Although bacteria are ubiquitous in the near-surface atmosphere and they can have important effects on human health, airborne bacteria have received relatively little attention and their spatial dynamics remain poorly understood. Owing to differences in meteorological conditions and the potential sources of airborne bacteria, we would expect the atmosphere over different land-use types to harbor distinct bacterial communities. To test this hypothesis, we sampled the near-surface atmosphere above three distinct land-use types (agricultural fields, suburban areas and forests) across northern Colorado, USA, sampling five sites per land-use type. Microbial abundances were stable across land-use types, with B10 5 -10 6 bacterial cells per m 3 of air, but the concentrations of biological ice nuclei, determined using a droplet freezing assay, were on average two and eight times higher in samples from agricultural areas than in the other two land-use types. Likewise, the composition of the airborne bacterial communities, assessed via bar-coded pyrosequencing, was significantly related to land-use type and these differences were likely driven by shifts in the sources of bacteria to the atmosphere across the land-uses, not local meteorological conditions. A metaanalysis of previously published data shows that atmospheric bacterial communities differ from those in potential source environments (leaf surfaces and soils), and we demonstrate that we may be able to use this information to determine the relative inputs of bacteria from these source environments to the atmosphere. This work furthers our understanding of bacterial diversity in the atmosphere, the terrestrial controls on this diversity and potential approaches for source tracking of airborne bacteria.

Infectious diseases rarely end in extinction. Yet the mechanisms that explain how epidemics subside are difficult to pinpoint. We investigated host-pathogen interactions after the emergence of a lethal fungal pathogen in a tropical amphibian assemblage. Some amphibian host species are recovering, but the pathogen is still present and is as pathogenic today as it was almost a decade ago. In addition, some species have defenses that are more effective now than they were before the epidemic. These results suggest that host recoveries are not caused by pathogen attenuation and may be due to shifts in host responses. Our findings provide insights into the mechanisms underlying disease transitions, which are increasingly important to understand in an era of emerging infectious diseases and unprecedented global pandemics.

B lymphocytes migrate among different micro-anatomic sites for diversification, selection, and eventual differentiation into antibody-secreting plasma cells. Emerging evidence supports the premise that aspects of the nutrient milieu vary within lymphoid micro-environments. However, the role of B cell-intrinsic metabolic programs in regulating B cell differentiation and antibody response quality remain unclear. We now show that the amino acid-sensing mTOR complex 1 (mTORC1) is essential for induction of Bcl6 and IRF4, key transcriptional regulators of germinal center and plasma cell fates. mTORC1 also enhances B cell proliferation upon exposure to antigen, increases the rate of somatic hyper-mutation, and is essential for generating high-affinity class switched antibodies. We also find that AMP-activated kinase (AMPK), an intracellular energy sensor, promotes plasma cell differentiation and antibody production. Collectively, these findings suggest mechanisms by which mTORC1 activity is critical for the germinal center reaction and producing class-switched, high-affinity antibodies, and indicate that AMPK can regulate the development and functional properties of terminally differentiated plasma cells. Supported by NIH R01 AI113292, HL106812, and NCI T32CA009592-29

Emerging evidence indicates that metabolic programs regulate B cell activation and antibody responses. However, the metabolic mediators that support the durability of the memory B cell and long-lived plasma cell populations are not fully elucidated. Adenosine monophosphate-activated protein kinase (AMPK) is an evolutionary conserved serine/threonine kinase that integrates cellular energy status and nutrient availability to intracellular signaling and metabolic pathways. Here, we use genetic mouse models to show that B cell restricted loss of the catalytic subunit, AMPKα1, leads to a defect in the long-term survival of the memory B cell population. AMPKα1-deficient memory B lymphocytes exhibited aberrant mitochondrial activity including impaired mitophagy and decreased mitochondrial spare respiratory capacity. In contrast, AMPKα1 was dispensable for the stability of the bone marrow-resident long-lived plasma cell population yet its absence led to increased rates of Ig synthesis and elevated serum antibody concentrations elicited by immunization. Collectively, our findings fit a model in which AMPKα1 supports longevity in the memory B cell compartment by promoting mitochondrial homeostasis but restrains rates of immunoglobulin production by plasma cells.