortion.
Highlights
Listeriosis is caused by gram-positive Listeria monocytogenes
We demonstrated that heme oxygenase (HO)-1 plays a role in inhibiting cell death induced by Brucella abortus infection
HO-1 was expressed in trophoblast giant (TG) cells, but its expression decreased on L. monocytogenes infection (Fig. 1A)
Summary
Listeriosis is caused by gram-positive Listeria monocytogenes. In humans, this pathogen has the ability to cross the intestinal, placental, and blood-brain barriers, leading to gastroenteritis, maternofetal infections, and meningoencephalitis, respectively. A key feature of the virulence of L. monocytogenes is its ability to avoid the killing mechanisms of professional and non- professional phagocytic host cells [1–4]. L. monocytogenes infections in humans are caused mainly by injection of contaminated food, such as daily products, raw vegetables, fish, poultry, processed chicken, and beef [5]. L. monocytogenes induces cell death in vitro and in vivo in various cell types including hepatocytes [6], lymphocytes [7], and dendritic cells [8]. Cell death induced by L. monocytogenes is associated with listeriolysin O, a pore-forming toxin that allows bacteria to lyse the phagosomal membrane and escape into the cytosol
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