Desulfovibrio (DSV) are sulfate-reducing bacteria (SRB) that are ubiquitously present in the environment and as resident commensal bacteria within the human gastrointestinal tract. Though they are minor residents of the healthy gut, DSV are opportunistic pathobionts that may overgrow in the setting of various intestinal and extra-intestinal diseases. An increasing number of studies have demonstrated a positive correlation between DSV overgrowth (bloom) and various human diseases. While the relationship between DSV bloom and disease pathology has not been clearly established, mounting evidence suggests a causal role for these bacteria in disease development. As DSV are the most predominant genera of SRB in the gut, this review summarizes current knowledge regarding the relationship between DSV and a variety of diseases. In this study, we also discuss the mechanisms by which these bacteria may contribute to disease pathology.

Mast cells (MCs) produce soluble mediators such as histamine and prostaglandins that are known to influence dendritic cell (DC) function by stimulating maturation and antigen processing. Whether direct cell–cell interactions are important in modulating MC/DC function is unclear. In this paper, we show that direct contact between MCs and DCs occurs and plays an important role in modulating the immune response. Activation of MCs through FcεRI cross-linking triggers the formation of stable cell–cell interactions with immature DCs that are reminiscent of the immunological synapse. Direct cellular contact differentially regulates the secreted cytokine profile, indicating that MC modulation of DC populations is influenced by the nature of their interaction. Synapse formation requires integrin engagement and facilitates the transfer of internalized MC-specific antigen from MCs to DCs. The transferred material is ultimately processed and presented by DCs and can activate T cells. The physiological outcomes of the MC–DC synapse suggest a new role for intercellular crosstalk in defining the immune response.

For decades, bacteriophage purification has followed structured protocols focused on generating high concentrations of phage in manageable volumes. As research moves toward understanding complex phage populations, purification needs have shifted to maximize the amount of phage while maintaining diversity and activity. The effects of standard phage purification procedures such as polyethylene glycol (PEG) precipitation and cesium chloride (CsCl) density gradients on both diversity and activity of a phage population are not known. We have examined the effects of PEG precipitation and CsCl density gradients on a number of known phage (M13, T4, and ΦX 174) of varying structure and size, individually and as mixed sample. Measurement of phage numbers and activity throughout the purification process was performed. We demonstrate that these methods, used routinely to generate “pure” phage samples, are in fact detrimental to retention of phage number and activity; even more so in mixed phage samples. As such, minimal amounts of processing are recommended to introduce less bias and maintain more of a phage population.

Bacteriophage and the bacteria they infect are the dominant members of the gastrointestinal microbiome. While bacteria are known to be central to maintenance of the structure, function, and health of the microbiome, it has only recently been recognized that phage too might serve a critical function. Along these lines, bacteria are not the only cells that are influenced by bacteriophage, and there is growing evidence of bacteriophage effects on epithelial, endothelial, and immune cells. The innate immune system is essential to protecting the Eukaryotic host from invading microorganisms, and bacteriophage have been demonstrated to interact with innate immune cells regularly. Here, we conduct a systematic review of the varying mechanisms allowing bacteriophage to access and interact with cells of the innate immune system and propose the potential importance of these interactions.

In addition to their central role in allergy, mast cells are involved in a wide variety of cellular interactions during homeostasis and disease. In this review, we discuss the ability of mast cells to extend their mechanisms for intercellular communication beyond the release of soluble mediators. These include formation of mast cell synapses on antigen presenting surfaces, as well as cell–cell contacts with dendritic cells and T cells. Release of membrane bound exosomes also provide for the transfer of antigen, mast cell proteins, and RNA to other leukocytes. With the recognition of the extended role mast cells have during immune modulation, further investigation of the processes in which mast cells are involved is necessary. This reopens mast cell research to exciting possibilities, demonstrating it to be an immunological frontier.