Metamorphosis in the Cirripede Crustacean Balanus amphitrite

Stalked and acorn barnacles (Cirripedia Thoracica) have a complex life cycle that includes a free-swimming nauplius larva, a cypris larva and a permanently attached sessile juvenile and adult barnacle. The barnacle cyprid is among the most highly specialized of marine invertebrate larvae and its settlement biology has been intensively studied. By contrast, surprisingly few papers have dealt with the critical series of metamorphic events from cementation of the cyprid to the substratum until the appearance of a suspension feeding juvenile. This metamorphosis is both ontogenetically complex and critical to the survival of the barnacle. Here we use video microscopy to present a timeline and description of morphological events from settled cyprid to juvenile barnacle in the model species Balanus amphitrite, representing an important step towards both a broader understanding of the settlement ecology of this species and a platform for studying the factors that control its metamorphosis. Metamorphosis in B. amphitrite involves a complex sequence of events: cementation, epidermis separation from the cypris cuticle, degeneration of cypris musculature, rotation of the thorax inside the mantle cavity, building of the juvenile musculature, contraction of antennular muscles, raising of the body, shedding of the cypris cuticle, shell plate and basis formation and, possibly, a further moult to become a suspension feeding barnacle. We compare these events with developmental information from other barnacle species and discuss them in the framework of barnacle settlement ecology

Lung microbiota promotes tolerance to allergens in neonates via PD-L1.

Epidemiological data point toward a critical period in early life during which environmental cues can set an individual on a trajectory toward respiratory health or disease. The neonatal immune system matures during this period, although little is known about the signals that lead to its maturation. Here we report that the formation of the lung microbiota is a key parameter in this process. Immediately following birth, neonatal mice were prone to develop exaggerated airway eosinophilia, release type 2 helper T cell cytokines and exhibit airway hyper-responsiveness following exposure to house dust mite allergens, even though their lungs harbored high numbers of natural CD4(+)Foxp3(+)CD25(+)Helios(+) regulatory T (Treg) cells. During the first 2 weeks after birth, the bacterial load in the lungs increased, and representation of the bacterial phyla shifts from a predominance of Gammaproteobacteria and Firmicutes towards Bacteroidetes. The changes in the microbiota were associated with decreased aeroallergen responsiveness and the emergence of a Helios(-) Treg cell subset that required interaction with programmed death ligand 1 (PD-L1) for development. Absence of microbial colonization(10) or blockade of PD-L1 during the first 2 weeks postpartum maintained exaggerated responsiveness to allergens through to adulthood. Adoptive transfer of Treg cells from adult mice to neonates before aeroallergen exposure ameliorated disease. Thus, formation of the airway microbiota induces regulatory cells early in life, which, when dysregulated, can lead to sustained susceptibility to allergic airway inflammation in adulthood