• Title/Summary/Keyword: Host-pathogen interaction

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Use of Germ-Free Animal Models in Microbiota-Related Research

  • Al-Asmakh, Maha;Zadjali, Fahad
    • Journal of Microbiology and Biotechnology
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    • v.25 no.10
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    • pp.1583-1588
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    • 2015
  • The large intestine is a home for trillions of microbiota, which confer many benefits on the host, including production of vitamins, absorption of nutrients, pathogen displacement, and development of the immune system. For several decades, germ-free animals have been used to study the interaction between the host and its microbiota. This minireview describes the technical aspects for establishing and maintaining germ-free animals and highlights the advantages and disadvantages for germ-free animals as experimental models.

Innate immune response to oral bacteria and the immune evasive characteristics of periodontal pathogens

  • Ji, Suk;Choi, Youngnim
    • Journal of Periodontal and Implant Science
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    • v.43 no.1
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    • pp.3-11
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    • 2013
  • Periodontitis is a chronic inflammation of periodontal tissue caused by subgingival plaque-associated bacteria. Periodontitis has long been understood to be the result of an excessive host response to plaque bacteria. In addition, periodontal pathogens have been regarded as the causative agents that induce a hyperinflammatory response from the host. In this brief review, host-microbe interaction of nonperiodontopathic versus periodontopathic bacteria with innate immune components encountered in the gingival sulcus will be described. In particular, we will describe the susceptibility of these microbes to antimicrobial peptides (AMPs) and phagocytosis by neutrophils, the induction of tissue-destructive mediators from neutrophils, the induction of AMPs and interleukin (IL)-8 from gingival epithelial cells, and the pattern recognition receptors that mediate the regulation of AMPs and IL-8 in gingival epithelial cells. This review indicates that true periodontal pathogens are poor activators/suppressors of a host immune response, and they evade host defense mechanisms.

Molecular determinants of the host specificity by Xanthomonas spp.

  • Heu, Sunggi;Choi, Min-Seon;Park, Hyoung-Joon;Lee, Seung-Don;Ra, Dong-Soo
    • Proceedings of the Korean Society of Plant Pathology Conference
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    • 2004.10a
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    • pp.65-67
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    • 2004
  • During initial interactions of bacteria with their host plants, most plants recognize the bacterial infections and repel the pathogen by plant defense mechanism. The most active plant defense mechanism is the hypersensitive response (HR) which is the localized induced cell death in the plant at the site of infection by a pathogen. A primary locus induced in gram-negative phytopathogenic bacteria during this initial interaction is the Hrp locus. The Hrp locus is composed of a cluster of genes that encodes the bacteral Type 111 machinery that is involved in the secretion and translocation of effector proteins to the plant cell. DNA sequence analysis of hrp gene in phytopathogenic bacteria has revealed a Hrp pathogenicity is]and (PAI) with a tripartite mosaic structure. For many gram-negative pathogenic bacteria, colonization of the host's tissue depends on the type III protein secretion system (TTSS) which secrets and translocates effector proteins into the host cell. Effectors can be divided into several groups including broad host range effectors, host specific effectors, disease specific effectors, and effectors inhibit host defenses. The role of effectors carrying LRR domain in plant resistance is very elusive since most known plant resistance gene carry LRR domain. Host specific effectors such as several avr gene products are involved in the determination of the host specificity. Almost all the phytopathogenic Xanthomonas spp. carry avrBs1, avrBs2, and avrBs3 homologs. Some strains of X. oryzae pv. oryzae carry more than 10 copies of avrBs3 homologs. However, the functions of all those avr genes in host specificity are not characterized well.;

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RNA-seq Gene Profiling Reveals Transcriptional Changes in the Late Phase during Compatible Interaction between a Korean Soybean Cultivar (Glycine max cv. Kwangan) and Pseudomonas syringae pv. syringae B728a

  • Myoungsub, Kim;Dohui, Lee;Hyun Suk, Cho;Young-Soo, Chung;Hee Jin, Park;Ho Won, Jung
    • The Plant Pathology Journal
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    • v.38 no.6
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    • pp.603-615
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    • 2022
  • Soybean (Glycine max (L) Merr.) provides plant-derived proteins, soy vegetable oils, and various beneficial metabolites to humans and livestock. The importance of soybean is highly underlined, especially when carbon-negative sustainable agriculture is noticeable. However, many diseases by pests and pathogens threaten sustainable soybean production. Therefore, understanding molecular interaction between diverse cultivated varieties and pathogens is essential to developing disease-resistant soybean plants. Here, we established a pathosystem of the Korean domestic cultivar Kwangan against Pseudomonas syringae pv. syringae B728a. This bacterial strain caused apparent disease symptoms and grew well in trifoliate leaves of soybean plants. To examine the disease susceptibility of the cultivar, we analyzed transcriptional changes in soybean leaves on day 5 after P. syringae pv. syringae B728a infection. About 8,900 and 7,780 differentially expressed genes (DEGs) were identified in this study, and significant proportions of DEGs were engaged in various primary and secondary metabolisms. On the other hand, soybean orthologs to well-known plant immune-related genes, especially in plant hormone signal transduction, mitogen-activated protein kinase signaling, and plant-pathogen interaction, were mainly reduced in transcript levels at 5 days post inoculation. These findings present the feature of the compatible interaction between cultivar Kwangan and P. syringae pv. syringae B728a, as a hemibiotroph, at the late infection phase. Collectively, we propose that P. syringae pv. syringae B728a successfully inhibits plant immune response in susceptible plants and deregulates host metabolic processes for their colonization and proliferation, whereas host plants employ diverse metabolites to protect themselves against infection with the hemibiotrophic pathogen at the late infection phase.

The Within-Host Population Dynamics of Normal Flora in the Presence of an Invading Pathogen and Antibiotic Treatments

  • Kim, Jung-Mo;Lee, Dong-Hwan;Song, Yoon-Seok;Kang, Seong-Woo;Kim, Seung-Wook
    • Journal of Microbiology and Biotechnology
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    • v.17 no.1
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    • pp.146-153
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    • 2007
  • A mathematical competition model between normal flora and an invading pathogen was devised to allow analysis of bacterial infections in a host. The normal flora includes the various microorganisms that live on or within the host and act as a primary human immune system. Despite the important role of the normal flora, no mathematical study has been undertaken on models of the interaction between it and invading pathogens against a background of antibiotic treatment. To quantify key elements of bacterial behavior in a host, pairs of nonlinear differential equations were used to describe three categories of human health conditions, namely, healthy, latent infection, and active infection. In addition, a cutoff value was proposed to represent the minimum population level required for survival. The recovery of normal flora after antibiotic treatment was also included in the simulation because of its relation to human health recovery. The significance of each simulation parameter for the bacterial growth model was investigated. The devised simulation showed that bacterial proliferation rate, carrying capacity, initial population levels, and competition intensity have a significant effect on bacterial behavior. Consequently, a model was established to describe competition between normal flora and an infiltrating pathogen. Unlike other population models, the recovery process described by the devised model can describe the human health recovery mechanism.

Antimicrobials, Gut Microbiota and Immunity in Chickens

  • Lee, Kyung-Woo;Lillehoj, Hyun S.
    • Korean Journal of Poultry Science
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    • v.38 no.2
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    • pp.155-164
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    • 2011
  • The use of antimicrobials will be soon removed due to an increase of occurrence of antibiotic-resistant bacteria or ionophore-resistant Eimeria species in poultry farms and consumers' preference on drug-free chicken meats or eggs. Although dietary antimicrobials contributed to the growth and health of the chickens, we do not fully understand their interrelationship among antimicrobials, gut microbiota, and host immunity in poultry. In this review, we explored the current understanding on the effects of antimicrobials on gut microbiota and immune systems of chickens. Based on the published literatures, it is clear that antibiotics and antibiotic ionophores, when used singly or in combination could influence gut microbiota. However, antimicrobial effect on gut microbiota varied depending on the samples (e.g., gut locations, digesta vs. mucosa) used and among the experiments. It was noted that the digesta vs. the mucosa is the preferred sample with the results of no change, increase, or decrease in gut microbiota community. In future, the mucosa-associated bacteria should be targeted as they are known to closely interact with the host immune system and pathogen control. Although limited, dietary antimicrobials are known to modulate humoral and cell-mediated immunities. Ironically, the evidence is increasing that dietary antimicrobials may play an important role in triggering enteric disease such as gangrenous dermatitis, a devastating disease in poultry industry. Future work should be done to unravel our understanding on the complex interaction of host-pathogen-microbiota-antimicrobials in poultry.

The Role of Immune Response in Periodontal Disease (치주질환의 면역학)

  • Kim, Kack-Kyun
    • IMMUNE NETWORK
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    • v.3 no.4
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    • pp.261-267
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    • 2003
  • The periodontal diseases are infections caused by bacteria in oral biofilm, a gelatinous mat commonly called dental plaque, which is a complex microbial community that forms and adhere to tooth surfaces. Host immune-pathogen interaction in periodontal disease appears to be a complex process, which is regulated not only by the acquired immunity to deal with ever-growing and -invading microorganisms in periodontal pockets, but also by genetic and/or environmental factors. However, our understanding of the pathogenesis in human periodontal diseases is limited by the lack of specific and sensitive tools or models to study the complex microbial challenges and their interactions with the host's immune system. Recent advances in cellular and molecular biology research have demonstrated the importance of the acquired immune system in fighting the virulent periodontal pathogens and in protecting the host from developing further devastating conditions in periodontal infections. The use of genetic knockout and immunodeficient mouse strains has shown that the acquired immune response, in particular, $CD4^+$ T-cells plays a pivotal role in controlling the ongoing infection, the immune/inflammatory responses, and the subsequent host's tissue destruction.

Interaction Proteome Analysis of Xanthomonas Hrp Proteins

  • Jang, Mi;Park, Byoung-Chul;Lee, Do-Hee;Bae, Kwang-Hee;Cho, Sa-Yeon;Park, Hyun-Seok;Lee, Baek-Rak;Park, Sung-Goo
    • Journal of Microbiology and Biotechnology
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    • v.17 no.2
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    • pp.359-363
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    • 2007
  • Because of the importance of the type III protein-secretion system in bacteria-plant interaction, its function in bacterial pathogenesis of plants has been intensively studied. To identity bacterial proteins interacting with Xanthomonas hrp gene products that are involved in pathogenicity, we performed the glutathione-bead binding analysis of Xanthomonas lysates containing GST-tagged Hrp proteins. Analysis of glutathione-bead bound proteins by 1-DE and MALDI-TOF has demonstrated that Avr proteins, RecA, and several components of the type III secretion system interact with HrpB protein. This proteomic approach could provide a powerful tool in finding interaction partners of Hrp proteins whose roles in host-pathogen interaction need further studies.

Functional Genomics of Vibrio vulnificus: from Survival to Toxigenesis

  • Choi Sang Ho
    • Proceedings of the Microbiological Society of Korea Conference
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    • 2004.05a
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    • pp.132-136
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    • 2004
  • Understanding the molecular pathogenesis of the multifaceted host-pathogen interaction is critical in the development of improved treatment and prevention, as well as elucidating how certain bacteria can circumvent host defenses, multiply in the host, and cause such extensive damage. Disease caused by infection with V. vulnificus is remarkable for the invasive nature of the infection, ensuing severe tissue damage, and rapidly fulminating course. The characterization of somatic as well as secreted products of V. vulnificus has yielded a large list of putative virulence attributes, whose known functions are easily imagined to explain the pathology of disease. These putative virulence factors include a carbohydrate capsule, lipopolysaccharide, a cytolysin/hemolysin, elastolytic metalloprotease, iron sequestering systems, lipase, and pili. However, only few among the putative virulence factors has been confirmed to be essential for virulence by the use of molecular Koch's postulates. This presentation describes molecular biological characterization of the virulence factors contributing to survival as well as to toxigenesis of V. vulnificus.

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Molecular Characterization of Survival and Toxigenesis of Vibrio vulnificus

  • Choi Sang Ho
    • Proceedings of the Microbiological Society of Korea Conference
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    • 2002.10a
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    • pp.56-58
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    • 2002
  • Understanding the molecular pathogenesis of the multifaceted host-pathogen interaction is critical in the development of improved treatment and prevention, as well as elucidating how certain bacteria can circumvent host defenses, multiply in the host, and cause such extensive damage. Disease caused by infection with V. vulnificus is remarkable for the invasive nature of the infection, ensuing severe tissue damage, and rapidly fulminating course. The characterization of somatic as well as secreted products of V. vulnificus has yielded a large list of putative virulence attributes, whose known functions are easily imagined to explain the pathology of disease. These putative virulence factors include a carbohydrate capsule, lipopolysaccharide, a cytolysin/hemolysin, elastolytic metalloprotease, iron sequestering systems, lipase, and pili. However, only few among the putative virulence factors has been confirmed to be essential for virulence by the use of molecular Koch's postulates. This presentation describes molecular biological characterization of the virulence factors contributing to survival as well as to toxigenesis of V. vulnificus.

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