Early Host Cell Targets of Yersinia pestis during Primary Pneumonic Plague

Inhalation of Yersinia pestis causes primary pneumonic plague, a highly lethal syndrome with mortality rates approaching 100%. Pneumonic plague progression is biphasic, with an initial pre-inflammatory phase facilitating bacterial growth in the absence of host inflammation, followed by a pro-inflammatory phase marked by extensive neutrophil influx, an inflammatory cytokine storm, and severe tissue destruction. Using a FRET-based probe to quantitate injection of effector proteins by the Y. pestis type III secretion system, we show that these bacteria target alveolar macrophages early during infection of mice, followed by a switch in host cell preference to neutrophils. We also demonstrate that neutrophil influx is unable to limit bacterial growth in the lung and is ultimately responsible for the severe inflammation during the lethal pro-inflammatory phase.     

Failed predation or transportation? Causes and consequences of phoretic behavior in the pseudoscorpionDinocheirus arizonensis (Pseudoscorpionida: Chernetidae)

The pseudoscorpion Dinocheirus arizonensisinhabits rotting saguaro cactus in the Sonoran Desert and has also been found attached to the legs of the cactophilic neriid fly, Odontoloxozus longicornis.Laboratory experiments demonstrated a higher incidence of phoresy on eclosing versus postteneral adult flies, a female bias in phoresy, and an increased rate in female phoresy through time. The pseudoscorpion may also prey on the fly, but predation rate was unaffected by fly category, pseudoscorpion gender, or food deprivation. A study of pseudoscorpion colonization in the field indicated that females were the first to colonize and the first to abandon the transient habitat of a saguaro rot and, thus, corroborated patterns of phoretic behavior in the laboratory. Taken together, these results establish that phoresy is a behavior functioning specifically for dispersal. The hypothesis that pseudoscorpion transport by other arthropods is accidental, motivated by hunger, and occurs because pseudoscorpions are incapable of consuming their hosts is rejected.     

PDK4 dictates metabolic resistance to ferroptosis by suppressing pyruvate oxidation and fatty acid synthesis

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Tissue expression of the vesicle protein pantophysin

The cell-type restricted expression of cytoplasmic microvesicle membrane protein isoforms may be a consequence of the functional adaptation of these vesicles to the execution of specialized processes in cells of different specialization. To characterize the expression of the vesicle protein pantophysin, an isoform of the synaptic vesicle proteins synaptophysin and synaptoporin, we have prepared and characterized antibodies useful for the immunological detection of pantophysin in vitro and in situ. Using these reagents, we show by immunoblot analyses that pantophysin expression is not homogeneous but differs significantly between various bovine tissues. Furthermore, these differences are not exactly paralleled by the expression of other vesicle proteins of the SCAMP (secretory carrier-associated membrane protein) and VAMP (vesicle-associated membrane protein) types that have previously been localized to pantophysin vesicles in cultured cells. By immunofluorescence microscopy, pantophysin expression is seen predominantly in non-neuroendocrine cells with pronounced membrane traffic. Pantophysin staining codistributes with SCAMP and VAMP immunoreactivities in most instances but differs in some. Remarkably, pantophysin staining in liver is restricted to cells surrounding sinusoids and is not detectable in hepatocytes, similar to that of the SCAMP and VAMP isoforms as detected by our reagents in tissue sections.