Journal of Microbiology

Volume 52(3); March 2014

Journal Article

EDITORIAL] Molecular Microbiology in Antibacterial Research: You-Hee Cho; J. Microbiol. 2014;52(3):185-187.; DOI: https://doi.org/10.1007/s12275-014-4088-y

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Abstract: The special issue of Journal of Microbiology contains six reviews dealing with cutting edge research achievements in the fields of molecular microbiology focusing on antibacterial research. In a more specific sense, this special issue helps outline the progress of 21st-century basic molecular microbiology that can encompass related disciplines regarding a variety of interactions involving bacteria during bacterial pathogenesis and their control: sociomicrobiology (interaction between bacteria), immunology (interaction between bacteria and their hosts), and bacteriophage (phage) virology (interaction between bacteria and their parasites). Recent advancements have rapidly been made in our understanding of the real situation regarding polymicrobial interactions during bacterial infection and in non-mammalian host infection models to uncover the molecular mechanisms of host-bacteria interactions, which will complement our growing knowledge about immune responses toward bacterial and environmental elicitors. Moreover, much attention has recently been paid to phages and phage products as potential antibacterial therapeutics in the era of antibiotic resistance. Below, I summarize the individual contributions in these distinct categories.

Reviews

REVIEW] Mechanisms of Synergy in Polymicrobial Infections: Justine L. Murray , Jodi L. Connell , Apollo Stacy , Keith H. Turner , Marvin Whiteley; J. Microbiol. 2014;52(3):188-199. Published online March 1, 2014; DOI: https://doi.org/10.1007/s12275-014-4067-3

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133 Citations

Abstract: Communities of microbes can live almost anywhere and contain many different species. Interactions between members of these communities often determine the state of the habitat in which they live. When these habitats include sites on the human body, these interactions can affect health and disease. Polymicrobial synergy can occur during infection, in which the combined effect of two or more microbes on disease is worse than seen with any of the individuals alone. Powerful genomic methods are increasingly used to study microbial communities, including metagenomics to reveal the members and genetic content of a community and metatranscriptomics to describe the activities of community members. Recent efforts focused toward a mechanistic understanding of these interactions have led to a better appreciation of the precise bases of polymicrobial synergy in communities containing bacteria, eukaryotic microbes, and/or viruses. These studies have benefited from advances in the development of in vivo models of polymicrobial infection and modern techniques to profile the spatial and chemical bases of intermicrobial communication. This review describes the breadth of mechanisms microbes use to interact in ways that impact pathogenesis and techniques to study polymicrobial communities.

REVIEW] Enterococcus Infection Biology: Lessons from Invertebrate Host Models: Grace J. Yuen , Frederick M. Ausubel; J. Microbiol. 2014;52(3):200-210. Published online March 1, 2014; DOI: https://doi.org/10.1007/s12275-014-4011-6

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35 Citations

Abstract: The enterococci are commensals of the gastrointestinal tract of many metazoans, from insects to humans. While they normally do not cause disease in the intestine, they can become pathogenic when they infect sites outside of the gut. Recently, the enterococci have become important nosocomial pathogens, with the majority of human enterococcal infections caused by two species, Enterococcus faecalis and Enterococcus faecium. Studies using invertebrate infection models have revealed insights into the biology of enterococcal infections, as well as general principles underlying host innate immune defense. This review highlights recent findings on Enterococcus infection biology from two invertebrate infection models, the greater wax moth Galleria mellonella and the free-living bacteriovorous nematode Caenorhabditis elegans.

REVIEW] Chronic Obstructive Pulmonary Disease (COPD): Evaluation From Clinical, Immunological and Bacterial Pathogenesis Perspectives: Daniel J. Hassett , Michael T. Borchers , Ralph J. Panos; J. Microbiol. 2014;52(3):211-226. Published online March 1, 2014; DOI: https://doi.org/10.1007/s12275-014-4068-2

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60 Citations

Abstract: Chronic obstructive pulmonary disease (COPD), a disease manifested by significantly impaired airflow, afflicts ~14.2 million cases in the United States alone with an estimated 63 million people world-wide. Although there are a number of causes, the predominant cause is excessive tobacco smoke. In fact, in China, there have been estimates of 315,000,000 people that smoke. Other less frequent causes are associated with indirect cigarette smoke, air pollutants, biomass fuels, and genetic mutations. COPD is often associated with heart disease, lung cancer, osteoporosis and conditions can worsen in patients with sudden falls. COPD also affects both innate and adaptive immune processes. Cigarette smoke increases the expression of matrix metalloproteases and proinflammatory chemokines and increases lung titers of natural killer cells and neutrophils. Yet, neutrophil reactive oxygen species (ROS) mediated by the phagocytic respiratory burst and phagocytosis is impaired by nicotine. In contrast to innate immunity in COPD, dendritic cells represent leukocytes recruited to the lung that link the innate immune responses to adaptive immune responses by activating naïve T cells through antigen presentation. The autoimmune process that is also a significant part of inflammation associated with COPD. Moreover, coupled with restricted FEV1 values, are the prevalence of patients with single or multiple infections by bacteria, viruses and fungi. Finally, we focus on one of the more problematic infectious agents, the Gram-negative opportunistic pathogenic bacterium, Pseudomonas aeruginosa. Specifically, we delve into the development of highly problematic biofilm infections that are highly refractory to conventional antibiotic therapies in COPD. We offer a nonconventional, biocidal treatment that may be effective for COPD airway infections as well as with combinations of current antibiotic regimens for more effective treatment outcomes and relief for patients with COPD.

REVIEW] Perturbation of Pulmonary Immune Functions by Carbon Nanotubes and Susceptibility to Microbial Infection: Brent E. Walling , Gee W. Lau; J. Microbiol. 2014;52(3):227-234. Published online March 1, 2014; DOI: https://doi.org/10.1007/s12275-014-3695-y

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6 Citations

Abstract: Occupational and environmental pulmonary exposure to carbon nanotubes (CNT) is considered to be a health risk with a very low threshold of tolerance as determined by the United States Center for Disease Control. Immortalized airway epithelial cells exposed to CNTs show a diverse range of effects including reduced viability, impaired proliferation, and elevated reactive oxygen species generation. Additionally, CNTs inhibit internalization of targets in multiple macrophage cell lines. Mice and rats exposed to CNTs often develop pulmonary granulomas and fibrosis. Furthermore, CNTs have immunomodulatory properties in these animal models. CNTs themselves are proinflammatory and can exacerbate the allergic response. However, CNTs may also be immunosuppressive, both locally and systemically. Studies that examined the relationship of CNT exposure prior to pulmonary infection have reached different conclusions. In some cases, pre-exposure either had no effect or enhanced clearance of infections while other studies showed CNTs inhibited clearance. Interestingly, most studies exploring this relationship use pathogens which are not considered primary pulmonary pathogens. Moreover, harmony across studies is difficult as different types of CNTs have dissimilar biological effects. We used Pseudomonas aeruginosa as model pathogen to study how helical multi-walled carbon nanotubes (HCNTs) affected internalization and clearance of the pulmonary pathogen. The results showed that, although HCNTs can inhibit internalization through multiple processes, bacterial clearance was not altered, which was attributed to an enhanced inflammatory response caused by pre-exposure to HCNTs. We compare and contrast our findings in relation to other studies to gauge the modulation of pulmonary immune response by CNTs.

REVIEW] When a Virus is not a Parasite: The Beneficial Effects of Prophages: Joseph Bondy-Denomy , Alan R. Davidson; J. Microbiol. 2014;52(3):235-242. Published online March 1, 2014; DOI: https://doi.org/10.1007/s12275-014-4083-3

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132 Citations

Abstract: Most organisms on the planet have viruses that infect them. Viral infection may lead to cell death, or to a symbiotic relationship where the genomes of both virus and host replicate together. In the symbiotic state, both virus and cell potentially experience increased fitness as a result of the other. The viruses that infect bacteria, called bacteriophages (or phages), well exemplify the symbiotic relationships that can develop between viruses and their host. In this review, we will discuss the many ways that prophages, which are phage genomes integrated into the genomes of their hosts, influence bacterial behavior and virulence.

REVIEW] Phage Lysis: Three Steps, Three Choices, One Outcome: Ryl Young; J. Microbiol. 2014;52(3):243-258. Published online March 1, 2014; DOI: https://doi.org/10.1007/s12275-014-4087-z

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284 Citations

Abstract: The lysis of bacterial hosts by double-strand DNA bacteriophages, once thought to reflect merely the accumulation of sufficient lysozyme activity during the infection cycle, has been revealed to recently been revealed to be a carefully regulated and temporally scheduled process. For phages of Gramnegative hosts, there are three steps, corresponding to subversion of each of the three layers of the cell envelope: inner membrane, peptidoglycan, and outer membrane. The pathway is controlled at the level of the cytoplasmic membrane. In canonical lysis, a phage encoded protein, the holin, accumulates harmlessly in the cytoplasmic membrane until triggering at an allele-specific time to form micron-scale holes. This allows the soluble endolysin to escape from the cytoplasm to degrade the peptidoglycan. Recently a parallel pathway has been elucidated in which a different type of holin, the pinholin, which, instead of triggering to form large holes, triggers to form small, heptameric channels that serve to depolarize the membrane. Pinholins are associated with SAR endolysins, which accumulate in the periplasm as inactive, membrane-tethered enzymes. Pinholin triggering collapses the proton motive force, allowing the SAR endolysins to refold to an active form and attack the peptidoglycan. Surprisingly, a third step, the disruption of the outer membrane is also required. This is usually achieved by a spanin complex, consisting of a small outer membrane lipoprotein and an integral cytoplasmic membrane protein, designated as o-spanin and i-spanin, respectively. Without spanin function, lysis is blocked and progeny virions are trapped in dead spherical cells, suggesting that the outer membrane has considerable tensile strength. In addition to two-component spanins, there are some single-component spanins, or u-spanins, that have an N-terminal outer-membrane lipoprotein signal and a C-terminal transmembrane domain. A possible mechanism for spanin function to disrupt the outer membrane is to catalyze fusion of the inner and outer membranes.

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