Warming temperatures drive at least half of the magnitude of long-term trait changes in European birds

Many wild populations are experiencing temporal changes in life-history and other phenotypic traits, and these changes are frequently assumed to be driven by climate change rather than nonclimatic drivers. However, this assumption relies on three conditions: that local climate is changing, traits are sensitive to climate variability, and other drivers are not also changing over time. Although many studies acknowledge one or more of these conditions, all three are rarely checked simultaneously. Consequently, the relative contribution of climate change to trait change, and the variation in this contribution across traits and species, remain unclear. We used long-term datasets on 60 bird species in Europe to test the three conditions in laying date, offspring number, and body condition and used a method that quantifies the contribution of warming temperatures to changes in traits relative to other effects. Across species, approximately half of the magnitude of changes in traits could be attributed to rising mean temperature, suggesting that increasing temperatures are likely the single most important contributor to temporal trends and emphasizes the impact that global warming is having on natural populations. There were also substantial nontemperature-related temporal trends (presumably due to other changes such as urbanization), which generally caused trait change in the same direction as warming. Attributing temporal trends solely to warming thus overestimates the impact of warming. Furthermore, contributions from nontemperature drivers explained most of the interspecific variation in trait changes, raising concerns about comparative studies that attribute differences in temporal trends to species differences in climate-change sensitivity

The Role of luxS in the Middle Ear Streptococcus pneumoniae Isolate 947

The LuxS protein, encoded by luxS, is required for the production of autoinducer 2 (AI-2) in Streptococcus pneumoniae. The AI-2 molecule serves as a quorum sensing signal, and thus regulates cellular processes such as carbohydrate utilisation and biofilm formation, as well as impacting virulence. The role of luxS in S. pneumoniae biology and lifestyle has been predominantly assessed in the laboratory strain D39. However, as biofilm formation, which is regulated by luxS, is critical for the ability of S. pneumoniae to cause otitis media, we investigated the role of luxS in a middle ear isolate, strain 947. Our results identified luxS to have a role in prevention of S. pneumoniae transition from colonisation of the nasopharynx to the ear, and in facilitating adherence to host epithelial cells.Alexandra Tikhomirova, Erin B. Brazel, Kimberley T. McLean, Hannah N. Agnew, James C. Paton and Claudia Trappett

Anti-tumour therapeutic efficacy of OX40L in murine tumour model

OX40 ligand (OX40L), a member of TNF superfamily, is a co-stimulatory molecule involved in T cell activation. Systemic administration of mOX40L fusion protein significantly inhibited the growth of experimental lung metastasis and subcutaneous (s.c.) established colon (CT26) and breast (4T1) carcinomas. Vaccination with OX40L was significantly enhanced by combination treatment with intra-tumour injection of a disabled infectious single cycle-herpes simplex virus (DISC-HSV) vector encoding murine granulocyte macrophage-colony stimulating factor (mGM-CSF). Tumour rejection in response to OX40L therapy required functional CD4+ and CD8+ T cells and correlated with splenocyte cytotoxic T lymphocytes (CTLs) activity against the AH-1 gp70 peptide of the tumour associated antigen expressed by CT26 cells. These results demonstrate the potential role of the OX40L in cancer immunotherapy

Streptococcus pneumoniae Strains Isolated From a Single Pediatric Patient Display Distinct Phenotypes

Streptococcus pneumoniae is the leading cause of bacterial paediatric meningitis after the neonatal period worldwide, but the bacterial factors and pathophysiology that drive pneumococcal meningitis are not fully understood. In this work, we have identified differences in raffinose utilization by S. pneumoniae isolates of identical serotype and sequence type from the blood and cerebrospinal fluid (CSF) of a single pediatric patient with meningitis. The blood isolate displayed defective raffinose metabolism, reduced transcription of the raffinose utilization pathway genes, and an inability to grow in vitro when raffinose was the sole carbon source. The fitness of these strains was then assessed using a murine intranasal infection model. Compared with the CSF isolate, mice infected with the blood isolate displayed higher bacterial numbers in the nose, but this strain was unable to invade the ears of infectedmice. A premature stop codon was identified in the aga gene in the raffinose locus, suggesting that this protein likely displays impaired alpha-galactosidase activity. These closely related strains were assessed by Illumina sequencing, which did not identify any single nucleotide polymorphisms (SNPs) between the two strains. However, these wider genomic analyses identified the presence of an alternative alpha-galactosidase gene that appeared to display altered sequence coverage between the strains, which may account for the observed differences in raffinose metabolic capacity. Together, these studies support previous findings that raffinose utilization capacity contributes to disease progression, and provide insight into a possible alternative means by which perturbation of this pathway may influence the behavior of pneumococci in the host environment, particularly in meningitis.Hannah N. Agnew, Erin B. Brazel, Alexandra Tikhomirova, Mark van der Linden, Kimberley T. McLean, James C. Paton, and Claudia Trappett