Cellular Microbiology Journal Impact Factor & Information

Publisher: Wiley

Journal description

Cellular Microbiology publishes the best original scientific contribution of the intersection of microbial on host-cell biology. The focus is the host cell responses elicited by the interaction of micro-organisms. Equal emphasis is placed on responses to prokaryotic, viral and eukaryotic micro-organisms. In addition to mammalion systems, papers addressing other hosts such as plants and insects are strongly encourage. Exploitation of host cell structure; Modification of cell signalling pathways; Molecular responses of the host cell; Responses of tissues and whole organs; Systemic effects elicited by micro-organisms; Induction of immune response; Modulation and exploitation of immune response; Remodelling of tissues; Co-pathogen interactions.

Current impact factor: 4.82

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 4.816
2012 Impact Factor 4.811
2011 Impact Factor 5.458
2010 Impact Factor 5.625
2009 Impact Factor 5.725
2008 Impact Factor 5.598
2007 Impact Factor 5.293
2006 Impact Factor 5.07
2005 Impact Factor 6.333
2004 Impact Factor 6.097
2003 Impact Factor 5.336
2002 Impact Factor 4.895
2001 Impact Factor 4.557
2000 Impact Factor 3.409

Impact factor over time

Impact factor
Year

Additional details

5-year impact 5.09
Cited half-life 5.30
Immediacy index 1.31
Eigenfactor 0.03
Article influence 1.85
Website Cellular Microbiology website
Other titles Cellular microbiology (Online)
ISSN 1462-5822
OCLC 42869627
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Wiley

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo
  • Conditions
    • Some journals have separate policies, please check with each journal directly
    • On author's personal website, institutional repositories, arXiv, AgEcon, PhilPapers, PubMed Central, RePEc or Social Science Research Network
    • Author's pre-print may not be updated with Publisher's Version/PDF
    • Author's pre-print must acknowledge acceptance for publication
    • Non-Commercial
    • Publisher's version/PDF cannot be used
    • Publisher source must be acknowledged with citation
    • Must link to publisher version with set statement (see policy)
    • If OnlineOpen is available, BBSRC, EPSRC, MRC, NERC and STFC authors, may self-archive after 12 months
    • If OnlineOpen is available, AHRC and ESRC authors, may self-archive after 24 months
    • Publisher last contacted on 07/08/2014
    • This policy is an exception to the default policies of 'Wiley'
  • Classification
    ​ yellow

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Anaplasma phagocytophilum is an emerging human pathogen and obligate intracellular bacterium. It inhabits a host cell-derived vacuole and cycles between replicative RC (reticulate cell) and infectious DC (dense-cored) morphotypes. Host-pathogen interactions that are critical for RC-to-DC conversion are undefined. We previously reported that A. phagocytophilum recruits GFP-tagged Rab10, a GTPase that directs exocytic traffic from the sphingolipid-rich trans-Golgi network (TGN), to its vacuole in a guanine nucleotide-independent manner. Here, we demonstrate that endogenous Rab10-positive TGN vesicles are not only routed to but also delivered into the A. phagocytophilum-occupied vacuole (ApV). Consistent with this finding, A. phagocytophilum incorporates sphingolipids while intracellular and retains them when naturally released from host cells. TGN vesicle delivery into the ApV is Rab10-dependent, upregulates expression of the DC-specific marker, APH1235, and is critical for the production of infectious progeny. The A. phagocytophilum surface protein, uridine monophosphate kinase, was identified as a guanine nucleotide-independent, Rab10-specific ligand. These data delineate why Rab10 is important for the A. phagocytophilum infection cycle and expands understanding of the benefits exploiting host cell membrane traffic affords intracellular bacterial pathogens. This article is protected by copyright. All rights reserved.
    Cellular Microbiology 08/2015; DOI:10.1111/cmi.12500
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    ABSTRACT: Borrelia burgdorferi surface-located membrane protein 1, also known as Lmp1, has been shown to play critical roles in pathogen evasion of host-acquired immune defenses, thereby facilitating persistent infection. Lmp1 possesses three regions representing potentially discrete domains, Lmp1N, Lmp1M, and Lmp1C. Due to its insignificant homology to known proteins, how Lmp1 or its specific regions contribute to microbial biology and infection remains enigmatic. Here we show that distinct from Lmp1N and Lmp1C, Lmp1M is composed of at least 70% alpha helices and completely lacks recognizable beta sheets. The region binds to host glycosaminoglycan chondroitin-6-sulfate molecules and facilitates mammalian cell attachment, suggesting an adhesin function of Lmp1M. Phenotypic analysis of the Lmp1-deficient mutant engineered to produce Lmp1M on the microbial surface suggests that Lmp1M can independently support B. burgdorferi infectivity in murine hosts. Further exploration of functions of Lmp1 distinct regions will shed new light on the intriguing biology and infectivity of spirochetes and help develop novel interventions to combat Lyme disease. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Cellular Microbiology 08/2015; DOI:10.1111/cmi.12487
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    ABSTRACT: The increasing interest in cytoplasmic factories generated by eukaryotic-infecting viruses stems from the realization that these highly ordered assemblies may contribute fundamental novel insights to the functional significance of order in cellular biology. Here we report the formation process and structural features of the cytoplasmic factories of the large dsDNA virus PBCV-1. By combining diverse imaging techniques, including Scanning-transmission EM (STEM) tomography and Focused Ion Beam (FIB) technologies, we show that the architecture and mode of formation of PBCV-1 factories are significantly different from those generated by their evolutionary relatives Vaccinia and Mimivirus. Specifically, PBCV-1 factories consist of a network of single membrane bilayers acting as capsid templates in the central region, and viral genomes spread throughout the host cytoplasm but excluded from the membrane-containing sites. In sharp contrast, factories generated by Mimivirus have viral genomes in their core, with membrane biogenesis region located at their periphery. Yet, all viral factories appear to share structural features that are essential for their function. In addition, our studies support the notion that PBCV-1 infection, which was recently reported to result in significant pathological outcomes in humans and mice, proceeds through a bacteriophage-like infection pathway. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Cellular Microbiology 08/2015; DOI:10.1111/cmi.12486
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    ABSTRACT: The Aggregatibactor actinomycetemcomitans cytolethal distending toxin (Cdt) induces G2 arrest and apoptosis in lymphocytes and other cell types. We have shown that the active subunit, CdtB, exhibits phosphatidylinositol-3,4,5-triphosphate (PIP3) phosphatase activity leading us to propose that Cdt toxicity is the result of PIP3 depletion and perturbation of PI-3 K/PIP3/Akt signaling. To further explore this relationship, we have focused our analysis on identifying residues that comprise the catalytic pocket and are critical to substrate binding rather than catalysis. In this context we have generated several CdtB mutants and demonstrate that, in each instance, the ability of the toxin to induce cell cycle arrest correlates with retention of phosphatase activity. We have also assessed the effect of Cdt on downstream components of the PI-3 K signaling pathway. In addition to depletion of intracellular concentrations of PIP3, toxin treated lymphocytes exhibit decreases in pAkt and pGSK3β. Further analysis indicates that toxin-treated cells exhibit a concomitant loss in Akt activity and increase in GSK3β kinase activity consistent with observed changes in their phosphorylation status. We demonstrate that cell susceptibility to Cdt is dependent upon dephosphorylation and concomitant activation of GSK3β as well as baseline levels of PIP3. Finally, we demonstrate that in addition to lymphocytes, HeLa cells exposed to a CdtB mutant that retains phosphatase activity and not DNase activity undergo G2 arrest in the absence of H2AX phosphorylation. Our results provide further insight into the mode of action by which Cdt may function as an immunotoxin and induce cell cycle arrest in target cells such as lymphocytes. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Cellular Microbiology 08/2015; DOI:10.1111/cmi.12497
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    ABSTRACT: Macrophages are critical effectors of the early innate response to bacteria in tissues. Phagocytosis and killing of bacteria are interrelated functions essential for bacterial clearance but the rate-limiting step when macrophages are challenged with large numbers of the major medical pathogen Staphylococcus aureus is unknown. We show that macrophages have a finite capacity for intracellular killing and fail to match sustained phagocytosis with sustained microbial killing when exposed to large inocula of S. aureus (Newman, SH1000 and USA300 strains). S. aureus ingestion by macrophages is associated with a rapid decline in bacterial viability immediately after phagocytosis. However not all bacteria are killed in the phagolysosome and we demonstrate reduced acidification of the phagolysosome, associated with failure of phagolysosomal maturation and reduced activation of cathepsin D. This results in accumulation of viable intracellular bacteria in macrophages. We show macrophages fail to engage apoptosis-associated bacterial killing. Ultimately macrophages with viable bacteria undergo cell lysis and viable bacteria are released and can be internalized by other macrophages. We show that cycles of lysis and reuptake maintain a pool of viable intracellular bacteria over time when killing is overwhelmed and demonstrate intracellular persistence in alveolar macrophages in the lung in a murine model. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Cellular Microbiology 08/2015; DOI:10.1111/cmi.12485
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    ABSTRACT: Leishmaniasis is a major health problem that affects more than 300 million people throughout the world. The morbidity associated with the disease causes serious economic burden in Leishmania endemic regions. Despite the morbidity and economic burden associated with Leishmaniasis, this disease rarely gets noticed and is still categorized under neglected tropical diseases. The lack of research combined with the ability of Leishmania to evade immune recognition has rendered our efforts to design therapeutic treatments or vaccines challenging. Herein, we review the literature on Leishmania from innate immune perspective and discuss potential problems as well as solutions and future directions that could aid in identifying novel therapeutic targets to eliminate this parasite. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Cellular Microbiology 08/2015; DOI:10.1111/cmi.12484
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    ABSTRACT: In mice, avirulent strains (e.g. types II and III) of the protozoan parasite Toxoplasma gondii are restricted by the immunity-related GTPase (IRG) resistance system. Loading of IRG proteins onto the PVM is required for vacuolar rupture resulting in parasite clearance. In virulent strain (e.g. type I) infections polymorphic effector proteins ROP5 and ROP18 cooperate to phosphorylate and thereby inactivate mouse IRG proteins to preserve PVM integrity. In this study we confirmed the dense granule protein GRA7 as an additional component of the ROP5/ROP18 kinase complex and identified GRA7 association with the PVM by direct binding to ROP5. The absence of GRA7 results in reduced phosphorylation of Irga6 correlated with increased vacuolar IRG protein amounts and attenuated virulence. Earlier work identified additional IRG proteins as targets of T. gondii ROP18 kinase. We show that the only specific target of ROP18 among IRG proteins is in fact Irga6. Similarily, we demonstrate that GRA7 is strictly an Irga6-specific virulence effector. This identifies T. gondii GRA7 as a regulator for ROP18-specific inactivation of Irga6. The structural diversity of the IRG proteins implies that certain family members constitute additional specific targets for other yet unknown T. gondii virulence effectors. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Cellular Microbiology 08/2015; DOI:10.1111/cmi.12499
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    ABSTRACT: Cross-kingdom interactions between bacteria and fungi are a common occurrence in the environment. Recent studies have identified various types of interactions that can either take the form of a synergistic relationship, or can result in an antagonistic interplay with the subsequent destruction or inhibition of growth of bacteria, fungi or both. This cross-kingdom communication is of particular significance in human health and disease, as bacteria and fungi commonly colonize various human surfaces and their interactions can at times alter the outcome of invasive infections. Moreover, mixed infections from both bacteria and fungi are relatively common among critically ill patients and individuals with weak immune responses. The purpose of this review is to summarize our knowledge on the type of interactions between bacteria and fungi and their relevance in human infections. This article is protected by copyright. All rights reserved.
    Cellular Microbiology 08/2015; DOI:10.1111/cmi.12493
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    ABSTRACT: The obligate intracellular pathogen Coxiella burnetii replicates in a large phagolysosomal-like vacuole. Currently, both host and bacterial factors required for creating this replicative parasitophorous C. burnetii-containing vacuole (PV) are poorly defined. Here, we assessed the contributions of the most abundant proteins of the lysosomal membrane, LAMP-1 and LAMP-2, to the establishment and maintenance of the PV. Whereas these proteins were not critical for uptake of C. burnetii, they influenced the intracellular replication of C. burnetii. In LAMP-1/2 double-deficient fibroblasts as well as in LAMP-1/2 knock-down cells C. burnetii establishes a significantly smaller, yet faster maturing vacuole, which harbored more bacteria. The accelerated maturation of PVs in LAMP double-deficient fibroblasts, which was partially or fully reversed by ectopic expression of LAMP-1 or LAMP-2, respectively, was characterized by an increased fusion rate with endosomes, lysosomes and bead-containing phagosomes, but not by different fusion kinetics with autophagy vesicles. These findings establish that LAMP proteins are critical for the maturation delay of PVs. Unexpectedly, neither the creation of the spacious vacuole nor the delay in maturation was found to be prerequisites for the intracellular replication of C. burnetii. This article is protected by copyright. All rights reserved.
    Cellular Microbiology 08/2015; DOI:10.1111/cmi.12494
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    ABSTRACT: Viral glycoproteins are highly variable in their primary structure but on the other hand feature a high functional conservation to fulfill their versatile tasks during the pathogenic lifecycle. Typically, all protein domains are optimized in that indispensable functions can be assigned to small conserved motifs or even individual amino acids. The cytoplasmic tail of many viral spike proteins, although of particular relevance for the virus biology, is often only insufficiently characterized. Hemagglutinin (HA), the receptor binding protein of the Influenza virus comprises a short cytoplasmic tail of 13 amino acids which exhibits three highly conserved palmitoylation sites. However, the particular importance of these modifications and the tail in general for intracellular trafficking and lateral membrane organization remain elusive. In this study we generated HA core proteins consisting of transmembrane domain, cytoplasmic tail and a minor part of the ectodomain, tagged with a yellow fluorescent protein. Different mutation and truncation variants of these chimeric proteins were investigated using confocal microscopy to characterize the role of cytoplasmic tail and palmitoylation for the intracellular trafficking to plasma membrane and Golgi apparatus. In addition we assessed raft partitioning of the variants by Foerster resonance energy transfer with an established raft marker. We revealed a substantial influence of the cytoplasmic tail length on the intracellular distribution and surface exposure of the proteins. A complete removal of the tail hampers a physiological trafficking of the protein whereas a partial truncation can be compensated by cytoplasmic palmitoylations. Plasma membrane raft partitioning on the other hand was found to imperatively require palmitoylations, and the cysteine at position 551 turned out to be of most relevance. Our data shed further light on the tight interconnection between cytoplasmic elements and intracellular trafficking and suggest a function of hemagglutinin palmitoylations in both, lateral sorting and anterograde trafficking of the glycoprotein. This article is protected by copyright. All rights reserved.
    Cellular Microbiology 08/2015; DOI:10.1111/cmi.12491
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    ABSTRACT: Viral hepatitis caused by HBV and HCV infections poses a significant burden to the public health system. Although HBV and HCV differ in structure and life cycles, they share unique characteristics, such as tropism to infect hepatocytes and association with hepatic and extrahepatic disorders that are of innate immunity nature. In response to HBV and HCV infection, the liver innate immune cells eradicate pathogens by recognizing specific molecules expressed by pathogens via distinct cellular pattern recognition receptors whose triggering activates intracellular signaling pathways inducing cytokines, interferons and anti-viral response genes whose function is to clear infections. However, HBV and HCV evolved strategies to inactivate innate signaling factors and as such establish persistent infections without being recognized by the innate immunity. We review recent insights into how HBV and HCV are sensed and how they evade innate immunity to establish chronicity. Understanding the mechanisms of viral hepatitis is mandatory to develop effective and safe therapies for eradication of viral hepatitis. This article is protected by copyright. All rights reserved.
    Cellular Microbiology 08/2015; DOI:10.1111/cmi.12489
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    ABSTRACT: Helicobacter pylori strains carrying the cag pathogenicity island (cagPAI) provoke an increased inflammatory response, conferring an increased risk of ulcer formation and carcinogenesis. How the immune system recognizes the presence of cagPAI positive strains is yet unclear. By comparing the transcriptional response of wild type and MyD88/Trif (-/-) bone marrow macrophages to infection with H. pylori we found that the majority of regulated genes were dependent on TLR signaling. To determine the role of TLR-independent responses, we analyzed the transcriptome of MyD88/Trif (-/-) bone marrow macrophages at different time points after infection with cagPAI positive vs. negative strains. We identified a group of genes that exhibited different kinetic behaviour depending on whether cagPAI was present. Analysis of their gene expression kinetics demonstrated that this responsiveness to cagPAI was observed only in MyD88/Trif (-/-) macrophages. This group of cagPAI sensing genes was enriched for AU-rich element-containing early response genes involved in immune regulation, including IL-1β and TNF-α. Recognition of cagPAI positive strains was found to be mediated by the type IV secretion system (CagT4SS), rather than its effector protein CagA. We hypothesize that anergic macrophages of the gastric mucosa initiate an innate immune response following detection the T4SS of H. pylori. This article is protected by copyright. All rights reserved.
    Cellular Microbiology 08/2015; DOI:10.1111/cmi.12492
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    ABSTRACT: A single layer of epithelial cells separates the intestinal lumen from the underlying sterile tissue. It is exposed to a multitude of nutrients and a large number of commensal bacteria. Although the presence of commensal bacteria significantly contributes to nutrient digestion, vitamin synthesis and tissue maturation, their high number represents a permanent challenge to the integrity of the epithelial surface keeping the local immune system constantly on alert. In addition, the intestinal mucosa is challenged by a variety of enteropathogenic microorganisms. In both circumstances, the epithelium actively contributes to maintaining host-microbial homeostasis and antimicrobial host defense. It deploys a variety of mechanisms to restrict the presence of commensal bacteria to the intestinal lumen and to prevent translocation of commensal and pathogenic microorganisms to the underlying tissue. Enteropathogenic microorganisms in turn have learnt to evade the host's immune system and circumvent the antimicrobial host response. In the present article, we review recent advances that illustrate the intense and intimate host-microbial interaction at the epithelial level and improve our understanding of the mechanisms that maintain the integrity of the intestinal epithelial barrier. This article is protected by copyright. All rights reserved.
    Cellular Microbiology 08/2015; DOI:10.1111/cmi.12501
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    ABSTRACT: Vascular injury is a serious complication of sepsis due to the gram-negative bacterium Neisseria meningitidis. One of the critical early steps in initiating this injury is via the interaction of leucocytes, particularly neutrophils, with adhesion molecules expressed on inflamed endothelium. We have previously demonstrated that both LPS and non-LPS components of meningococci can induce very high levels of expression of the vascular endothelial cell adhesion molecule E-selectin, which is critical for early tethering and capture of neutrophils onto endothelium under flow. Using an LPS deficient strain of meningococcus, we showed that very high levels of expression can be induced in primary endothelial cells, even in the context of weak activation of the major host signal transduction factor NF-κB. In this study, we show that the particular propensity for N. meningitidis to induce high levels of expression is regulated at a transcriptional level, and demonstrate a significant role for phosphorylation of the ATF2 transcription factor, likely via MAP kinases, on the activity of the E-selectin promoter. Furthermore, inhibition of E-selectin expression in response to the lpxA- strain by a p38 inhibitor indicate a significant role of a p38-dependent MAPK signalling pathway in ATF-2 activation. Collectively, this data highlight the role that LPS and other bacterial components have in modulating endothelial function and their involvement in the pathogenesis of meningococcal sepsis. Better understanding of these multiple mechanisms induced by complex stimuli such as bacteria, and the specific inflammatory pathways they activate, may lead to improved, focused interventions in both meningococcal and potentially bacterial sepsis more generally. This article is protected by copyright. All rights reserved.
    Cellular Microbiology 07/2015; DOI:10.1111/cmi.12483
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    ABSTRACT: Many intracellular pathogens co-opt actin in host cells, but little is known about these interactions in vivo. We study the in vivo trafficking and exit of the microsporidian Nematocida parisii, which is an intracellular pathogen that infects intestinal cells of the nematode Caenorhabditis elegans. We recently demonstrated that N. parisii uses directional exocytosis to escape out of intestinal cells into the intestinal tract. Here, we show that an intestinal-specific isoform of C. elegans actin called ACT-5 forms coats around membrane compartments that contain single exocytosing spores, and that these coats appear to form after fusion with the apical membrane. We performed a genetic screen for host factors required for actin coat formation and identified small GTPases important for this process. Through analysis of animals defective in these factors, we found that actin coats are not required for pathogen exit although they may boost exocytic output. Later during infection, we find that ACT-5 also forms coats around membrane-bound vesicles that contain multiple spores. These vesicles are likely formed by clathrin-dependent compensatory endocytosis to retrieve membrane material that has been trafficked to the apical membrane as part of the exocytosis process. These findings provide insight into microsporidia interaction with host cells, and provide novel in vivo examples of the manner in which intracellular pathogens co-opt host actin during their life cycle. This article is protected by copyright. All rights reserved.
    Cellular Microbiology 07/2015; DOI:10.1111/cmi.12481