Perforin-2 (MPEG1) is a pore-forming, antibacterial protein with broad-spectrum activity. Perforin-2 is expressed constitutively in phagocytes and inducibly in parenchymal, tissue-forming cells. In vitro, Perforin-2 prevents the intracellular replication and proliferation of bacterial pathogens in these cells. Perforin-2 knockout mice are unable to control the systemic dissemination of methicillin-resistant Staphylococcus aureus (MRSA) or Salmonella typhimurium and perish shortly after epicutaneous or orogastric infection respectively. In contrast, Perforin-2-sufficient littermates clear the infection. Perforin-2 is a transmembrane protein of cytosolic vesicles -derived from multiple organelles- that translocate to and fuse with bacterium containing vesicles. Subsequently, Perforin-2 polymerizes and forms large clusters of 100 Å pores in the bacterial surface with Perforin-2 cleavage products present in bacteria. Perforin-2 is also required for the bactericidal activity of reactive oxygen and nitrogen species and hydrolytic enzymes. Perforin-2 constitutes a novel and apparently essential bactericidal effector molecule of the innate immune system.DOI: http://dx.doi.org/10.7554/eLife.06508.001

Understanding what happens at the time of embryo implantation has been the subject of significant research. Investigators from many differing fields including maternal fetal medicine, microbiology, genetics, reproductive endocrinology and immunology have all been studying the moment the embryo interacts with the maternal endometrium. A perfect relationship between the uterus and the embryo, mediated by a tightly controlled interaction between the embryo and the endometrium, is required for successful implantation. Any factors affecting this communication, such as altered microbiome may lead to poor reproductive outcomes. Current theories suggest that altered microbiota may trigger an inflammatory response in the endometrium that affects the success of embryo implantation, as inflammatory mediators are tightly regulated during the adhesion of the blastocyst to the epithelial endometrial wall. In this review, we will highlight the various microbiome found during the periconceptual period, the microbiomes interaction with immunological responses surrounding the time of implantation, its effect on implantation, placentation and ultimately maternal and neonatal outcomes.

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Purpose of Review Following the recent association of Zika virus with microcephaly in Brazil, there has been a multitude of studies attempting to elucidate the relationship between Zika virus infection in pregnancy and congenital anomalies. The American Congress of Obstetricians and Gynecologists (ACOG), the U.S. Centers for Disease Control and Prevention (CDC), and the Society for Maternal Fetal Medicine (SMFM) have all issued guidelines governing the screening and management of pregnant patients with Zika exposure. These guidelines have rapidly evolved as the scientific evidence supporting causation of microcephaly in cases of Zika Virus infection has continued to mount. The purpose of this article is to review the current guidelines and the available evidence on which they are based. Recent Findings A series of experiments on animals and human cell lines have demonstrated that Zika virus is neurotropic. Further, examinations of amniotic fluid, fetal tissues, and placenta have confirmed the ability of Zika virus to cross the placenta. With the currently available evidence, the CDC has recently concluded that Zika virus infection in pregnancy is a cause of microcephaly. Summary Recently, it has become clear that Zika virus infection during pregnancy is responsible for congenital brain anomalies and microcephaly in the offspring. What remains unclear is the rate of vertical transmission from mother to fetus, the risk of microcephaly, and other CNS anomalies in fetuses when maternal infection is proven and the time from exposure or infection to clinical manifestations including ultrasound anomalies. Further studies are needed to answer these important questions.