Listeria faecal carriage by renal transplant recipients, haemodialysis patients and patients in general practice: its relation to season, drug therapy, foreign travel, animal exposure and diet

Ghanem

Clinical Infectious Diseases

et al. 2012

Section: Discussionmentioning

confidence: 99%

Listeriosis at a Tertiary Care Hospital in Beijing, China: High Prevalence of Nonclustered Healthcare-Associated Cases Among Adult Patients

Ghanem

Clinical Infectious Diseases

et al. 2012

“…Using this bacterium to investigate the underlying pathogenesis of prenatal infection is clearly important given the ubiquitous presence of this pathogen in our food supply, colonization within the gastrointestinal tract, propensity for disseminated infection during pregnancy, and alarming rate of morbidity and mortality associated with human prenatal infection (Gellin and Broome 1989, Iida, et al 1998, MacGowan, et al 1991, Mylonakis, et al 2002, Silver 1998, Southwick and Purich 1996). Here, a somewhat surprising degree of resistance to L. monocytogenes infection for placental cells has been described using human organ cultures (Abrahams, et al 2006, Koga and Mor 2008, Robbins and Bakardjiev 2012).…”

Section: Infection Induced Shifts In Treg Suppression and Pregnancy Cmentioning

confidence: 99%

Regulatory T cells and the immune pathogenesis of prenatal infection

Rowe¹,

Ertelt²,

Luo³

et al. 2013

Reproduction

Pregnancy in placental mammals offers exceptional comprehensive benefits of in utero protection, nutrition, and elimination of metabolic waste for the developing fetus. However, these advantages also require durable strategies to mitigate maternal rejection of fetal tissue expressing foreign paternal antigens. Since the initial postulate of expanded maternal immune tolerance by Sir Peter Medawar 60 years ago, an amazingly elaborate assortment of molecular and cellular modifications acting both locally at the maternal placental interface and systemically have been shown to silence potentially detrimental maternal immune responses. In turn, simultaneously maintaining host defense against the infinite array of potential pathogens during pregnancy is equally important. Fortunately, resistance against most infections is preserved seamlessly throughout gestation. On the other hand, recent studies on pathogens with unique predisposition for prenatal infection have uncovered distinctive holes in host defense associated with the reproductive process. Using these infections to probe the response during pregnancy, the immune suppressive regulatory subset of maternal CD4 T cells has been increasingly shown to dictate the inter-workings between prenatal infection susceptibility and pathogenesis of ensuing pregnancy complications. Herein, the recent literature suggesting a necessity for maternal regulatory T cells in pregnancy induced immunological shifts that sustain fetal tolerance is reviewed. Additional discussion is focused on how expansion of maternal regulatory T cell suppression may become exploited by pathogens that cause prenatal infection, and the perilous potential of infection induced immune activation that may mitigate fetal tolerance and inadvertently inject hostility into the protective in utero environment.

“…Nevertheless, Lm can be shed asymptomatically, persist in human and animal feces and be released in the environment [15], [16]. Lm is a ubiquitous bacterium that also thrives in diverse external environments such as soil, water, decaying plants, and silage, exposing wild animals and cattle to multiple opportunities of ingestion and perpetuating Lm transmission [17].…”

Section: Introductionmentioning

confidence: 99%

ActA Promotes Listeria monocytogenes Aggregation, Intestinal Colonization and Carriage

et al. 2013

Listeria monocytogenes (Lm) is a ubiquitous bacterium able to survive and thrive within the environment and readily colonizes a wide range of substrates, often as a biofilm. It is also a facultative intracellular pathogen, which actively invades diverse hosts and induces listeriosis. So far, these two complementary facets of Lm biology have been studied independently. Here we demonstrate that the major Lm virulence determinant ActA, a PrfA-regulated gene product enabling actin polymerization and thereby promoting its intracellular motility and cell-to-cell spread, is critical for bacterial aggregation and biofilm formation. We show that ActA mediates Lm aggregation via direct ActA-ActA interactions and that the ActA C-terminal region, which is not involved in actin polymerization, is essential for aggregation in vitro. In mice permissive to orally-acquired listeriosis, ActA-mediated Lm aggregation is not observed in infected tissues but occurs in the gut lumen. Strikingly, ActA-dependent aggregating bacteria exhibit an increased ability to persist within the cecum and colon lumen of mice, and are shed in the feces three order of magnitude more efficiently and for twice as long than bacteria unable to aggregate. In conclusion, this study identifies a novel function for ActA and illustrates that in addition to contributing to its dissemination within the host, ActA plays a key role in Lm persistence within the host and in transmission from the host back to the environment.