Cryo-electron tomography of stationary phase .

species belonging to the pseudomallei group include significant human and animal pathogens as well as the non-pathogenic species . These bacteria co-opt the host cell machinery for their replication and spread between host cells. Thus, it is of interest to understand the structural features of these cells that contribute to host cell colonization and virulence.

Critical roles of outer membrane protein B (OmpB) in the tick host.

is a pathogen of public health concern and transmitted by the Gulf Coast tick, . Rickettsiae are obligate intracellular bacteria that enter and replicate in diverse host cells. Rickettsial outer membrane protein B (OmpB) functions in bacterial adhesion, invasion, and avoidance of cell-autonomous immunity in mammalian cell infection, but the function of OmpB in arthropod infection is unknown.

FAZ assembly in bloodstream form requires kinesin KIN-E.

, the causative agent of African sleeping sickness, uses its flagellum for movement, cell division, and signaling. The flagellum is anchored to the cell body membrane the flagellum attachment zone (FAZ), a complex of proteins, filaments, and microtubules that spans two membranes with elements on both flagellum and cell body sides. How FAZ components are carried into place to form this complex is poorly understood.

Manipulation of host cell plasma membranes by intracellular bacterial pathogens.

Manipulation of the host cell plasma membrane is critical during infection by intracellular bacterial pathogens, particularly during bacterial entry into and exit from host cells. To manipulate host cells, bacteria deploy secreted proteins that modulate or modify host cell components. Here, we review recent advances that suggest common themes by which bacteria manipulate the host cell plasma membrane.

A patatin-like phospholipase mediates Rickettsia parkeri escape from host membranes.

Rickettsia species of the spotted fever group are arthropod-borne obligate intracellular bacteria that can cause mild to severe human disease. These bacteria invade host cells, replicate in the cell cytosol, and spread from cell to cell. To access the host cytosol and avoid immune detection, they escape membrane-bound vacuoles by expressing factors that disrupt host membranes.

A glycine-rich PE_PGRS protein governs mycobacterial actin-based motility.

Many key insights into actin regulation have been derived through examining how microbial pathogens intercept the actin cytoskeleton during infection. Mycobacterium marinum, a close relative of the human pathogen Mycobacterium tuberculosis, polymerizes host actin at the bacterial surface to drive intracellular movement and cell-to-cell spread during infection. However, the mycobacterial factor that commandeers actin polymerization has remained elusive.

Plasma membrane protrusions mediate host cell-cell fusion induced by .

Cell-cell fusion is important for biological processes including fertilization, development, immunity, and microbial pathogenesis. Bacteria in the pseudomallei group of the species, including , spread between host cells by inducing cell-cell fusion. Previous work showed that -induced cell-cell fusion requires intracellular bacterial motility and a bacterial protein secretion apparatus called the type VI secretion system-5 (T6SS-5), including the T6SS-5 protein VgrG5.

Interferon receptor-deficient mice are susceptible to eschar-associated rickettsiosis.

Arthropod-borne rickettsial pathogens cause mild and severe human disease worldwide. The tick-borne pathogen elicits skin lesions (eschars) and disseminated disease in humans; however, inbred mice are generally resistant to infection. We report that intradermal infection of mice lacking both interferon receptors () with as few as 10 .

Lysine methylation shields an intracellular pathogen from ubiquitylation and autophagy.

Many intracellular pathogens avoid detection by their host cells. However, it remains unknown how they avoid being tagged by ubiquitin, an initial step leading to antimicrobial autophagy. Here, we show that the intracellular bacterial pathogen uses two protein-lysine methyltransferases (PKMTs) to modify outer membrane proteins (OMPs) and prevent their ubiquitylation.

Baculovirus actin-rearrangement-inducing factor ARIF-1 induces the formation of dynamic invadosome clusters.

The baculovirus  multiple nucleopolyhedrovirus (AcMNPV), a pathogen of lepidopteran insects, has a striking dependence on the host cell actin cytoskeleton. During the delayed-early stage of infection, AcMNPV was shown to induce the accumulation of actin at the cortex of infected cells. However, the dynamics and molecular mechanism of cortical actin assembly remained unknown.

Mechanical competition triggered by innate immune signaling drives the collective extrusion of bacterially infected epithelial cells.

Intracellular pathogens alter their host cells' mechanics to promote dissemination through tissues. Conversely, host cells may respond to the presence of pathogens by altering their mechanics to limit infection. Here, we monitored epithelial cell monolayers infected with intracellular bacterial pathogens, Listeria monocytogenes or Rickettsia parkeri, over days.

Trypanosomes have divergent kinesin-2 proteins that function differentially in flagellum biosynthesis and cell viability.

, the causative agent of African sleeping sickness, has a flagellum that is crucial for motility, pathogenicity, and viability. In most eukaryotes, the intraflagellar transport (IFT) machinery drives flagellum biogenesis, and anterograde IFT requires kinesin-2 motor proteins. In this study, we investigated the function of the two kinesin-2 proteins, TbKin2a and TbKin2b, in bloodstream form trypanosomes.

Systematic review of primary total hip arthroplasty using titanium-titanium modular-neck prostheses: the true risk of revision.

Aims: Modular-neck femoral implants are used to enable more variability in femoral neck version, offset and length. It has been reported that these implants carry a higher rate of revision. The aim of this review was to assess the overall and cause-specific revision rate of titanium-titanium alloy modular-neck implants in primary total hip arthroplasty (THA).

Inflammasome-mediated antagonism of type I interferon enhances Rickettsia pathogenesis.

The innate immune system fights infection with inflammasomes and interferons. Facultative bacterial pathogens that inhabit the host cytosol avoid inflammasomes and are often insensitive to type I interferons (IFN-I), but are restricted by IFN-γ. However, it remains unclear how obligate cytosolic bacterial pathogens, including Rickettsia species, interact with innate immunity.

A Metabolic Dependency for Host Isoprenoids in the Obligate Intracellular Pathogen Rickettsia parkeri Underlies a Sensitivity to the Statin Class of Host-Targeted Therapeutics.

Gram-negative bacteria in the order have an obligate intracellular growth requirement, and some species cause human diseases such as typhus and spotted fever. The bacteria have evolved a dependence on essential nutrients and metabolites from the host cell as a consequence of extensive genome reduction. However, it remains largely unknown which nutrients they acquire and whether their metabolic dependency can be exploited therapeutically.

Evasion of autophagy mediated by Rickettsia surface protein OmpB is critical for virulence.

Rickettsia are obligate intracellular bacteria that evade antimicrobial autophagy in the host cell cytosol by unknown mechanisms. Other cytosolic pathogens block different steps of autophagy targeting, including the initial step of polyubiquitin-coat formation. One mechanism of evasion is to mobilize actin to the bacterial surface.

Baculovirus Actin-Based Motility Drives Nuclear Envelope Disruption and Nuclear Egress.

Viruses that replicate in the host cell nucleus face challenges in usurping cellular pathways to enable passage through the nuclear envelope [1]. Baculoviruses are enveloped, double-stranded DNA viruses that infect lepidopteran insects and are tools for protein expression, cell transduction, and pest management [2-4]. The type species Autographa californica M nucleopolyhedrovirus (AcMNPV) shares with other pathogens an ability to assemble host actin monomers (G-actin) into actin filaments (F-actin) to drive motility [5].

RECON-Dependent Inflammation in Hepatocytes Enhances Listeria monocytogenes Cell-to-Cell Spread.

The oxidoreductase RECON is a high-affinity cytosolic sensor of bacterium-derived cyclic dinucleotides (CDNs). CDN binding inhibits RECON's enzymatic activity and subsequently promotes inflammation. In this study, we sought to characterize the effects of RECON on the infection cycle of the intracellular bacterium , which secretes cyclic di-AMP (c-di-AMP) into the cytosol of infected host cells.