Journal articles: 'Host-bacterial interaction'

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Mosher, Deane. "Targeting the bacterial-host interaction." Virulence 3, no. 4 (July 2012): 349–50. http://dx.doi.org/10.4161/viru.21269.

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Wu, Yao-Wen, and Fu Li. "Bacterial interaction with host autophagy." Virulence 10, no. 1 (January 1, 2019): 352–62. http://dx.doi.org/10.1080/21505594.2019.1602020.

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Barnett, Timothy C., Jin Yan Lim, Amelia T. Soderholm, Tania Rivera-Hernandez, Nicholas P. West, and Mark J. Walker. "Host–pathogen interaction during bacterial vaccination." Current Opinion in Immunology 36 (October 2015): 1–7. http://dx.doi.org/10.1016/j.coi.2015.04.002.

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Libbing, Cassandra L., Adam R. McDevitt, Rea-Mae P. Azcueta, Ahila Ahila, and Minal Mulye. "Lipid Droplets: A Significant but Understudied Contributor of Host–Bacterial Interactions." Cells 8, no. 4 (April 15, 2019): 354. http://dx.doi.org/10.3390/cells8040354.

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Lipid droplets (LDs) are cytosolic lipid storage organelles that are important for cellular lipid metabolism, energy homeostasis, cell signaling, and inflammation. Several bacterial, viral and protozoal pathogens exploit host LDs to promote infection, thus emphasizing the importance of LDs at the host–pathogen interface. In this review, we discuss the thus far reported relation between host LDs and bacterial pathogens including obligate and facultative intracellular bacteria, and extracellular bacteria. Although there is less evidence for a LD–extracellular bacterial interaction compared to interactions with intracellular bacteria, in this review, we attempt to compare the bacterial mechanisms that target LDs, the host signaling pathways involved and the utilization of LDs by these bacteria. Many intracellular bacteria employ unique mechanisms to target host LDs and potentially obtain nutrients and lipids for vacuolar biogenesis and/or immune evasion. However, extracellular bacteria utilize LDs to either promote host tissue damage or induce host death. We also identify several areas that require further investigation. Along with identifying LD interactions with bacteria besides the ones reported, the precise mechanisms of LD targeting and how LDs benefit pathogens should be explored for the bacteria discussed in the review. Elucidating LD–bacterial interactions promises critical insight into a novel host–pathogen interaction.

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Yang, Huiying, Yuehua Ke, Jian Wang, Yafang Tan, Sebenzile K. Myeni, Dong Li, Qinghai Shi, et al. "Insight into Bacterial Virulence Mechanisms against Host Immune Response via the Yersinia pestis-Human Protein-Protein Interaction Network." Infection and Immunity 79, no. 11 (September 12, 2011): 4413–24. http://dx.doi.org/10.1128/iai.05622-11.

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ABSTRACTAYersinia pestis-human protein interaction network is reported here to improve our understanding of its pathogenesis. Up to 204 interactions between 66Y. pestisbait proteins and 109 human proteins were identified by yeast two-hybrid assay and then combined with 23 previously published interactions to construct a protein-protein interaction network. Topological analysis of the interaction network revealed that human proteins targeted byY. pestiswere significantly enriched in the proteins that are central in the human protein-protein interaction network. Analysis of this network showed that signaling pathways important for host immune responses were preferentially targeted byY. pestis, including the pathways involved in focal adhesion, regulation of cytoskeleton, leukocyte transendoepithelial migration, and Toll-like receptor (TLR) and mitogen-activated protein kinase (MAPK) signaling. Cellular pathways targeted byY. pestisare highly relevant to its pathogenesis. Interactions with host proteins involved in focal adhesion and cytoskeketon regulation pathways could account for resistance ofY. pestisto phagocytosis. Interference with TLR and MAPK signaling pathways byY. pestisreflects common characteristics of pathogen-host interaction that bacterial pathogens have evolved to evade host innate immune response by interacting with proteins in those signaling pathways. Interestingly, a large portion of human proteins interacting withY. pestis(16/109) also interacted with viral proteins (Epstein-Barr virus [EBV] and hepatitis C virus [HCV]), suggesting that viral and bacterial pathogens attack common cellular functions to facilitate infections. In addition, we identified vasodilator-stimulated phosphoprotein (VASP) as a novel interaction partner of YpkA and showed that YpkA could inhibitin vitroactin assembly mediated by VASP.

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Sun, Hongmin. "The Interaction Between Pathogens and the Host Coagulation System." Physiology 21, no. 4 (August 2006): 281–88. http://dx.doi.org/10.1152/physiol.00059.2005.

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There is mounting evidence that the hemostatic system is critical in host responses to bacterial infection. Invasive bacteria have evolved virulence strategies to interact with host hemostatic factors such as plasminogen and fibrinogen for infection. Furthermore, genetic variations in host hemostatic factors also influence host response to bacterial infection.

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Ceri, Howard, and Yolande Westra. "Host binding proteins and bacterial adhesion: ecology and binding model." Biochemistry and Cell Biology 66, no. 6 (June 1, 1988): 541–48. http://dx.doi.org/10.1139/o88-064.

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Defining the involvement of specific recognition and (or) adhesion molecules in the precise association formed between cells of an organism during development or between bacteria and specific host tissues has become a focus of extensive research. The possibility that the same molecules responsible for cellular adhesion in the host may also play a major role in determining host–bacterial interactions is now becoming more evident. The following review looks at the interaction of a group of host binding proteins, including lectins, fibronectin, and laminin, with respect to their specific association with bacteria. This information is dealt with both from the perspective of the ecology of the host and its autochthonous and pathogenic bacterial populations, as well as in terms of the difficulties in defining the nature of ligand associations even in the more simplified bacterial–host interaction.

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Khan, M. A., H. Satoh, T. Mino, H. Katayama, F. Kurisu, and T. Matsuo. "Bacteriophage-host interaction in the enhanced biological phosphate removing activated sludge system." Water Science and Technology 46, no. 1-2 (July 1, 2002): 39–43. http://dx.doi.org/10.2166/wst.2002.0453.

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Bacteriophages were isolated from a laboratory scale enhanced biological phosphate removing (EBPR) activated sludge process, and their host range was examined. Bacterial isolates to host the bacteriophages were isolated from the EBPR activated sludge process. Bacteriophages were eluted from the EBPR activated sludge, enriched by incubation with the bacterial isolates, and then tested for plaque formation on each of the bacterial isolates. Out of 12 bacterial isolates isolated, 4 supported plaque formation. Four bacteriophages were obtained from the plaques. The host range test was conducted with the combination of the bacteriophage isolates and the bacterial isolates. Three of the bacteriophages were found to form plaques on more than one host, and one of them formed plaques on both Gram +ve and Gram −ve bacterial isolates. Two of the four bacteriophages failed to form plaques on their original bacterial host, indicating the existence of mutation on either both or one of the host and the bacteriophage. This study strongly suggests that bacteriophages are an active part of the activated sludge microbial ecosystem, having very complex interaction with their host bacteria.

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Lin, Borong, Xue Qing, Jinling Liao, and Kan Zhuo. "Role of Protein Glycosylation in Host-Pathogen Interaction." Cells 9, no. 4 (April 20, 2020): 1022. http://dx.doi.org/10.3390/cells9041022.

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Host-pathogen interactions are fundamental to our understanding of infectious diseases. Protein glycosylation is one kind of common post-translational modification, forming glycoproteins and modulating numerous important biological processes. It also occurs in host-pathogen interaction, affecting host resistance or pathogen virulence often because glycans regulate protein conformation, activity, and stability, etc. This review summarizes various roles of different glycoproteins during the interaction, which include: host glycoproteins prevent pathogens as barriers; pathogen glycoproteins promote pathogens to attack host proteins as weapons; pathogens glycosylate proteins of the host to enhance virulence; and hosts sense pathogen glycoproteins to induce resistance. In addition, this review also intends to summarize the roles of lectin (a class of protein entangled with glycoprotein) in host-pathogen interactions, including bacterial adhesins, viral lectins or host lectins. Although these studies show the importance of protein glycosylation in host-pathogen interaction, much remains to be discovered about the interaction mechanism.

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Ling, Jessmi M. L., and Anthony B. Schryvers. "Perspectives on interactions between lactoferrin and bacteriaThis paper is one of a selection of papers published in this Special Issue, entitled 7th International Conference on Lactoferrin: Structure, Function, and Applications, and has undergone the Journal's usual peer review process." Biochemistry and Cell Biology 84, no. 3 (June 2006): 275–81. http://dx.doi.org/10.1139/o06-044.

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Lactoferrin has long been recognized for its antimicrobial properties, initially attributed primarily to iron sequestration. It has since become apparent that interaction between the host and bacteria is modulated by a complex series of interactions between lactoferrin and bacteria, lactoferrin and bacterial products, and lactoferrin and host cells. The primary focus of this review is the interaction between lactoferrin and bacteria, but interactions with the lactoferrin-derived cationic peptide lactoferricin will also be discussed. We will summarize what is currently known about the interaction between lactoferrin (or lactoferricin) and surface or secreted bacterial components, comment on the potential physiological relevance of the findings, and identify key questions that remain unanswered.

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NV, Beloborodova. "Low-Molecular Weight Bacterial Metabolites in Host-Microbial Interaction." Infectious & Non Infectious Diseases 2, no. 1 (June 9, 2016): 1–11. http://dx.doi.org/10.24966/inid-8654/100011.

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Kuehn, M. J. "Bacterial outer membrane vesicles and the host-pathogen interaction." Genes & Development 19, no. 22 (November 15, 2005): 2645–55. http://dx.doi.org/10.1101/gad.1299905.

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Maudet, Claire, Miguel Mano, and Ana Eulalio. "MicroRNAs in the interaction between host and bacterial pathogens." FEBS Letters 588, no. 22 (August 12, 2014): 4140–47. http://dx.doi.org/10.1016/j.febslet.2014.08.002.

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Day, Christopher J., Elizabeth N. Tran, Evgeny A. Semchenko, Greg Tram, Lauren E. Hartley-Tassell, Preston S. K. Ng, Rebecca M. King, et al. "Glycan:glycan interactions: High affinity biomolecular interactions that can mediate binding of pathogenic bacteria to host cells." Proceedings of the National Academy of Sciences 112, no. 52 (December 16, 2015): E7266—E7275. http://dx.doi.org/10.1073/pnas.1421082112.

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Cells from all domains of life express glycan structures attached to lipids and proteins on their surface, called glycoconjugates. Cell-to-cell contact mediated by glycan:glycan interactions have been considered to be low-affinity interactions that precede high-affinity protein–glycan or protein–protein interactions. In several pathogenic bacteria, truncation of surface glycans, lipooligosaccharide (LOS), or lipopolysaccharide (LPS) have been reported to significantly reduce bacterial adherence to host cells. Here, we show that the saccharide component of LOS/LPS have direct, high-affinity interactions with host glycans. Glycan microarrays reveal that LOS/LPS of four distinct bacterial pathogens bind to numerous host glycan structures. Surface plasmon resonance was used to determine the affinity of these interactions and revealed 66 high-affinity host–glycan:bacterial–glycan pairs with equilibrium dissociation constants (KD) ranging between 100 nM and 50 µM. These glycan:glycan affinity values are similar to those reported for lectins or antibodies with glycans. Cell assays demonstrated that glycan:glycan interaction-mediated bacterial adherence could be competitively inhibited by either host cell or bacterial glycans. This is the first report to our knowledge of high affinity glycan:glycan interactions between bacterial pathogens and the host. The discovery of large numbers of glycan:glycan interactions between a diverse range of structures suggests that these interactions may be important in all biological systems.

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Raftery, Tara D., Heidi Lindler, and Tamara L. McNealy. "Altered Host Cell–Bacteria Interaction due to Nanoparticle Interaction with a Bacterial Biofilm." Microbial Ecology 65, no. 2 (September 30, 2012): 496–503. http://dx.doi.org/10.1007/s00248-012-0128-5.

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Auweter, Sigrid D., Amit P. Bhavsar, Carmen L. de Hoog, Yuling Li, Y. Alina Chan, Joris van der Heijden, Michael J. Lowden, et al. "Quantitative Mass Spectrometry Catalogues Salmonella Pathogenicity Island-2 Effectors and Identifies Their Cognate Host Binding Partners." Journal of Biological Chemistry 286, no. 27 (May 12, 2011): 24023–35. http://dx.doi.org/10.1074/jbc.m111.224600.

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Gram-negative bacterial pathogens have developed specialized secretion systems to transfer bacterial proteins directly into host cells. These bacterial effectors are central to virulence and reprogram host cell processes to favor bacterial survival, colonization, and proliferation. Knowing the complete set of effectors encoded by a particular pathogen is the key to understanding bacterial disease. In addition, the identification of the molecular assemblies that these effectors engage once inside the host cell is critical to determining the mechanism of action of each effector. In this work we used stable isotope labeling of amino acids in cell culture (SILAC), a powerful quantitative proteomics technique, to identify the proteins secreted by the Salmonella pathogenicity island-2 type three secretion system (SPI-2 T3SS) and to characterize the host interaction partners of SPI-2 effectors. We confirmed many of the known SPI-2 effectors and were able to identify several novel substrate candidates of this secretion system. We verified previously published host protein-effector binding pairs and obtained 11 novel interactions, three of which were investigated further and confirmed by reciprocal co-immunoprecipitation. The host cell interaction partners identified here suggest that Salmonella SPI-2 effectors target, in a concerted fashion, cellular processes such as cell attachment and cell cycle control that are underappreciated in the context of infection. The technology outlined in this study is specific and sensitive and serves as a robust tool for the identification of effectors and their host targets that is readily amenable to the study of other bacterial pathogens.

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Li, Yajuan, Yuelong Li, Hylemariam Mihiretie Mengist, Cuixiao Shi, Caiying Zhang, Bo Wang, Tingting Li, Ying Huang, Yuanhong Xu, and Tengchuan Jin. "Structural Basis of the Pore-Forming Toxin/Membrane Interaction." Toxins 13, no. 2 (February 9, 2021): 128. http://dx.doi.org/10.3390/toxins13020128.

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With the rapid growth of antibiotic-resistant bacteria, it is urgent to develop alternative therapeutic strategies. Pore-forming toxins (PFTs) belong to the largest family of virulence factors of many pathogenic bacteria and constitute the most characterized classes of pore-forming proteins (PFPs). Recent studies revealed the structural basis of several PFTs, both as soluble monomers, and transmembrane oligomers. Upon interacting with host cells, the soluble monomer of bacterial PFTs assembles into transmembrane oligomeric complexes that insert into membranes and affect target cell-membrane permeability, leading to diverse cellular responses and outcomes. Herein we have reviewed the structural basis of pore formation and interaction of PFTs with the host cell membrane, which could add valuable contributions in comprehensive understanding of PFTs and searching for novel therapeutic strategies targeting PFTs and interaction with host receptors in the fight of bacterial antibiotic-resistance.

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Wang, Xueying, and Jin Wang. "Modeling the within-host dynamics of cholera: bacterial–viral interaction." Journal of Biological Dynamics 11, sup2 (December 22, 2016): 484–501. http://dx.doi.org/10.1080/17513758.2016.1269957.

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Yermak, I. M., and V. N. Davydova. "Interaction of bacterial lipopolysaccharides with host soluble proteins and polycations." Biochemistry (Moscow) Supplement Series A: Membrane and Cell Biology 2, no. 4 (December 2008): 279–95. http://dx.doi.org/10.1134/s1990747808040016.

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Lu, Qiuhe, Shan Li, and Feng Shao. "Sweet Talk: Protein Glycosylation in Bacterial Interaction With the Host." Trends in Microbiology 23, no. 10 (October 2015): 630–41. http://dx.doi.org/10.1016/j.tim.2015.07.003.

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Niddam, Alexandra F., Rhodaba Ebady, Anil Bansal, Anne Koehler, Boris Hinz, and Tara J. Moriarty. "Plasma fibronectin stabilizes Borrelia burgdorferi–endothelial interactions under vascular shear stress by a catch-bond mechanism." Proceedings of the National Academy of Sciences 114, no. 17 (April 10, 2017): E3490—E3498. http://dx.doi.org/10.1073/pnas.1615007114.

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Bacterial dissemination via the cardiovascular system is the most common cause of infection mortality. A key step in dissemination is bacterial interaction with endothelia lining blood vessels, which is physically challenging because of the shear stress generated by blood flow. Association of host cells such as leukocytes and platelets with endothelia under vascular shear stress requires mechanically specialized interaction mechanisms, including force-strengthened catch bonds. However, the biomechanical mechanisms supporting vascular interactions of most bacterial pathogens are undefined. Fibronectin (Fn), a ubiquitous host molecule targeted by many pathogens, promotes vascular interactions of the Lyme disease spirochete Borrelia burgdorferi. Here, we investigated how B. burgdorferi exploits Fn to interact with endothelia under physiological shear stress, using recently developed live cell imaging and particle-tracking methods for studying bacterial–endothelial interaction biomechanics. We found that B. burgdorferi does not primarily target insoluble matrix Fn deposited on endothelial surfaces but, instead, recruits and induces polymerization of soluble plasma Fn (pFn), an abundant protein in blood plasma that is normally soluble and nonadhesive. Under physiological shear stress, caps of polymerized pFn at bacterial poles formed part of mechanically loaded adhesion complexes, and pFn strengthened and stabilized interactions by a catch-bond mechanism. These results show that B. burgdorferi can transform a ubiquitous but normally nonadhesive blood constituent to increase the efficiency, strength, and stability of bacterial interactions with vascular surfaces. Similar mechanisms may promote dissemination of other Fn-binding pathogens.

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Meurer, Marita, Sophie Öhlmann, Marta C. Bonilla, Peter Valentin-Weigand, Andreas Beineke, Isabel Hennig-Pauka, Christian Schwerk, et al. "Role of Bacterial and Host DNases on Host-Pathogen Interaction during Streptococcus suis Meningitis." International Journal of Molecular Sciences 21, no. 15 (July 25, 2020): 5289. http://dx.doi.org/10.3390/ijms21155289.

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Streptococcus suis is a zoonotic agent causing meningitis in pigs and humans. Neutrophils, as the first line of defense against S. suis infections, release neutrophil extracellular traps (NETs) to entrap pathogens. In this study, we investigated the role of the secreted nuclease A of S. suis (SsnA) as a NET-evasion factor in vivo and in vitro. Piglets were intranasally infected with S. suis strain 10 or an isogenic ssnA mutant. DNase and NET-formation were analyzed in cerebrospinal fluid (CSF) and brain tissue. Animals infected with S. suis strain 10 or S. suis 10ΔssnA showed the presence of NETs in CSF and developed similar clinical signs. Therefore, SsnA does not seem to be a crucial virulence factor that contributes to the development of meningitis in pigs. Importantly, DNase activity was detectable in the CSF of both infection groups, indicating that host nucleases, in contrast to bacterial nuclease SsnA, may play a major role during the onset of meningitis. The effect of DNase 1 on neutrophil functions was further analyzed in a 3D-cell culture model of the porcine blood–CSF barrier. We found that DNase 1 partially contributes to enhanced killing of S. suis by neutrophils, especially when plasma is present. In summary, host nucleases may partially contribute to efficient innate immune response in the CSF.

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Alkatheri, Asma Hussain, Polly Soo-Xi Yap, Aisha Abushelaibi, Kok-Song Lai, Wan-Hee Cheng, and Swee-Hua Erin Lim. "Host–Bacterial Interactions: Outcomes of Antimicrobial Peptide Applications." Membranes 12, no. 7 (July 19, 2022): 715. http://dx.doi.org/10.3390/membranes12070715.

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The bacterial membrane is part of a secretion system which plays an integral role to secrete proteins responsible for cell viability and pathogenicity; pathogenic bacteria, for example, secrete virulence factors and other membrane-associated proteins to invade the host cells through various types of secretion systems (Type I to Type IX). The bacterial membrane can also mediate microbial communities’ communication through quorum sensing (QS), by secreting auto-stimulants to coordinate gene expression. QS plays an important role in regulating various physiological processes, including bacterial biofilm formation while providing increased virulence, subsequently leading to antimicrobial resistance. Multi-drug resistant (MDR) bacteria have emerged as a threat to global health, and various strategies targeting QS and biofilm formation have been explored by researchers worldwide. Since the bacterial secretion systems play such a crucial role in host–bacterial interactions, this review intends to outline current understanding of bacterial membrane systems, which may provide new insights for designing approaches aimed at antimicrobials discovery. Various mechanisms pertaining interaction of the bacterial membrane with host cells and antimicrobial agents will be highlighted, as well as the evolution of bacterial membranes in evasion of antimicrobial agents. Finally, the use of antimicrobial peptides (AMPs) as a cellular device for bacterial secretion systems will be discussed as emerging potential candidates for the treatment of multidrug resistance infections.

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Farahani, Ali Safaie, and Mohsen Taghavi. "Changes of antioxidant enzymes of mung bean [Vigna radiata (L.) R. Wilczek] in response to host and non-host bacterial pathogens." Journal of Plant Protection Research 56, no. 1 (January 1, 2016): 95–99. http://dx.doi.org/10.1515/jppr-2016-0016.

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Abstract The natural resistance against the majority of potential pathogens that exist in most plant species is known as non-host resistance. Several reports suggest the role of antioxidant enzymes in non-host resistance. We assayed the expression or activity of four scavenging enzymes during non-host pathogen-plant interaction (Xanthomonas hortorum pv. pelargonii/mung bean) and host pathogen-plant interaction (Xanthomonas axonopodis pv. phaseoli/mung bean). The expression of superoxide dismutase (SOD) and ascorbate peroxidase (APX) and the enzyme activity of catalase (CAT) and peroxidase (POX) were investigated. The activities of CAT and POX were higher during non-host pathogen invasion vs. host pathogen attack. The expression of SOD and APX were also different between compatible and incompatible interactions. The expression of SOD and APX were higher in the incompatible compared to the compatible interaction. Additionally, induction of the antioxidant enzymes in response to non-host pathogen was earlier than induction in response to host pathogen. Such information is important for plant breeders, and useful when looking for alternative control strategies as well.

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Kumar, P. S., M. F. Monteiro, S. M. Dabdoub, G. L. Miranda, M. Z. Casati, F. V. Ribeiro, F. R. Cirano, S. P. Pimentel, and R. C. V. Casarin. "Subgingival Host-Microbial Interactions in Hyperglycemic Individuals." Journal of Dental Research 99, no. 6 (March 16, 2020): 650–57. http://dx.doi.org/10.1177/0022034520906842.

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Type 2 diabetes mellitus (T2DM) is an established risk factor for periodontitis, yet its contribution to creating host-bacterial disequilibrium in the subgingival crevice is poorly understood. The present investigation aimed to quantify the impact of hyperglycemia on host-bacterial interactions in established periodontitis and to map shifts in these dynamics following mechanical nonsurgical therapy. Seventeen T2DM and 17 non-T2DM subjects with generalized severe chronic periodontitis were recruited along with 20 periodontally healthy individuals. Subjects with periodontitis were treated with scaling and root planing (SRP). Samples of subgingival biofilm and gingival crevicular fluid were collected at baseline and at 1-, 3-, and 6 mo postoperatively. Correlations were generated between 13.7 million 16S ribosomal DNA sequences and 8 immune mediators. Intermicrobial and host-microbial interactions were modeled using differential network analysis. Periodontal health was characterized by a sparse interbacterial and highly connected cytokine-bacterial network, while both normoglycemics and T2DM subjects with periodontitis demonstrated robust congeneric and intergeneric hubs but significantly fewer cytokine-bacterial connections. Following SRP, the cytokine-bacterial edges demonstrated a 2-fold increase 1 mo postoperatively and a 10-fold increase at 6 mo in normoglycemics. In hyperglycemics, there was a doubling at 1 mo but no further changes thereafter. These shifts accompanied an increasingly sparse interbacterial network. In normoglycemics, the nodes anchored by interleukin (IL)–4, IL-6, and IL-10 demonstrated greatest rewiring, while in hyperglycemics, IL-1β, IL-6, INF-γ, and IL-17 exhibited progressive rewiring. Thus, the present investigation points to a breakdown in host-bacterial mutualism in periodontitis, with interbacterial interactions rather than host-bacterial interactions primarily determining community assembly. Hyperglycemia further exacerbates this uncoupled mutualism. Our data also demonstrate that while nonsurgical therapy might not consistently alter microbial abundances or lower proinflammatory molecules, it “reboots” the interaction between the immunoinflammatory system and the newly colonizing microbiome, restoring a role for the immune system in determining bacterial colonization. However, this outcome is lower and delayed in hyperglycemics.

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Loessner, Holger, Insea Schlattmeier, Marie Anders-Maurer, Isabelle Bekeredjian-Ding, Christine Rohde, Johannes Wittmann, Cornelia Pokalyuk, Oleg Krut, and Christel Kamp. "Kinetic Fingerprinting Links Bacteria-Phage Interactions with Emergent Dynamics: Rapid Depletion of Klebsiella pneumoniae Indicates Phage Synergy." Antibiotics 9, no. 7 (July 14, 2020): 408. http://dx.doi.org/10.3390/antibiotics9070408.

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The specific temporal evolution of bacterial and phage population sizes, in particular bacterial depletion and the emergence of a resistant bacterial population, can be seen as a kinetic fingerprint that depends on the manifold interactions of the specific phage–host pair during the course of infection. We have elaborated such a kinetic fingerprint for a human urinary tract Klebsiella pneumoniae isolate and its phage vB_KpnP_Lessing by a modeling approach based on data from in vitro co-culture. We found a faster depletion of the initially sensitive bacterial population than expected from simple mass action kinetics. A possible explanation for the rapid decline of the bacterial population is a synergistic interaction of phages which can be a favorable feature for phage therapies. In addition to this interaction characteristic, analysis of the kinetic fingerprint of this bacteria and phage combination revealed several relevant aspects of their population dynamics: A reduction of the bacterial concentration can be achieved only at high multiplicity of infection whereas bacterial extinction is hardly accomplished. Furthermore the binding affinity of the phage to bacteria is identified as one of the most crucial parameters for the reduction of the bacterial population size. Thus, kinetic fingerprinting can be used to infer phage–host interactions and to explore emergent dynamics which facilitates a rational design of phage therapies.

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Haley, Kathryn P., and Jennifer A. Gaddy. "Helicobacter pylori: Genomic Insight into the Host-Pathogen Interaction." International Journal of Genomics 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/386905.

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The advent of genomic analyses has revolutionized the study of human health. Infectious disease research in particular has experienced an explosion of bacterial genomic, transcriptomic, and proteomic data complementing the phenotypic methods employed in traditional bacteriology. Together, these techniques have revealed novel virulence determinants in numerous pathogens and have provided information for potential chemotherapeutics. The bacterial pathogen,Helicobacter pylori, has been recognized as a class 1 carcinogen and contributes to chronic inflammation within the gastric niche. Genomic analyses have uncovered remarkable coevolution between the human host andH. pylori. Perturbation of this coevolution results in dysregulation of the host-pathogen interaction, leading to oncogenic effects. This review discusses the relationship ofH. pyloriwith the human host and environment and the contribution of each of these factors to disease progression, with an emphasis on features that have been illuminated by genomic tools.

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Meyer, Margaux De, Joren De Ryck, Sofie Goormachtig, and Petra Van Damme. "Keeping in Touch with Type-III Secretion System Effectors: Mass Spectrometry-Based Proteomics to Study Effector–Host Protein–Protein Interactions." International Journal of Molecular Sciences 21, no. 18 (September 19, 2020): 6891. http://dx.doi.org/10.3390/ijms21186891.

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Manipulation of host cellular processes by translocated bacterial effectors is key to the success of bacterial pathogens and some symbionts. Therefore, a comprehensive understanding of effectors is of critical importance to understand infection biology. It has become increasingly clear that the identification of host protein targets contributes invaluable knowledge to the characterization of effector function during pathogenesis. Recent advances in mapping protein–protein interaction networks by means of mass spectrometry-based interactomics have enabled the identification of host targets at large-scale. In this review, we highlight mass spectrometry-driven proteomics strategies and recent advances to elucidate type-III secretion system effector–host protein–protein interactions. Furthermore, we highlight approaches for defining spatial and temporal effector–host interactions, and discuss possible avenues for studying natively delivered effectors in the context of infection. Overall, the knowledge gained when unravelling effector complexation with host factors will provide novel opportunities to control infectious disease outcomes.

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Riahi Rad, Zohreh, Zahra Riahi Rad, Hossein Goudarzi, Mehdi Goudarzi, Mohammad Mahmoudi, Javad Yasbolaghi Sharahi, and Ali Hashemi. "MicroRNAs in the interaction between host–bacterial pathogens: A new perspective." Journal of Cellular Physiology 236, no. 9 (February 18, 2021): 6249–70. http://dx.doi.org/10.1002/jcp.30333.

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Fels, Ursula, Kris Gevaert, and Petra Van Damme. "Proteogenomics in Aid of Host–Pathogen Interaction Studies: A Bacterial Perspective." Proteomes 5, no. 4 (October 11, 2017): 26. http://dx.doi.org/10.3390/proteomes5040026.

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Stewart, Graham R., and Douglas B. Young. "Heat-shock proteins and the host–pathogen interaction during bacterial infection." Current Opinion in Immunology 16, no. 4 (August 2004): 506–10. http://dx.doi.org/10.1016/j.coi.2004.05.007.

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Shibl, Atef M. "Clinical Pharmacology of Antibiotics: Do Antibiotics Interfere with Host/Bacterial Interaction?" Infection Control 6, no. 8 (August 1985): 326–28. http://dx.doi.org/10.1017/s0195941700063207.

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Antibiotics exert a number of effects on bacteria other than simply killing them or inhibiting their growth. Increasing evidence that exposure of bacteria to antibiotics induces profound alterations in the interaction between bacteria and host defense has been noted. The effect of antibiotics on polymorphonuclear leukocytes and the immune specific response of mononuclear cells is reviewed. An understanding of such effects would allow a more rational application of antibiotics, as well as provide direction in the development of new antibiotics that have both specific antibacterial action and positive effects on host defense mechanisms.

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Taslem Mourosi, Jarin, Ayobami Awe, Wenzheng Guo, Himanshu Batra, Harrish Ganesh, Xiaorong Wu, and Jingen Zhu. "Understanding Bacteriophage Tail Fiber Interaction with Host Surface Receptor: The Key “Blueprint” for Reprogramming Phage Host Range." International Journal of Molecular Sciences 23, no. 20 (October 12, 2022): 12146. http://dx.doi.org/10.3390/ijms232012146.

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Bacteriophages (phages), as natural antibacterial agents, are being rediscovered because of the growing threat of multi- and pan-drug-resistant bacterial pathogens globally. However, with an estimated 1031 phages on the planet, finding the right phage to recognize a specific bacterial host is like looking for a needle in a trillion haystacks. The host range of a phage is primarily determined by phage tail fibers (or spikes), which initially mediate reversible and specific recognition and adsorption by susceptible bacteria. Recent significant advances at single-molecule and atomic levels have begun to unravel the structural organization of tail fibers and underlying mechanisms of phage–host interactions. Here, we discuss the molecular mechanisms and models of the tail fibers of the well-characterized T4 phage’s interaction with host surface receptors. Structure–function knowledge of tail fibers will pave the way for reprogramming phage host range and will bring future benefits through more-effective phage therapy in medicine. Furthermore, the design strategies of tail fiber engineering are briefly summarized, including machine-learning-assisted engineering inspired by the increasingly enormous amount of phage genetic information.

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Hajdamowicz, Natalia H., Rebecca C. Hull, Simon J. Foster, and Alison M. Condliffe. "The Impact of Hypoxia on the Host-Pathogen Interaction between Neutrophils and Staphylococcus aureus." International Journal of Molecular Sciences 20, no. 22 (November 7, 2019): 5561. http://dx.doi.org/10.3390/ijms20225561.

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Neutrophils are key to host defence, and impaired neutrophil function predisposes to infection with an array of pathogens, with Staphylococcus aureus a common and sometimes life-threatening problem in this setting. Both infiltrating immune cells and replicating bacteria consume oxygen, contributing to the profound tissue hypoxia that characterises sites of infection. Hypoxia in turn has a dramatic effect on both neutrophil bactericidal function and the properties of S. aureus, including the production of virulence factors. Hypoxia thereby shapes the host–pathogen interaction and the progression of infection, for example promoting intracellular bacterial persistence, enabling local tissue destruction with the formation of an encaging abscess capsule, and facilitating the establishment and propagation of bacterial biofilms which block the access of host immune cells. Elucidating the molecular mechanisms underlying host–pathogen interactions in the setting of hypoxia will enable better understanding of persistent and recalcitrant infections due to S. aureus and may uncover novel therapeutic targets and strategies.

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Urban, Martin, Alayne Cuzick, James Seager, Valerie Wood, Kim Rutherford, Shilpa Yagwakote Venkatesh, Jashobanta Sahu, et al. "PHI-base in 2022: a multi-species phenotype database for Pathogen–Host Interactions." Nucleic Acids Research 50, no. D1 (November 12, 2021): D837—D847. http://dx.doi.org/10.1093/nar/gkab1037.

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Abstract Since 2005, the Pathogen–Host Interactions Database (PHI-base) has manually curated experimentally verified pathogenicity, virulence and effector genes from fungal, bacterial and protist pathogens, which infect animal, plant, fish, insect and/or fungal hosts. PHI-base (www.phi-base.org) is devoted to the identification and presentation of phenotype information on pathogenicity and effector genes and their host interactions. Specific gene alterations that did not alter the in host interaction phenotype are also presented. PHI-base is invaluable for comparative analyses and for the discovery of candidate targets in medically and agronomically important species for intervention. Version 4.12 (September 2021) contains 4387 references, and provides information on 8411 genes from 279 pathogens, tested on 228 hosts in 18, 190 interactions. This provides a 24% increase in gene content since Version 4.8 (September 2019). Bacterial and fungal pathogens represent the majority of the interaction data, with a 54:46 split of entries, whilst protists, protozoa, nematodes and insects represent 3.6% of entries. Host species consist of approximately 54% plants and 46% others of medical, veterinary and/or environmental importance. PHI-base data is disseminated to UniProtKB, FungiDB and Ensembl Genomes. PHI-base will migrate to a new gene-centric version (version 5.0) in early 2022. This major development is briefly described.

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Bonazzi, Matteo, Lavanya Vasudevan, Adeline Mallet, Martin Sachse, Anna Sartori, Marie-Christine Prevost, Allison Roberts, et al. "Clathrin phosphorylation is required for actin recruitment at sites of bacterial adhesion and internalization." Journal of Cell Biology 195, no. 3 (October 31, 2011): 525–36. http://dx.doi.org/10.1083/jcb.201105152.

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Bacterial pathogens recruit clathrin upon interaction with host surface receptors during infection. Here, using three different infection models, we observed that host–pathogen interactions induce tyrosine phosphorylation of clathrin heavy chain. This modification was critical for recruitment of actin at bacteria–host adhesion sites during bacterial internalization or pedestal formation. At the bacterial interface, clathrin assembled to form coated pits of conventional size. Because such structures cannot internalize large particles such as bacteria, we propose that during infection, clathrin-coated pits serve as platforms to initiate actin rearrangements at bacteria–host adhesion sites. We then showed that the clathrin–actin interdependency is initiated by Dab2 and depends on the presence of clathrin light chain and its actin-binding partner Hip1R, and that the fully assembled machinery can recruit Myosin VI. Together, our study highlights a physiological role for clathrin heavy chain phosphorylation and reinforces the increasingly recognized function of clathrin in actin cytoskeletal organization in mammalian cells.

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Blasche, Sonja, Stefan Wuchty, Seesandra V. Rajagopala, and Peter Uetz. "The Protein Interaction Network of Bacteriophage Lambda with Its Host, Escherichia coli." Journal of Virology 87, no. 23 (September 18, 2013): 12745–55. http://dx.doi.org/10.1128/jvi.02495-13.

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Although most of the 73 open reading frames (ORFs) in bacteriophage λ have been investigated intensively, the function of many genes in host-phage interactions remains poorly understood. Using yeast two-hybrid screens of all lambda ORFs for interactions with its hostEscherichia coli, we determined a raw data set of 631 host-phage interactions resulting in a set of 62 high-confidence interactions after multiple rounds of retesting. These links suggest novel regulatory interactions between theE. colitranscriptional network and lambda proteins. Targeted host proteins and genes required for lambda infection are enriched among highly connected proteins, suggesting that bacteriophages resemble interaction patterns of human viruses. Lambda tail proteins interact with both bacterial fimbrial proteins andE. coliproteins homologous to other phage proteins. Lambda appears to dramatically differ from other phages, such as T7, because of its unusually large number of modified and processed proteins, which reduces the number of host-virus interactions detectable by yeast two-hybrid screens.

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Portet, Anaïs, Eve Toulza, Ana Lokmer, Camille Huot, David Duval, Richard Galinier, and Benjamin Gourbal. "Experimental Infection of the Biomphalaria glabrata Vector Snail by Schistosoma mansoni Parasites Drives Snail Microbiota Dysbiosis." Microorganisms 9, no. 5 (May 18, 2021): 1084. http://dx.doi.org/10.3390/microorganisms9051084.

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Host-parasite interaction can result in a strong alteration of the host-associated microbiota. This dysbiosis can affect the fitness of the host; can modify pathogen interaction and the outcome of diseases. Biomphalaria glabrata is the snail intermediate host of the trematode Schistosoma mansoni, the agent of human schistosomiasis, causing hundreds of thousands of deaths every year. Here, we present the first study of the snail bacterial microbiota in response to Schistosoma infection. We examined the interplay between B. glabrata, S. mansoni and host microbiota. Snails were infected and the microbiota composition was analysed by 16S rDNA amplicon sequencing approach. We demonstrated that the microbial composition of water did not affect the microbiota composition. Then, we characterised the Biomphalaria bacterial microbiota at the individual scale in both naive and infected snails. Sympatric and allopatric strains of parasites were used for infections and re-infections to analyse the modification or dysbiosis of snail microbiota in different host-parasite co-evolutionary contexts. Concomitantly, using RNAseq, we investigated the link between bacterial microbiota dysbiosis and snail anti-microbial peptide immune response. This work paves the way for a better understanding of snail/schistosome interaction and should have critical consequences in terms of snail control strategies for fighting schistosomiasis disease in the field.

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Shlykova, D. S., V. M. Pisarev, A. M. Gaponov, and A. V. Tutelyan. "Interaction of bacterial extracellular microvesicles with eukaryotic cells." Medical Immunology (Russia) 22, no. 6 (January 10, 2021): 1065–84. http://dx.doi.org/10.15789/1563-0625-iob-2079.

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Bacterial extracellular microvesicles (BMV) are formed by nonpathogenic, pathogenic and opportunistic bacteria. BMV are spherical bilayer-membrane organelles containing different cargoes: lipopolysaccharides, pathogen associated molecular patterns (PUMP), DNA, RNA, signal molecules, proteins, antibiotic resistance factors, virulence factors, toxins providing various immune response options and conducive to the survival and pathogen dissemination in the human body. BMVs secretion play an important role in the ability of microorganisms to cause various diseases. BMV are involved in biofilms formation, help bacteria to obtain nutrition in a nutrient-poor conditions, to evade the host's immune response, provide communication and surviving in a stressful environment during infection inside the host. The heterogeneity of the biogenesis mechanisms causes differences in the BMV and their characteristics including virulence rate. BMVs host cells entering is mediated by several mechanisms and helps to activate innate and adaptive immune reactions. This review focuses on interaction study of BMV with various eukaryotic cells types including neutrophils, dendritic cells, macrophages, epithelial, endothelial cells. This interaction depends on bacteria species, type of target cell and number of vesicles and can lead to different responses: non-immunogenic, pro-inflammatory, cytotoxic. Subcellular and molecular mechanisms related to the involvement of extracellular microvesicles in host's immune response modulation are presented. Stimulation of immune response is provided by increased secretion of proinflammatory cytokines and chemokines. In some cases BMV use mechanisms to evade immune surveillance: anti-inflammatory cytokines secretion, alterations of phagocytosis and chemotaxis of macrophages, increasing the proteolytic cleavage of CD14 on the macrophage surface, alterations of antigen-presenting function of dendritic cells, T-cell proliferation suppression, reducing the pro-inflammatory cytokines secretion, evasion of host-immune cells direct interactions, destruction of neutrophilic traps. These features allow bacterial cells to survive in the human body, increase their invasive potential, and reduce the excessive inflammatory reactions leading to death of the pathogen itself and life-threatening damage of tissues and organs of the host. Further studies of these mechanisms will improve existing therapeutic approaches to the infectious diseases treatment.

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Baldassarre, Laura, Adam M. Reitzel, and Sebastian Fraune. "Genotype–environment interactions determine microbiota plasticity in the sea anemone Nematostella vectensis." PLOS Biology 21, no. 1 (January 23, 2023): e3001726. http://dx.doi.org/10.1371/journal.pbio.3001726.

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Most multicellular organisms harbor microbial colonizers that provide various benefits to their hosts. Although these microbial communities may be host species- or even genotype-specific, the associated bacterial communities can respond plastically to environmental changes. In this study, we estimated the relative contribution of environment and host genotype to bacterial community composition in Nematostella vectensis, an estuarine cnidarian. We sampled N. vectensis polyps from 5 different populations along a north–south gradient on the Atlantic coast of the United States and Canada. In addition, we sampled 3 populations at 3 different times of the year. While half of the polyps were immediately analyzed for their bacterial composition by 16S rRNA gene sequencing, the remaining polyps were cultured under laboratory conditions for 1 month. Bacterial community comparison analyses revealed that laboratory maintenance reduced bacterial diversity by 4-fold, but maintained a population-specific bacterial colonization. Interestingly, the differences between bacterial communities correlated strongly with seasonal variations, especially with ambient water temperature. To decipher the contribution of both ambient temperature and host genotype to bacterial colonization, we generated 12 clonal lines from 6 different populations in order to maintain each genotype at 3 different temperatures for 3 months. The bacterial community composition of the same N. vectensis clone differed greatly between the 3 different temperatures, highlighting the contribution of ambient temperature to bacterial community composition. To a lesser extent, bacterial community composition varied between different genotypes under identical conditions, indicating the influence of host genotype. In addition, we identified a significant genotype x environment interaction determining microbiota plasticity in N. vectensis. From our results we can conclude that N. vectensis-associated bacterial communities respond plastically to changes in ambient temperature, with the association of different bacterial taxa depending in part on the host genotype. Future research will reveal how this genotype-specific microbiota plasticity affects the ability to cope with changing environmental conditions.

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de Vos, Marjon G. J., Marcin Zagorski, Alan McNally, and Tobias Bollenbach. "Interaction networks, ecological stability, and collective antibiotic tolerance in polymicrobial infections." Proceedings of the National Academy of Sciences 114, no. 40 (September 18, 2017): 10666–71. http://dx.doi.org/10.1073/pnas.1713372114.

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Polymicrobial infections constitute small ecosystems that accommodate several bacterial species. Commonly, these bacteria are investigated in isolation. However, it is unknown to what extent the isolates interact and whether their interactions alter bacterial growth and ecosystem resilience in the presence and absence of antibiotics. We quantified the complete ecological interaction network for 72 bacterial isolates collected from 23 individuals diagnosed with polymicrobial urinary tract infections and found that most interactions cluster based on evolutionary relatedness. Statistical network analysis revealed that competitive and cooperative reciprocal interactions are enriched in the global network, while cooperative interactions are depleted in the individual host community networks. A population dynamics model parameterized by our measurements suggests that interactions restrict community stability, explaining the observed species diversity of these communities. We further show that the clinical isolates frequently protect each other from clinically relevant antibiotics. Together, these results highlight that ecological interactions are crucial for the growth and survival of bacteria in polymicrobial infection communities and affect their assembly and resilience.

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Nassif, X., and M. So. "Interaction of pathogenic neisseriae with nonphagocytic cells." Clinical Microbiology Reviews 8, no. 3 (July 1995): 376–88. http://dx.doi.org/10.1128/cmr.8.3.376.

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The ability to interact with nonphagocytic cells is a crucial virulence attribute of the meningococcus and the genococcus. Like most bacterial pathogens, Neisseria meningitidis and Neisseria gonorrhoeae initiate infections by colonizing the mucosal epithelium, which serves as the site of entry. After this step, both bacteria cross the intact mucosal barrier. While N. gonorrhoeae is likely to remain in the subepithelial matrix, where it initiates an intense inflammatory reaction, N. meningitidis enters the bloodstream, and eventually the cerebrospinal fluid to cause meningitis. Both pathogens have evolved very similar mechanisms for interacting with host cells. Surface structures that influence bacterium-host interactions include pili, the meningococcal class 5 outer membrane proteins or the gonococcal opacity proteins, lipooligosaccharide, and the meningococcal capsule. This review examines what is known about the roles these structures play in bacterial adhesion and invasion, with special emphasis, on pilus-mediated adhesion. Finally, the importance of these structures in neisserial pathogenesis is discussed.

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Andrian, E., D. Grenier, and M. Rouabhia. "Porphyromonas gingivalis-Epithelial Cell Interactions in Periodontitis." Journal of Dental Research 85, no. 5 (May 2006): 392–403. http://dx.doi.org/10.1177/154405910608500502.

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Emerging data on the consequences of the interactions between invasive oral bacteria and host cells have provided new insights into the pathogenesis of periodontal disease. Indeed, modulation of the mucosal epithelial barrier by pathogenic bacteria appears to be a critical step in the initiation and progression of periodontal disease. Periodontopathogens such as Porphyromonas gingivalis have developed different strategies to perturb the structural and functional integrity of the gingival epithelium. P. gingivalis adheres to, invades, and replicates within human epithelial cells. Adhesion of P. gingivalis to host cells is multimodal and involves the interaction of bacterial cell-surface adhesins with receptors expressed on the surfaces of epithelial cells. Internalization of P. gingivalis within host cells is rapid and requires both bacterial contact-dependent components and host-induced signaling pathways. P. gingivalis also subverts host responses to bacterial challenges by inactivating immune cells and molecules and by activating host processes leading to tissue destruction. The adaptive ability of these pathogens that allows them to survive within host cells and degrade periodontal tissue constituents may contribute to the initiation and progression of periodontitis. In this paper, we review current knowledge on the molecular cross-talk between P. gingivalis and gingival epithelial cells in the development of periodontitis.

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Xie, Kaibo, Christina Bunse, Katrin Marcus, and Lars I. Leichert. "Quantifying changes in the bacterial thiol redox proteome during host-pathogen interaction." Redox Biology 21 (February 2019): 101087. http://dx.doi.org/10.1016/j.redox.2018.101087.

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Schertzer, Jeffrey W., and Marvin Whiteley. "Bacterial Outer Membrane Vesicles in Trafficking, Communication and the Host-Pathogen Interaction." Journal of Molecular Microbiology and Biotechnology 23, no. 1-2 (2013): 118–30. http://dx.doi.org/10.1159/000346770.

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da Silva, Mauricio C. A., Jean-Marie Zahm, Delphine Gras, Odile Bajolet, Michel Abely, Jocelyne Hinnrasky, Magali Milliot, et al. "Dynamic interaction between airway epithelial cells andStaphylococcus aureus." American Journal of Physiology-Lung Cellular and Molecular Physiology 287, no. 3 (September 2004): L543—L551. http://dx.doi.org/10.1152/ajplung.00256.2003.

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Staphylococcus aureus is a major cause of pulmonary infection, particularly in cystic fibrosis (CF) patients. However, few aspects of the interplay between S. aureus and host airway epithelial cells have been investigated thus far. We investigated by videomicroscopy the time- and bacterial concentration-dependent (104, 106, and 108CFU/ml) effect of S. aureus on adherence, internalization, and the associated damage of the airway epithelial cells. The balance between the secretion by S. aureus of the α-toxin virulence factor and by the airway cells of the antibacterial secretory leukoproteinase inhibitor (SLPI) was also analyzed. After 1 h of interaction, whatever the initial bacterial concentration, a low percentage of S. aureus (<8%) adhered to airway cells, and no airway epithelial cell damage was observed. In contrast, after 24 h of incubation, more bacteria adhered to airway epithelial cells, internalized bacteria were observed, and a bacterial concentration-dependent effect on airway cell damage was observed. At 24 h, most airway cells incubated with bacteria at 108CFU/ml exhibited a necrotic phenotype. The necrosis was preceded by a transient apoptotic process. In parallel, we observed a time- and bacterial concentration-dependent decrease in SLPI and increase in α-toxin expression. These results suggest that airway cells can defend against S. aureus in the early stages of infection. However, in later phases, there is a marked imbalance between the bactericidal capacity of host cells and bacterial virulence. These findings reinforce the potential importance of S. aureus in the pathogenicity of airway infections, including those observed early in CF patients.

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Galle, Jan N., and Johannes H. Hegemann. "Exofacial phospholipids at the plasma membrane: ill-defined targets for early infection processes." Biological Chemistry 400, no. 10 (October 25, 2019): 1323–34. http://dx.doi.org/10.1515/hsz-2019-0187.

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Abstract The eukaryotic plasma membrane (PM) consists largely of phospholipids and proteins, and separates the intracellular compartments from the extracellular space. It also serves as a signaling platform for cell-to-cell communication and an interaction platform for the molecular crosstalk between pathogens and their target cells. Much research has been done to elucidate the interactions between pathogens and host membrane proteins. However, little is known about the interactions between pathogens and membrane phospholipids, although reports have described a contribution of phospholipids to cell recognition and/or invasion during early infection by diverse pathogens. Thus, during adhesion to the host cell, the obligate intracellular bacterial pathogens Chlamydia spp., the facultative intracellular pathogen Helicobacter pylori and the facultative aerobic pathogen Vibrio parahaemolyticus, interact with exofacial phospholipids. This review focuses on several prominent instances of pathogen interaction with host-cell phospholipids.

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Ellefson, D., D. Parker, and F. Heffron. "Identification of MHC-I Accessible Proteins from Salmonella Typhimurium." Microscopy and Microanalysis 7, S2 (August 2001): 616–17. http://dx.doi.org/10.1017/s1431927600029159.

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Intracellular bacterial pathogens such as Salmonella typhimurium secrete proteins into the host cell after infection. These proteins alter the normal structural and metabolic machinery of the host cell and benefit the bacterium by facilitating replication and avoidance of host immune surveillance. Since the host cytoplasmic localization of these proteins infers access to the class-I MHC antigen processing and presentation machinery of the host cell, we collectively refer to these proteins as Class- I Accessible Proteins (CAPs).The design of vaccines for new and emerging bacterial pathogens is often constrained by the selection of appropriate and specific antigens. While vaccine design is being greatly aided by whole genome analysis of bacterial pathogens, it has been of limited use in the assignment of function and host subcellular localization of a large percentage of bacterial proteins. in addition, analysis of the bacteria/host interaction is further complicated by the complex lifestyle of the pathogen.

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Radhakrishnan, Girish K., and Gary A. Splitter. "Modulation of host microtubule dynamics by pathogenic bacteria." BioMolecular Concepts 3, no. 6 (December 1, 2012): 571–80. http://dx.doi.org/10.1515/bmc-2012-0030.

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AbstractThe eukaryotic cytoskeleton is a vulnerable target of many microbial pathogens during the course of infection. Rearrangements of host cytoskeleton benefit microbes in various stages of their infection cycle such as invasion, motility, and persistence. Bacterial pathogens deliver a number of effector proteins into host cells for modulating the dynamics of actin and microtubule cytoskeleton. Alteration of the actin cytoskeleton is generally achieved by bacterial effectors that target the small GTPases of the host. Modulation of microtubule dynamics involves direct interaction of effector proteins with the subunits of microtubules or recruiting cellular proteins that affect microtubule dynamics. This review will discuss effector proteins from animal and human bacterial pathogens that either destabilize or stabilize host microtubules to advance the infectious process. A compilation of these research findings will provide an overview of known and unknown strategies used by various bacterial effectors to modulate the host microtubule dynamics. The present review will undoubtedly help direct future research to determine the mechanisms of action of many bacterial effector proteins and contribute to understanding the survival strategies of diverse adherent and invasive bacterial pathogens.

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Wang, Qi, Nadia Shakoor, Adam Boyher, Kira M. Veley, Jeffrey C. Berry, Todd C. Mockler, and Rebecca S. Bart. "Escalation in the host-pathogen arms race: A host resistance response corresponds to a heightened bacterial virulence response." PLOS Pathogens 17, no. 1 (January 11, 2021): e1009175. http://dx.doi.org/10.1371/journal.ppat.1009175.

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The zig-zag model of host-pathogen interaction describes the relative strength of defense response across a spectrum of pathogen-induced plant phenotypes. A stronger defense response results in increased resistance. Here, we investigate the strength of pathogen virulence during disease and place these findings in the context of the zig-zag model. Xanthomonas vasicola pv. holcicola (Xvh) causes sorghum bacterial leaf streak. Despite being widespread, this disease has not been described in detail at the molecular level. We divided diverse sorghum genotypes into three groups based on disease symptoms: water-soaked lesions, red lesions, and resistance. Bacterial growth assays confirmed that these three phenotypes represent a range of resistance and susceptibility. To simultaneously reveal defense and virulence responses across the spectrum of disease phenotypes, we performed dual RNA-seq on Xvh-infected sorghum. Consistent with the zig-zag model, the expression of plant defense-related genes was strongest in the resistance interaction. Surprisingly, bacterial virulence genes related to the type III secretion system (T3SS) and type III effectors (T3Es) were also most highly expressed in the resistance interaction. This expression pattern was observed at multiple time points within the sorghum-Xvh pathosystem. Further, a similar expression pattern was observed in Arabidopsis infected with Pseudomonas syringae for effector-triggered immunity via AvrRps4 but not AvrRpt2. Specific metabolites were able to repress the Xvh virulence response in vitro and in planta suggesting a possible signaling mechanism. Taken together, these findings reveal multiple permutations of the continually evolving host-pathogen arms race from the perspective of host defense and pathogen virulence responses.

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Journal articles on the topic 'Host-bacterial interaction'

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