scholarly journals Cnidarian Interaction with Microbial Communities: From Aid to Animal’s Health to Rejection Responses

Marine Drugs ◽  
2018 ◽  
Vol 16 (9) ◽  
pp. 296 ◽  
Author(s):  
Loredana Stabili ◽  
Maria Parisi ◽  
Daniela Parrinello ◽  
Matteo Cammarata
Keyword(s):  
Microbial Communities ◽  
Environmental Changes ◽  
Defense Mechanism ◽  
Immune Defense ◽  
Innate Immune ◽  
Animal Disease ◽  
Normal Microbiota ◽  
Essential Components ◽  
Pathogenic Agents ◽  
And Behavior

The phylum Cnidaria is an ancient branch in the tree of metazoans. Several species exert a remarkable longevity, suggesting the existence of a developed and consistent defense mechanism of the innate immunity capable to overcome the potential repeated exposure to microbial pathogenic agents. Increasing evidence indicates that the innate immune system in Cnidarians is not only involved in the disruption of harmful microorganisms, but also is crucial in structuring tissue-associated microbial communities that are essential components of the Cnidarian holobiont and useful to the animal’s health for several functions, including metabolism, immune defense, development, and behavior. Sometimes, the shifts in the normal microbiota may be used as “early” bio-indicators of both environmental changes and/or animal disease. Here the Cnidarians relationships with microbial communities and the potential biotechnological applications are summarized and discussed.

scholarly journals Combined Stimulation of Toll-Like Receptor 5 and NOD1 Strongly Potentiates Activity of NF-κB, Resulting in Enhanced Innate Immune Reactions and Resistance to Salmonella enterica Serovar Typhimurium Infection

2013 ◽  
Vol 81 (10) ◽  
pp. 3855-3864 ◽  
Author(s):  
Amir I. Tukhvatulin ◽  
Ilya I. Gitlin ◽  
Dmitry V. Shcheblyakov ◽  
Natalia M. Artemicheva ◽  
Lyudmila G. Burdelya ◽  
...  
Keyword(s):  
Critical Role ◽  
Immune Defense ◽  
Innate Immune ◽  
Microbial Infection ◽  
Immune Reactions ◽  
Content Type ◽  
Essential Components ◽  
Stimulation Of

ABSTRACTPathogen recognition receptors (PRRs) are essential components of host innate immune systems that detect specific conserved pathogen-associated molecular patterns (PAMPs) presented by microorganisms. Members of two families of PRRs, transmembrane Toll-like receptors (TLRs 1, 2, 4, 5, and 6) and cytosolic NOD receptors (NOD1 and NOD2), are stimulated upon recognition of various bacterial PAMPs. Such stimulation leads to induction of a number of immune defense reactions, mainly triggered via activation of the transcription factor NF-κB. While coordination of responses initiated via different PRRs sensing multiple PAMPS present during an infection makes clear biological sense for the host, such interactions have not been fully characterized. Here, we demonstrate that combined stimulation of NOD1 and TLR5 (as well as other NOD and TLR family members) strongly potentiates activity of NF-κB and induces enhanced levels of innate immune reactions (e.g., cytokine production) bothin vitroandin vivo. Moreover, we show that an increased level of NF-κB activity plays a critical role in formation of downstream responses. In live mice, synergy between these receptors resulting in potentiation of NF-κB activity was organ specific, being most prominent in the gastrointestinal tract. Coordinated activity of NOD1 and TLR5 significantly increased protection of mice against enteroinvasiveSalmonellainfection. Obtained results suggest that cooperation of NOD and TLR receptors is important for effective responses to microbial infectionin vivo.

scholarly journals Indoleamine 2,3-Dioxygenase 1 Is a Lung-Specific Innate Immune Defense Mechanism That Inhibits Growth of Francisella tularensis Tryptophan Auxotrophs

2010 ◽  
Vol 78 (6) ◽  
pp. 2723-2733 ◽  
Author(s):  
Kaitian Peng ◽  
Denise M. Monack
Keyword(s):  
Francisella Tularensis ◽  
Defense Mechanisms ◽  
Defense Mechanism ◽  
Immune Defense ◽  
The Body ◽  
Innate Immune ◽  
Microbial Pathogens ◽  
Immune Mechanisms ◽  
Indoleamine 2,3 Dioxygenase ◽  
Organ Specific

ABSTRACT Upon microbial challenge, organs at various anatomic sites of the body employ different innate immune mechanisms to defend against potential infections. Accordingly, microbial pathogens evolved to subvert these organ-specific host immune mechanisms to survive and grow in infected organs. Francisella tularensis is a bacterium capable of infecting multiple organs and thus encounters a myriad of organ-specific defense mechanisms. This suggests that F. tularensis may possess specific factors that aid in evasion of these innate immune defenses. We carried out a microarray-based, negative-selection screen in an intranasal model of Francisella novicida infection to identify Francisella genes that contribute to bacterial growth specifically in the lungs of mice. Genes in the bacterial tryptophan biosynthetic pathway were identified as being important for F. novicida growth specifically in the lungs. In addition, a host tryptophan-catabolizing enzyme, indoleamine 2,3-dioxygenase 1 (IDO1), is induced specifically in the lungs of mice infected with F. novicida or Streptococcus pneumoniae. Furthermore, the attenuation of F. novicida tryptophan mutant bacteria was rescued in the lungs of IDO1−/− mice. IDO1 is a lung-specific innate immune mechanism that controls pulmonary Francisella infections.

scholarly journals Epigenetic adaptations of the masticatory mucosa to periodontal inflammation

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Gesa M. Richter ◽  
Jochen Kruppa ◽  
H. Gencay Keceli ◽  
Emel Tuğba Ataman-Duruel ◽  
Christian Graetz ◽  
...  
Keyword(s):  
Oral Mucosa ◽  
Genetic Information ◽  
Environmental Changes ◽  
Immune Defense ◽  
Innate Immune ◽  
Fine Tuning ◽  
Mucosal Barrier ◽  
Epigenetic Changes ◽  
Periodontal Inflammation

Abstract Background In mucosal barrier interfaces, flexible responses of gene expression to long-term environmental changes allow adaptation and fine-tuning for the balance of host defense and uncontrolled not-resolving inflammation. Epigenetic modifications of the chromatin confer plasticity to the genetic information and give insight into how tissues use the genetic information to adapt to environmental factors. The oral mucosa is particularly exposed to environmental stressors such as a variable microbiota. Likewise, persistent oral inflammation is the most important intrinsic risk factor for the oral inflammatory disease periodontitis and has strong potential to alter DNA-methylation patterns. The aim of the current study was to identify epigenetic changes of the oral masticatory mucosa in response to long-term inflammation that resulted in periodontitis. Methods and results Genome-wide CpG methylation of both inflamed and clinically uninflamed solid gingival tissue biopsies of 60 periodontitis cases was analyzed using the Infinium MethylationEPIC BeadChip. We validated and performed cell-type deconvolution for infiltrated immune cells using the EpiDish algorithm. Effect sizes of DMPs in gingival epithelial and fibroblast cells were estimated and adjusted for confounding factors using our recently developed “intercept-method”. In the current EWAS, we identified various genes that showed significantly different methylation between periodontitis-inflamed and uninflamed oral mucosa in periodontitis patients. The strongest differences were observed for genes with roles in wound healing (ROBO2, PTP4A3), cell adhesion (LPXN) and innate immune response (CCL26, DNAJC1, BPI). Enrichment analyses implied a role of epigenetic changes for vesicle trafficking gene sets. Conclusions Our results imply specific adaptations of the oral mucosa to a persistent inflammatory environment that involve wound repair, barrier integrity, and innate immune defense.

scholarly journals Plant Antimicrobial Peptides as Potential Anticancer Agents

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Jaquelina Julia Guzmán-Rodríguez ◽  
Alejandra Ochoa-Zarzosa ◽  
Rodolfo López-Gómez ◽  
Joel E. López-Meza
Keyword(s):  
Antimicrobial Peptides ◽  
Anticancer Agents ◽  
Pathogenic Bacteria ◽  
Defense Mechanism ◽  
Immune Defense ◽  
Innate Immune ◽  
High Morbidity ◽  
Anticancer Activities ◽  
Innate Immune Defense ◽  
Wide Range

Antimicrobial peptides (AMPs) are part of the innate immune defense mechanism of many organisms and are promising candidates to treat infections caused by pathogenic bacteria to animals and humans. AMPs also display anticancer activities because of their ability to inactivate a wide range of cancer cells. Cancer remains a cause of high morbidity and mortality worldwide. Therefore, the development of methods for its control is desirable. Attractive alternatives include plant AMP thionins, defensins, and cyclotides, which have anticancer activities. Here, we provide an overview of plant AMPs anticancer activities, with an emphasis on their mode of action, their selectivity, and their efficacy.

scholarly journals Pattern Recognition Receptors and Cytokines inMycobacterium tuberculosisInfection—The Double-Edged Sword?

2013 ◽  
Vol 2013 ◽  
pp. 1-18 ◽  
Author(s):  
Md. Murad Hossain ◽  
Mohd-Nor Norazmi
Keyword(s):  
Pattern Recognition ◽  
Innate Immunity ◽  
Defense Mechanisms ◽  
Defense Mechanism ◽  
Adaptive Immune Response ◽  
Protective Role ◽  
Pattern Recognition Receptors ◽  
Immune Defense ◽  
Innate Immune ◽  
Intercellular Adhesion Molecule

Tuberculosis, an infectious disease caused byMycobacterium tuberculosis(Mtb), remains a major cause of human death worldwide. Innate immunity provides host defense against Mtb. Phagocytosis, characterized by recognition of Mtb by macrophages and dendritic cells (DCs), is the first step of the innate immune defense mechanism. The recognition of Mtb is mediated by pattern recognition receptors (PRRs), expressed on innate immune cells, including toll-like receptors (TLRs), complement receptors, nucleotide oligomerization domain like receptors, dendritic cell-specific intercellular adhesion molecule grabbing nonintegrin (DC-SIGN), mannose receptors, CD14 receptors, scavenger receptors, and FCγreceptors. Interaction of mycobacterial ligands with PRRs leads macrophages and DCs to secrete selected cytokines, which in turn induce interferon-γ- (IFNγ-) dominated immunity. IFNγand other cytokines like tumor necrosis factor-α(TNFα) regulate mycobacterial growth, granuloma formation, and initiation of the adaptive immune response to Mtb and finally provide protection to the host. However, Mtb can evade destruction by antimicrobial defense mechanisms of the innate immune system as some components of the system may promote survival of the bacteria in these cells and facilitate pathogenesis. Thus, although innate immunity components generally play a protective role against Mtb, they may also facilitate Mtb survival. The involvement of selected PRRs and cytokines on these seemingly contradictory roles is discussed.

scholarly journals Nilotinib: A Tyrosine Kinase Inhibitor Mediates Resistance to Intracellular Mycobacterium Via Regulating Autophagy

Cells ◽  
2019 ◽  
Vol 8 (5) ◽  
pp. 506 ◽  
Author(s):  
Tariq Hussain ◽  
Deming Zhao ◽  
Syed Zahid Ali Shah ◽  
Naveed Sabir ◽  
Jie Wang ◽  
...  
Keyword(s):  
Immune Responses ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitor ◽  
Bacterial Infections ◽  
Defense Mechanism ◽  
Kinase Inhibitor ◽  
Mycobacterium Avium Subspecies Paratuberculosis ◽  
Immune Defense ◽  
Innate Immune

Nilotinib, a tyrosine kinase inhibitor, has been studied extensively in various tumor models; however, no information exists about the pharmacological action of nilotinib in bacterial infections. Mycobacterium bovis (M. bovis) and Mycobacterium avium subspecies paratuberculosis (MAP) are the etiological agents of bovine tuberculosis and Johne’s disease, respectively. Although M. bovis and MAP cause distinct tissue tropism, both of them infect, reside, and replicate in mononuclear phagocytic cells of the infected host. Autophagy is an innate immune defense mechanism for the control of intracellular bacteria, regulated by diverse signaling pathways. Here we demonstrated that nilotinib significantly inhibited the intracellular survival and growth of M. bovis and MAP in macrophages by modulating host immune responses. We showed that nilotinib induced autophagic degradation of intracellular mycobacterium occurred via the inhibition of PI3k/Akt/mTOR axis mediated by abelson (c-ABL) tyrosine kinase. In addition, we observed that nilotinib promoted ubiquitin accumulation around M. bovis through activation of E3 ubiquitin ligase parkin. From in-vivo experiments, we found that nilotinib effectively controlled M. bovis growth and survival through enhanced parkin activity in infected mice. Altogether, our data showed that nilotinib regulates protective innate immune responses against intracellular mycobacterium, both in-vitro and in-vivo, and can be exploited as a novel therapeutic remedy for the control of M. bovis and MAP infections.

The roles of grouper TANK in innate immune defense against iridovirus and nodavirus infections

2020 ◽  
Vol 104 ◽  
pp. 506-516
Author(s):  
Jingguang Wei ◽  
Chen Li ◽  
Jisheng Ou ◽  
Xin Zhang ◽  
Zetian Liu ◽  
...  
Keyword(s):  
Immune Defense ◽  
Innate Immune ◽  
Innate Immune Defense
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