Simulations inform design of regional occupancy‐based monitoring for a sparsely distributed,territorial species

Sparsely distributed species attract conservation concern, but insufficient information on population trends challenges conservation and funding prioritization. Occupancy‐based monitoring is attractive for these species, but appropriate sampling design and inference depend on particulars of the study system. We employed spatially explicit simulations to identify minimum levels of sampling effort for a regional occupancy monitoring study design, using white‐headed woodpeckers (Picoides albolvartus), a sparsely distributed, territorial species threatened by habitat decline and degradation, as a case study. We compared the original design with commonly proposed alternatives with varying targets of inference (i.e., species range, space use, or abundance) and spatial extent of sampling. Sampling effort needed to achieve adequate power to observe a long‐term population trend (≥80% chance to observe a 2% yearly decline over 20 years) with the previously used study design consisted of annually monitoring ≥120 transects using a single‐survey approach or ≥90 transects surveyed twice per year using a repeat‐survey approach. Designs that shifted inference toward finer‐resolution trends in abundance and extended the spatial extent of sampling by shortening transects, employing a single‐survey approach to monitoring, and incorporating a panel design (33% of units surveyed per year) improved power and reduced error in estimating abundance trends. In contrast, efforts to monitor coarse‐scale trends in species range or space use with repeat surveys provided extremely limited statistical power. Synthesis and applications. Sampling resolutions that approximate home range size, spatially extensive sampling, and designs that target inference of abundance trends rather than range dynamics are probably best suited and most feasible for broad‐scale occupancy‐based monitoring of sparsely distributed territorial animal species.     

Trefoil Factor 2 Negatively Regulates Type 1 Immunity against Toxoplasma gondii

IL-12-mediated type 1 inflammation confers host protection against the parasitic protozoan Toxoplasma gondii. However, production of IFN-γ, another type 1 inflammatory cytokine, also drives lethality from excessive injury to the intestinal epithelium. As mechanisms that restore epithelial barrier function following infection remain poorly understood, this study investigated the role of trefoil factor 2 (TFF2), a well-established regulator of mucosal tissue repair. Paradoxically, TFF2 antagonized IL-12 release from dendritic cells (DCs) and macrophages, which protected TFF2-deficient (TFF2(-/-)) mice from T. gondii pathogenesis. Dysregulated intestinal homeostasis in naive TFF2(-/-) mice correlated with increased IL-12/23p40 levels and enhanced T cell recruitment at baseline. Infected TFF2(-/-) mice displayed low rates of parasite replication and reduced gut immunopathology, whereas wild-type (WT) mice experienced disseminated infection and lethal ileitis. p38 MAPK activation and IL-12p70 production was more robust from TFF2(-/-)CD8(+) DC compared with WT CD8(+) DC and treatment of WT DC with rTFF2 suppressed TLR-induced IL-12/23p40 production. Neutralization of IFN-γ and IL-12 in TFF2(-/-) animals abrogated resistance shown by enhanced parasite replication and infection-induced morbidity. Hence, TFF2 regulated intestinal barrier function and type 1 cytokine release from myeloid phagocytes, which dictated the outcome of oral T. gondii infection in mice.     

The enzymatic activity of phosphoglucose isomerase is not required for its cytokine function

PGI is a housekeeping gene encoding phosphoglucose isomerase (PGI) a glycolytic enzyme that also functions as a cytokine (autocrine motility factor (AMF)/neuroleukin/maturation factor) upon secretion from the cell and binding to its 78 kDa seven-transmembrane domain receptor (gp78/AMF-R). PGI contains a CXXC motif, characteristic of redox proteins and possibly evolutionarily related to the CC and CXC motif of the chemokine gene family. Using site-directed mutagenesis, single- and double-deletion (CXC, CC) mutants were created by deleting amino acids 331 and 332 of human PGI, respectively. The mutant proteins lost their enzymatic activity; however, neither of the deletions augmented the proteins' binding affinity to the receptor and all maintained cytokine function. The results demonstrate that the enzymatic activity of PGI is not essential for either receptor binding or cytokine function of human PGI.