Microbiologically influenced corrosion (MIC) is a phenomenon of increasing concern that affects various materials and sectors of society. MIC describes the effects, often negative, that a material can experience due to the presence of microorganisms. Unfortunately, although several research groups and industrial actors worldwide have already addressed MIC, discussions are fragmented, while information sharing and willingness to reach out to other disciplines are limited. A truly interdisciplinary approach, which would be logical for this material/biology/chemistry-related challenge, is rarely taken. In this review, we highlight critical non-biological aspects of MIC that can sometimes be overlooked by microbiologists working on MIC but are highly relevant for an overall understanding of this phenomenon. Here, we identify gaps, methods, and approaches to help solve MIC-related challenges, with an emphasis on the MIC of metals. We also discuss the application of existing tools and approaches for managing MIC and propose ideas to promote an improved understanding of MIC. Furthermore, we highlight areas where the insights and expertise of microbiologists are needed to help progress this field.

Wastewater treatment systems are important sources of contaminants of emerging substances, including pharmaceuticals, and personal care products. Onsite wastewater treatment systems provide alternative solutions to centralized systems; although they are becoming increasingly popular, little is known about the effect of maintenance on their performance. In the current study, chemical and microbiological parameters in the effluents from two identical on-site wastewater treatment systems were analyzed, one being properly maintained while the other not maintained at all. Taxonomic profiles vastly differed from each other, and organic micropollutants are present at higher concentrations in the effluent of the non-maintained unit. The results highlight the importance of proper maintenance.

To predict variation of maximum localized penetration with exposure time, long-term localized corrosion was assessed in an emergency cooling water system composed of two carbon steel pipelines of 700 mm diameter transporting raw river water at flow velocities of 1 m/s and 0.1 m/ s.Field tests, visual inspection, ultrasonic testing, BART testing, SEM-EDS and metagenomic analyses were performed to assess the progress of long-term corrosion and determine the influ-ence of microbes in the corrosion process.High corrosion was linked to sulphate reducing bacteria and potentially to methanogenic archaea in the low-velocity pipeline, while moderate corrosion was linked to non-sulphate reducing bacteria in the higher velocity pipeline. Using historical and literature data available as well as our own test results, an empirical model was developed to predict Maximum Localized Penetration change over time to be applied in the ageing management of cooling water systems.Molecular Microbiological Methods in combination with traditional techniques are useful tools in the ageing management of pipelines. By applying the empirical model developed and the approach presented, unexpected through-wall leaking can be avoided, thus, saving costs and assets.

On-site wastewater treatment systems are gaining popularity in areas where centralized wastewater treatment is not available. In the current case study a domestic activated sludge system was investigated, where treated effluent was stored in a short-term (1 week turn-over time) and a long-term (over 2-3 months) storage tank and was then used for irrigation. This design provided a unique opportunity to assess the chemical and microbial changes of the effluent upon storage. Long-term storage greatly improved both the chemical quality and the degradation efficiency of most organic micropollutants examined, including petroleum hydrocarbons and the pesticide diethyltoluamide. Taxonomic profile of the core microbiome of the effluent was also influenced upon storage. Relative abundance values of the members of Azoarcus and Thauera genera, which are important in degrading polycyclic aromatic hydrocarbons compounds, clearly indicated the biodegrading activity of these microbes across samples. The abundance of xenobiotics degradation functions correlated with the observed organic micropollutant degradation values indicating efficient microbial decomposition of these contaminants. Functions related to infectious diseases also had the highest abundance in the short-term storage tank corresponding well with the relative abundance of indicator organisms and implying to the significance of storage time in the elimination of pathogens. Based on these results, small, on-site wastewater treatment systems could benefit from long-term storage of wastewater effluent.

Here we report the results of our decades-long study on epiphytic communities from two tributary systems of the Szigetköz section of the Danube River. The main goal of the investigation was to detect changes in the epiphytic communities at structural (core species, changes in the relative abundance of common species) and functional (trait changes) levels as a result of the most important anthropogenic effects on Szigetköz, i.e., hydro-morphological modifications. We also examined the impact of rehabilitation on the tributary systems in terms of ecological potential. We discovered that mainly motile diatom species characterized the epiphyton due to reduced water volume were introduced into the tributary system after the diversion of the Danube. The ecosystem stabilized in the rehabilitated section, while the non-rehabilitated section showed a worsening tendency, mainly in the parapotamic branches. Our long-term data sets may provide a good basis for comparisons of different aquatic ecosystems, to define changes in the abundance of core species and in the structure of community in response to different anthropogenic pressures. It is fundamental to determine adaptive traits in assessing the impact of global warming stressors on biodiversity.

Corrosion degradation was observed in a nuclear power plant spent fuel cooling system. A systematic and comprehensive investigation program was developed to reveal the root cause of the degradation. Series of corrosion tests, mechanical, microstructural and microbiological investigations were carried out. Also, simulations of the operating conditions and welding parameters were performed. Based on the results, the major contributors to the degradation process were identified and a possible degradation mechanism was proposed.

The gene encoding T cell immunoglobulin and mucin domain-1 (Tim-1) is linked to atopy and asthma susceptibility in mice and humans. Tim-1 is a transmembrane protein expressed on activated lymphocytes and appears to have a role as a co-stimulatory receptor in T cells. The protein has not been shown to have enzymatic activity but contains a site within its cytoplasmic tail predicted to be a target for tyrosine kinases. Here, we show that Tim-1 can associate with the kinase Fyn, a member of the Src family of tyrosine kinases. This association does not require Fyn's kinase activity and is independent of the phosphorylation of a conserved tyrosine present within the cytoplasmic tail of Tim-1. Fyn is necessary for phosphorylation of this tyrosine in Tim-1 and the phosphorylation of Tim-1 varies with the levels of Fyn present in cells. These data suggest a role for Fyn in the signaling downstream of Tim-1.

SOCS-1 is a critical regulator of multiple signaling pathways, including those activated by cytokines that regulate Ig H chain class switching to IgE. Analysis of mice with mutations in the SOCS-1 gene demonstrated that IgE levels increase with loss of SOCS-1 alleles. This suggested that overall SOCS-1 acts as an inhibitor of IgE expression in vivo. A genetic association study was performed in 474 children enrolled in the Tucson Children’s Respiratory Study to determine if genetic variation in the SOCS-1 locus correlates with altered levels of IgE. Carriers of the C-allele for a novel, 3′ genomic single nucleotide polymorphism (SNP) in the SOCS-1 gene (SOCS1+1125G > C; rs33932899) were found to have significantly lower levels of serum IgE compared with those of homozygotes for the G-allele. Analysis demonstrated that the SOCS1+1125G > C SNP was in complete linkage disequilibrium with an SNP at position SOCS1−820G > T (rs33977706) of the SOCS-1 promoter. Carriers of the T-allele at the SOCS1−820G > T were also found to be associated with the decreased IgE. The promoter SNP increased transcriptional activity of the SOCS-1 promoter in reporter assays and human B cells. Consistent with this observation, the presence of this polymorphism within the promoter abolished binding of yin yang-1, which is identified as a negative regulator of SOCS-1 transcriptional activity. These data suggest that genetic variation in the SOCS-1 promoter may affect IgE production.

A recessive mutation named Justy was found that abolishes B lymphopoiesis but does not impair other major aspects of hematopoiesis. Transplantation experiments showed that homozygosity for Justy prevented hematopoietic progenitors from generating B cells but did not affect the ability of bone marrow stroma to support B lymphopoiesis. In bone marrow from mutant mice, common lymphoid progenitors and pre-pro-B cells appeared normal, but cells at subsequent stages of B lymphopoiesis were dramatically reduced in number. Under culture conditions that promoted B lymphopoiesis, mutant pre-pro-B cells remained alive and began expressing the B cell marker CD19 but failed to proliferate. In contrast, these cells were able to generate myeloid or T/NK precursors. Genetic and molecular analysis demonstrated that Justy is a point mutation within the Gon4-like (Gon4l) gene, which encodes a protein with homology to transcriptional regulators. This mutation was found to disrupt Gon4l pre-mRNA splicing and dramatically reduce expression of wild-type Gon4l RNA and protein. Consistent with a role for Gon4l in transcriptional regulation, the levels of RNA encoding C/EBPalpha and PU.1 were abnormally high in mutant B cell progenitors. Our findings indicate that the Gon4l protein is required for B lymphopoiesis and may function to regulate gene expression during this process.

The Suppressor of Cytokine Signaling (SOCS) protein family plays a central role in the negative regulation of cytokine action and has been implicated in the development of atopic diseases. Lack of SOCS7 is associated with severe skin disease in mice. We sought to explore the underlying mechanisms resulting in this phenotype. Skin samples were analyzed and serum immunoglobulin production was measured. Cytokine production by bone marrow derived mast cells was determined by ELISA. Mast cell thymic stromal lymphopoietin (TSLP) production was assessed by quantitative real-time PCR. Data obtained revealed that Socs7−/− mice have increased serum IgE and IgG1 production and exhibit an increased mast cell infiltrate, as well as un-provoked mast cell degranulation in the dermis as compared to controls. In vitro, bone marrow derived mast cells from Socs7−/− mice are hyperactive to IgE-mediated stimuli, with elevated production of pro-inflammatory cytokines (IL-13, IL-6, TNF-α). Further, activated Socs7−/− bone marrow derived mast cells have increased IL-7Rα transcript, which is part of the heterodimeric receptor for TSLP. Finally, lack of SOCS7 was accompanied by an increase in TSLP mRNA and protein production by mast cells following FcεRI aggregation. These data implicate SOCS7 in the modulation of allergic inflammation and demonstrate that SOCS7 is involved in the regulation of TSLP signaling in mast cells.

The immunopathological hallmark of allergic diseases is elevated total and allergen specific serum IgE levels along with inflammation. This inflammation results from the activation of a cadre of hematopoietic and nonhematopoetic cells. This coordinated activation is the result of the increased production of a variety of soluble factors including chemokines and cytokines. The magnitude and the duration of cytokine action will determine the response to an allergen, either mounting a low-grade immunologic response or resulting in exaggerated reaction such as asthma or atopic dermatitis. Thus, the action of cytokines is tightly regulated both developmentally and within the cell. The suppressor of cytokine signaling (SOCS) protein family represents a novel group of cytoplasmic negative feedback regulators of type I and II cytokines. Several of the signaling pathways regulated by SOCS proteins are important in allergic immune responses. Thus, SOCS proteins may be important regulators of atopy.

Otoconia are biominerals of the vestibular system that are indispensable for the perception of gravity. Despite their importance, the process of otoconia genesis is largely unknown. Reactive oxygen species (ROS) have been recognized for their toxic effects in antimicrobial host defense as well as in aging and carcinogenesis. Enzymes evolved for ROS production belong to the recently discovered NADPH oxidase (Nox) enzyme family [1]. Here we show that the inactivation of a regulatory subunit, NADPH oxidase organizer 1 (Noxo1), resulted in the severe balance deficit seen in the spontaneous mutant “head slant” (hslt) mice whose phenotype was rescued by Noxo1 transgenes. Wild-type Noxo1 was expressed in the vestibular and cochlear epithelia and was required for ROS production by an oxidase complex. In contrast, the hslt mutation of Noxo1 was biochemically inactive and led to an arrest of otoconia genesis, characterized by a complete lack of calcium carbonate mineralization and an accumulation of otoconial protein, otoconin-90/95 (OC-90/95). These results suggest that ROS generated by a Noxo1-dependent vestibular oxidase are critical for otoconia formation and may be required for interactions among otoconial components. Noxo1 mutants implicate a constructive developmental role for ROS, in contrast to their previously described toxic effects.

Reactive oxygen species (ROS) play a major role in drug-, noise-, and age-dependent hearing loss, but the source of ROS in the inner ear remains largely unknown. Herein, we demonstrate that NADPH oxidase (NOX) 3, a member of the NOX/dual domain oxidase family of NADPH oxidases, is highly expressed in specific portions of the inner ear. As assessed by real-time PCR, NOX3 mRNA expression in the inner ear is at least 50-fold higher than in any other tissues where its expression has been observed (e.g. fetal kidney, brain, skull). Microdissection and in situ hybridization studies demonstrated that NOX3 is localized to the vestibular and cochlear sensory epithelia and to the spiral ganglions. Transfection of human embryonic kidney 293 cells with NOX3 revealed that it generates low levels of ROS on its own but produces high levels of ROS upon co-expression with cytoplasmic NOX subunits. NOX3-dependent superoxide production required a stimulus in the absence of subunits and upon co-expression with phagocyte NADPH oxidase subunits p47phox and p67phox, but it was stimulus-independent upon co-expression with colon NADPH oxidase subunits NOX organizer 1 and NOX activator 1. Pre-incubation of NOX3-transfected human embryonic kidney 293 cells with the ototoxic drug cisplatin markedly enhanced superoxide production, in both the presence and the absence of subunits. Our data suggest that NOX3 is a relevant source of ROS generation in the cochlear and vestibular systems and that NOX3-dependent ROS generation might contribute to hearing loss and balance problems in response to ototoxic drugs.

NADPH oxidase 5 (NOX5) is a homologue of the gp91(phox) subunit of the phagocyte NADPH oxidase. NOX5 is expressed in lymphoid organs and testis and distinguished from the other NADPH oxidases by its unique N terminus, which contains three canonical EF-hands, Ca2+-binding domains. Upon heterologous expression, NOX5 was shown to generate superoxide in response to intracellular Ca2+ elevations. In this study, we have analyzed the mechanism of Ca2+ activation of NOX5. In a cell-free system, Ca2+ elevations triggered superoxide production by NOX5 (K-m = 1.06 muM) in an NADPH- and FAD-dependent but cytosol-independent manner. That result indicated a role for the N-terminal EF-hands in NOX5 activation. Therefore, we generated recombinant proteins of NOX5 N terminus and investigated their interactions with Ca2+. Flow dialysis experiments showed that NOX5 N terminus contained four Ca2+-binding sites and allowed us to define the hitherto unidentified fourth, non-canonical EF-hand. The EF-hands of NOX5 formed two pairs: the very N-terminal pair had relatively low affinity for Ca2+, whereas the more C-terminal pair bound Ca2+ with high affinity. Ca2+-binding caused a marked conformation change in the N terminus, which exposed its hydrophobic core, and became able to bind melittin, a model peptide for calmodulin targets. Using a pull-down assay, we demonstrate that the regulatory N terminus and the catalytic C terminus of NOX5 interact in a Ca2+-dependent way. Our results indicate that the Ca2+-induced conformation change of NOX5 N terminus led to enzyme activation through an intra-molecular interaction. That represents a novel mechanism of activation among NAD(P) H oxidases and Ca2+-activated enzymes.