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Arbuscular Mycorrhizal Symbiosis Affects Plant Immunity to Viral Infection and Accumulation.
Hao, Z, Xie, W, Chen, B
Viruses. 2019;(6)
Abstract
Arbuscular mycorrhizal (AM) fungi, as root symbionts of most terrestrial plants, improve plant growth and fitness. In addition to the improved plant nutritional status, the physiological changes that trigger metabolic changes in the root via AM fungi can also increase the host ability to overcome biotic and abiotic stresses. Plant viruses are one of the important limiting factors for the commercial cultivation of various crops. The effect of AM fungi on viral infection is variable, and considerable attention is focused on shoot virus infection. This review provides an overview of the potential of AM fungi as bioprotection agents against viral diseases and emphasizes the complex nature of plant-fungus-virus interactions. Several mechanisms, including modulated plant tolerance, manipulation of induced systemic resistance (ISR), and altered vector pressure are involved in such interactions. We propose that using "omics" tools will provide detailed insights into the complex mechanisms underlying mycorrhizal-mediated plant immunity.
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Toward a microbial Neolithic revolution in buildings.
Thaler, DS
Microbiome. 2016;:14
Abstract
The Neolithic revolution--the transition of our species from hunter and gatherer to cultivator--began approximately 14,000 years ago and is essentially complete for macroscopic food. Humans remain largely pre-Neolithic in our relationship with microbes but starting with the gut we continue our hundred-year project of approaching the ability to assess and cultivate benign microbiomes in our bodies. Buildings are analogous to the body and it is time to ask what it means to cultivate benign microbiomes in our built environment. A critical distinction is that we have not found, or invented, niches in buildings where healthful microbial metabolism occurs and/or could be cultivated. Key events affecting the health and healthfulness of buildings such as a hurricane leading to a flood or a burst pipe occur only rarely and unpredictably. The cause may be transient but the effects can be long lasting and, e.g., for moisture damage, cumulative. Non-invasive "building tomography" could find moisture and "sentinel microbes" could record the integral of transient growth. "Seed" microbes are metabolically inert cells able to grow when conditions allow. All microbes and their residue present actinic molecules including immunological epitopes (molecular shapes). The fascinating hygiene and microbial biodiversity hypotheses propose that a healthy immune system requires exposure to a set of microbial epitopes that is rich in diversity. A particular conjecture is that measures of the richness of diversity derived from microbiome next-generation sequencing (NGS) can be mechanistically coupled to--rather than merely correlated with some measures of--human health. These hypotheses and conjectures inspire workers and funders but an alternative is also consequent to the first Neolithic revolution: That the genetic uniformity of contemporary foods may also decrease human exposure to molecular biodiversity in a heath-relevant manner. Understanding the consequences--including the unintended consequences of the first Neolithic revolution--will inform and help us benignly implement the second--the microbial--Neolithic revolution.
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Systems-wide analyses of mucosal immune responses to Helicobacter pylori at the interface between pathogenicity and symbiosis.
Kronsteiner, B, Bassaganya-Riera, J, Philipson, C, Viladomiu, M, Carbo, A, Abedi, V, Hontecillas, R
Gut microbes. 2016;(1):3-21
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Abstract
Helicobacter pylori is the dominant member of the gastric microbiota in over half of the human population of which 5-15% develop gastritis or gastric malignancies. Immune responses to H. pylori are characterized by mixed T helper cell, cytotoxic T cell and NK cell responses. The presence of Tregs is essential for the control of gastritis and together with regulatory CX3CR1+ mononuclear phagocytes and immune-evasion strategies they enable life-long persistence of H. pylori. This H. pylori-induced regulatory environment might contribute to its cross-protective effect in inflammatory bowel disease and obesity. Here we review host-microbe interactions, the development of pro- and anti-inflammatory immune responses and how the latter contribute to H. pylori's role as beneficial member of the gut microbiota. Furthermore, we present the integration of existing and new data into a computational/mathematical model and its use for the investigation of immunological mechanisms underlying initiation, progression and outcomes of H. pylori infection.
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4.
Commensal Microbiome Promotes Resistance to Local and Systemic Infections.
Zhang, N, He, QS
Chinese medical journal. 2015;(16):2250-5
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Abstract
OBJECTIVE In this review, to illustrate the resistance mechanism for pathogen insult, we discussed the role of the intestinal microbiome in promoting resistance to local gastrointestinal tract infections and to respiratory tract infections. DATA SOURCES The review was based on data obtained from the published research articles. STUDY SELECTION A total of 49 original articles were selected in accordance with our main objective to illustrate the resistance mechanism(s) by which commensal microbiota can contribute to host defense against local and systemic infections. RESULTS Diverse microorganisms colonize human environmentally exposed surfaces such as skin, respiratory tract, and gastrointestinal tract. Co-evolution has resulted in these microbes with extensive and diverse impacts on multiple aspects of host biological functions. During the last decade, high-throughput sequencing technology developed has been applied to study commensal microbiota and their impact on host biological functions. By using pathogen recognition receptors pathway and nucleotide binding oligomerization domain-like receptors pathway, the commensal microbiome promotes resistance to local and systemic infections, respectively. To protect against the local infections, the microbiome functions contain the following: the competing for sites of colonization, direct production of inhibition molecules or depletion of nutrients needed for pathogens, and priming immune defenses against pathogen insult. At the same time, with the purpose to maintain homeostasis, the commensal bacteria can program systemic signals toward not only local tissue but also distal tissue to modify their function for infections accordingly. CONCLUSIONS Commensal bacteria play an essential role in protecting against infections, shaping and regulating immune responses, and maintaining host immune homeostasis.
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Beyond the red complex and into more complexity: the polymicrobial synergy and dysbiosis (PSD) model of periodontal disease etiology.
Hajishengallis, G, Lamont, RJ
Molecular oral microbiology. 2012;(6):409-19
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Abstract
Recent advancements in the periodontal research field are consistent with a new model of pathogenesis according to which periodontitis is initiated by a synergistic and dysbiotic microbial community rather than by select 'periopathogens', such as the 'red complex'. In this polymicrobial synergy, different members or specific gene combinations within the community fulfill distinct roles that converge to shape and stabilize a disease-provoking microbiota. One of the core requirements for a potentially pathogenic community to arise involves the capacity of certain species, termed 'keystone pathogens', to modulate the host response in ways that impair immune surveillance and tip the balance from homeostasis to dysbiosis. Keystone pathogens also elevate the virulence of the entire microbial community through interactive communication with accessory pathogens. Other important core functions for pathogenicity require the expression of diverse molecules (e.g. appropriate adhesins, cognate receptors, proteolytic enzymes and proinflammatory surface structures/ligands), which in combination act as community virulence factors to nutritionally sustain a heterotypic, compatible and proinflammatory microbial community that elicits a non-resolving and tissue-destructive host response. On the basis of the fundamental concepts underlying this model of periodontal pathogenesis, that is, polymicrobial synergy and dysbiosis, we term it the PSD model.
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The role of chitin detection in plant--pathogen interactions.
Kombrink, A, Sánchez-Vallet, A, Thomma, BP
Microbes and infection. 2011;(14-15):1168-76
Abstract
Despite the deployment of antifungal defence strategies, fungal diseases occur in all types of multicellular organisms. In plants, the role of fungal chitin as pathogen-associated molecular pattern that activates host defence is well established. Interestingly, plants employ homologs of the chitin immune receptors to initiate microbial symbiosis. Accumulating evidence shows that fungal pathogens developed secreted effectors to disarm chitin-triggered host immunity.