The Path Less Explored: Innate Immune Reactions in Cnidarians

2008 ◽  
pp. 27-42 ◽  
Author(s):  
Thomas C. G. Bosch
Keyword(s):  
Innate Immune ◽  
Immune Reactions

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 Exploration of Pattern Recognition Receptor Agonists as Candidate Adjuvants

2021 ◽  
Vol 11 ◽  
Author(s):  
Guang Han Ong ◽  
Benedict Shi Xiang Lian ◽  
Takumi Kawasaki ◽  
Taro Kawai
Keyword(s):  
Immune Responses ◽  
Molecular Mechanisms ◽  
Innate Immune ◽  
Host Cells ◽  
Vaccine Adjuvants ◽  
Immune Reactions ◽  
Safety And Reliability ◽  
Pathogen Recognition Receptors ◽  
Acquired Immune Responses ◽  
Molecular Patterns

Adjuvants are used to maximize the potency of vaccines by enhancing immune reactions. Components of adjuvants include pathogen-associated molecular patterns (PAMPs) and damage-associate molecular patterns (DAMPs) that are agonists for innate immune receptors. Innate immune responses are usually activated when pathogen recognition receptors (PRRs) recognize PAMPs derived from invading pathogens or DAMPs released by host cells upon tissue damage. Activation of innate immunity by PRR agonists in adjuvants activates acquired immune responses, which is crucial to enhance immune reactions against the targeted pathogen. For example, agonists for Toll-like receptors have yielded promising results as adjuvants, which target PRR as adjuvant candidates. However, a comprehensive understanding of the type of immunological reaction against agonists for PRRs is essential to ensure the safety and reliability of vaccine adjuvants. This review provides an overview of the current progress in development of PRR agonists as vaccine adjuvants, the molecular mechanisms that underlie activation of immune responses, and the enhancement of vaccine efficacy by these potential adjuvant candidates.

scholarly journals Sex- and region-biased depletion of microglia/macrophages attenuates CLN1 disease in mice

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Kristina Berve ◽  
Brian L. West ◽  
Rudolf Martini ◽  
Janos Groh
Keyword(s):  
Visual Acuity ◽  
Immune Cells ◽  
Term Treatment ◽  
Innate Immune ◽  
Neuronal Ceroid Lipofuscinoses ◽  
Innate Immune Cells ◽  
Immune Reactions ◽  
Neuron Loss ◽  
Long Term Treatment

Abstract Background The neuronal ceroid lipofuscinoses (CLN diseases) are fatal lysosomal storage diseases causing neurodegeneration in the CNS. We have previously shown that neuroinflammation comprising innate and adaptive immune reactions drives axonal damage and neuron loss in the CNS of palmitoyl protein thioesterase 1-deficient (Ppt1−/−) mice, a model of the infantile form of the diseases (CLN1). Therefore, we here explore whether pharmacological targeting of innate immune cells modifies disease outcome in CLN1 mice. Methods We applied treatment with PLX3397 (150 ppm in the chow), a potent inhibitor of the colony stimulating factor-1 receptor (CSF-1R) to target innate immune cells in CLN1 mice. Experimental long-term treatment was non-invasively monitored by longitudinal optical coherence tomography and rotarod analysis, as well as analysis of visual acuity, myoclonic jerks, and survival. Treatment effects regarding neuroinflammation, neural damage, and neurodegeneration were subsequently analyzed by histology and immunohistochemistry. Results We show that PLX3397 treatment attenuates neuroinflammation in CLN1 mice by depleting pro-inflammatory microglia/macrophages. This leads to a reduction of T lymphocyte recruitment, an amelioration of axon damage and neuron loss in the retinotectal system, as well as reduced thinning of the inner retina and total brain atrophy. Accordingly, long-term treatment with the inhibitor also ameliorates clinical outcomes in CLN1 mice, such as impaired motor coordination, visual acuity, and myoclonic jerks. However, we detected a sex- and region-biased efficacy of CSF-1R inhibition, with male microglia/macrophages showing higher responsiveness toward depletion, especially in the gray matter of the CNS. This results in a better treatment outcome in male Ppt1−/− mice regarding some histopathological and clinical readouts and reflects heterogeneity of innate immune reactions in the diseased CNS. Conclusions Our results demonstrate a detrimental impact of innate immune reactions in the CNS of CLN1 mice. These findings provide insights into CLN pathogenesis and may guide in the design of immunomodulatory treatment strategies.

Innate immune reactions stimulated by a lipopolysaccharide-like component of the alga Prototheca (strain 289)

2001 ◽  
Vol 88 (11) ◽  
pp. 482-485 ◽  
Author(s):  
Jon C. Bedick ◽  
Alex Shnyra ◽  
David W. Stanley ◽  
R. Pardy
Keyword(s):  
Innate Immune ◽  
Immune Reactions

Mechanisms of meconium-induced innate immune-reactions: Role of complement and CD14/TLR4/MD-2

2009 ◽  
Vol 46 (14) ◽  
pp. 2865-2866
Author(s):  
Bodil Salvesen ◽  
Carlo Rossetti ◽  
Tom Eirik Mollnes
Keyword(s):  
Innate Immune ◽  
Immune Reactions

scholarly journals Mosquito Phenoloxidase and Defensin Colocalize in Melanization Innate Immune Responses

2005 ◽  
Vol 53 (6) ◽  
pp. 689-698 ◽  
Author(s):  
Julián F. Hillyer ◽  
Bruce M. Christensen
Keyword(s):  
Immune Responses ◽  
Micrococcus Luteus ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Melanin Biosynthesis ◽  
Immune Reactions ◽  
Transmission Electron ◽  
Cellular Immune ◽  
Rate Limiting

Mosquitoes mount strong humoral and cellular immune responses against foreign organisms. Two components of the mosquito immune response that have received much attention are the phenoloxidase cascade that leads to melanization and antimicrobial peptides. The purpose of the current study was to use immunocytochemistry and transmission electron microscopy to identify the location of the melanization rate-limiting enzyme phenoloxidase and the antimicrobial peptide defensin in innate immune reactions against Escherichia coli and Micrococcus luteus by the mosquito Aedes aegypti. Our results show that both phenoloxidase and defensin are present at the sites of melanin biosynthesis in immune reactions against bacteria. Furthermore, both proteins are often present inside the same melanotic capsules. When hemocytes were analyzed, phenoloxidase was present in the cytosol of oenocytoids, but no significant amounts of defensin were detected inside any hemocytes. In summary, these data show that phenoloxidase and defensin colocalize in melanization reactions against bacteria and argue for further studies into the potential role of defensin in phenoloxidase-based melanization innate immune responses in mosquitoes.

Neutrophil extracellular trap formation as innate immune reactions against the apicomplexan parasite Eimeria bovis

2010 ◽  
Vol 133 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Jan Hillern Behrendt ◽  
Antonio Ruiz ◽  
Horst Zahner ◽  
Anja Taubert ◽  
Carlos Hermosilla
Keyword(s):  
Apicomplexan Parasite ◽  
Innate Immune ◽  
Neutrophil Extracellular Trap ◽  
Immune Reactions ◽  
Trap Formation ◽  
Extracellular Trap ◽  
Eimeria Bovis

scholarly journals Innate Immune Signal-Regulated Hematopoiesis

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. SCI-1-SCI-1
Author(s):  
Hitoshi Takizawa
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Hematopoietic Stem Cells ◽  
Host Defense ◽  
Immune Cells ◽  
Innate Immune ◽  
Immune Memory ◽  
Bone Marrow Niche ◽  
Hematopoietic Stem ◽  
Immune Reactions

Adult bone marrow (BM) had been long thought to be an immune-privileged organ where little immune reactions occur upon immunological challenges, and thus to form an advantageous environment to preserve long-lived hematopoietic and immune cells, e.g., hematopoietic stem cells (HSCs) that maintain lifelong hematopoiesis. They are mostly kept in quiescence, i.e., very slowly dividing within the steady state BM microenvironment, often referred to as niche, which consists of various type of non-hematopoietic cells such as endothelial cells, mesenchymal stromal cells1. In contrast, recent studies have suggested that a broad range of immunological and inflammatory responses occur in BM and largely influence HSC function2. Upon hematopoietic challenges, e.g., infection, inflammation, cancer, both HSCs and the surrounding niche cells can sense hematopoietic demand signals and integrate it to hematopoiesis via direct (HSC-mediated) and indirect (niche-mediated) sensing mechanisms. As a consequence, primitive HSC and their differentiated progenitors (HSPCs) migrate to inflamed organs, proliferate and differentiate into specific cell lineages that are locally consumed and to be replenished. Infection is one of hemato-immunological challenges that are highly conserved in evolution and relevant to pathogenesis of many diseases, e.g., cancer. Host defense against infection is initiated by rapid but relatively non-specific responses that involve innate immune effector cells, e.g., macrophages, granulocytes, and then is followed by slower but specific responses that involve acquired immunity. Recent studies have shown that not only immune cells but also HSPCs express innate immune sensors, such as Toll-like receptors (TLRs), and the ligation of receptors results in secretion of pro-inflammatory cytokines, cell migration, proliferation and differentiation into myeloid lineage cells (King, Nat Rev Immunol 2016). We have also shown that systemic infection of gram negative bacterial activates quiescent HSCs to proliferation through its cognate receptor, TLR4, and eventually impairs their hematopoietic repopulating ability3. More recently, we have found that intestinal tissue damage activates early hematopoiesis in BM via microbial signals and direct early HSPCs to inflamed lymph node to produce myeloid cells and promote tissue repair. Given the fact that innate immune cells are epigenetically programmed with innate immune memory upon sensitization ("training") infection to resist future infectious insults4, and that HSPCs are long-lived and immune-responsive, it has been demonstrated that upon exposure to pathogen, HSPCs also are able to memorize infection through metabolic and epigenetic changes, and build hemato-immune system with better protection to subsequent pathogen insults5. Taken together, these findings define the BM not as an immune-privileged reservoir, but rather as an organ of active immune reactions where immature HSPCs are capable of adapting the demand signal to hematopoiesis in response to hemato-immunological challenges, and of being trained by innate immune activation to reconstitute host defense with more resistance against future infection. Morrison SJ, Scadden DT. The bone marrow niche for haematopoietic stem cells. Nature. 2014 Jan 16;505(7483):327-34 Takizawa H, Boettcher S, Manz MG. Demand-adapted regulation of early hematopoiesis in infection and inflammation.Blood. 2012 Mar 29;119(13):2991-3002. Takizawa H, Fritsch K, Kovtonyuk LV, et al. Pathogen-Induced TLR4-TRIF Innate Immune Signaling in Hematopoietic Stem Cells Promotes Proliferation but Reduces Competitive Fitness.Cell Stem Cell. 2017 Aug 3;21(2):225-240.e5. Netea MG, Joosten LA, Latz E, et al. Trained immunity: A program of innate immune memory in health and disease.Science. 2016 Apr 22;352(6284):aaf1098. Kopf M, Nielsen PJ. Training myeloid precursors with fungi, bacteria and chips. Nat Immunol. 2018 Apr;19(4):320-322. Disclosures No relevant conflicts of interest to declare.

scholarly journals Innate Immune Reactions in Septic and Aseptic Osteolysis around Hip Implants

2014 ◽  
Vol 24 (4) ◽  
pp. 283-296 ◽  
Author(s):  
Jukka Pajarinen ◽  
Eemeli Jamsen ◽  
Yrjo T. Konttinen ◽  
Stuart B. Goodman
Keyword(s):  
Innate Immune ◽  
Hip Implants ◽  
Immune Reactions
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