Faculty Opinions recommendation of Hemocyte differentiation mediates innate immune memory in Anopheles gambiae mosquitoes.

2010 ◽  
Author(s):  
Sara Cherry
Keyword(s):  
Anopheles Gambiae ◽  
Innate Immune ◽  
Immune Memory

scholarly journals Hemocyte Differentiation Mediates Innate Immune Memory in Anopheles gambiae Mosquitoes

Science ◽  
2010 ◽  
Vol 329 (5997) ◽  
pp. 1353-1355 ◽  
Author(s):  
Janneth Rodrigues ◽  
Fábio André Brayner ◽  
Luiz Carlos Alves ◽  
Rajnikant Dixit ◽  
Carolina Barillas-Mury
Keyword(s):  
Epithelial Cells ◽  
Gut Microbiota ◽  
Anopheles Gambiae ◽  
Direct Contact ◽  
Malaria Parasite ◽  
Innate Immune ◽  
Immune Memory ◽  
Mosquito Midgut ◽  
Necessary And Sufficient

Mosquito midgut invasion by ookinetes of the malaria parasite Plasmodium disrupts the barriers that normally prevent the gut microbiota from coming in direct contact with epithelial cells. This triggers a long-lived response characterized by increased abundance of granulocytes, a subpopulation of hemocytes that circulates in the insect’s hemocoel, and enhanced immunity to bacteria that indirectly reduces survival of Plasmodium parasites upon reinfection. In mosquitoes, differentiation of hemocytes was necessary and sufficient to confer innate immune memory.

scholarly journals “Proliferation of DBLOX Peroxidase-Expressing Oenocytes Maintains Innate Immune Memory in Primed Mosquitoes”

2020 ◽  
Author(s):  
Fabio M. Gomes ◽  
Miles D.W. Tyner ◽  
Ana Beatriz F. Barletta ◽  
Lampougin Yenkoidiok-Douti ◽  
Gaspar E. Canepa ◽  
...  
Keyword(s):  
Anopheles Gambiae ◽  
Cellular Immunity ◽  
Histone Acetyltransferase ◽  
Direct Evidence ◽  
Fat Body ◽  
Immune Surveillance ◽  
Innate Immune ◽  
Body Tissue ◽  
Immune Memory ◽  
Immune Priming

AbstractImmune priming in Anopheles gambiae mosquitoes following infection with Plasmodium parasites is mediated by the systemic release of a hemocyte differentiation factor (HDF), a complex of lipoxin A4 bound to Evokin, a lipid carrier. HDF increases the proportion of circulating granulocytes and enhances mosquito cellular immunity. We found that Evokin is constitutively produced by hemocytes and fat-body cells, but expression increases in response to infection. Insects synthesize lipoxins, but lack lipoxygenases. Here, we show that the Double Peroxidase (DBLOX) enzyme, present in insects but not in vertebrates, is essential for HDF synthesis. DBLOX is highly expressed in oenocytes in the fat body tissue, and these cells proliferate in response to Plasmodium challenge. We provide direct evidence that modifications mediated by the histone acetyltransferase AgTip60 (AGAP01539) are essential for sustained oenocyte proliferation, HDF synthesis and immune priming. We propose that oenocytes function as a population of “memory” cells that continuously release lipoxin to orchestrate and maintain a broad, systemic and long-lasting state of enhanced immune surveillance.

Innate immune memory mediates increased susceptibility to Alzheimeŕs disease-like pathology in sepsis surviving mice

2021 ◽  
Author(s):  
Virginia L. De Sousa ◽  
Suzana B. Araújo ◽  
Leticia M. Antonio ◽  
Mariana Silva-Queiroz ◽  
Lilian C. Colodeti ◽  
...  
Keyword(s):  
Innate Immune ◽  
Immune Memory ◽  
Alzheimers Disease ◽  
Increased Susceptibility

scholarly journals The Role of Cell Metabolism in Innate Immune Memory

2020 ◽  
pp. 1-9
Author(s):  
Anaisa Valido Ferreira ◽  
Jorge Domiguéz-Andrés ◽  
Mihai Gheorghe Netea
Keyword(s):  
Metabolic Pathways ◽  
Tricarboxylic Acid Cycle ◽  
Cell Metabolism ◽  
Innate Immune ◽  
Immune Memory ◽  
Functional Changes ◽  
Trained Immunity ◽  
Health And Disease

Immunological memory is classically attributed to adaptive immune responses, but recent studies have shown that challenged innate immune cells can display long-term functional changes that increase nonspecific responsiveness to subsequent infections. This phenomenon, coined <i>trained immunity</i> or <i>innate immune memory</i>, is based on the epigenetic reprogramming and the rewiring of intracellular metabolic pathways. Here, we review the different metabolic pathways that are modulated in trained immunity. Glycolysis, oxidative phosphorylation, the tricarboxylic acid cycle, amino acid, and lipid metabolism are interplaying pathways that are crucial for the establishment of innate immune memory. Unraveling this metabolic wiring allows for a better understanding of innate immune contribution to health and disease. These insights may open avenues for the development of future therapies that aim to harness or dampen the power of the innate immune response.

scholarly journals The Role of the Pathogen Dose and PI3Kγ in Immunometabolic Reprogramming of Microglia for Innate Immune Memory

2021 ◽  
Vol 22 (5) ◽  
pp. 2578
Author(s):  
Trim Lajqi ◽  
Christian Marx ◽  
Hannes Hudalla ◽  
Fabienne Haas ◽  
Silke Große ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Immune Tolerance ◽  
Immune Cells ◽  
Low Dose ◽  
Innate Immune ◽  
Immune Memory ◽  
Innate Immune Cells ◽  
Atp Production ◽  
Dose Dependent

Microglia, the innate immune cells of the CNS, exhibit long-term response changes indicative of innate immune memory (IIM). Our previous studies revealed IIM patterns of microglia with opposing immune phenotypes: trained immunity after a low dose and immune tolerance after a high dose challenge with pathogen-associated molecular patterns (PAMP). Compelling evidence shows that innate immune cells adopt features of IIM via immunometabolic control. However, immunometabolic reprogramming involved in the regulation of IIM in microglia has not been fully addressed. Here, we evaluated the impact of dose-dependent microglial priming with ultra-low (ULP, 1 fg/mL) and high (HP, 100 ng/mL) lipopolysaccharide (LPS) doses on immunometabolic rewiring. Furthermore, we addressed the role of PI3Kγ on immunometabolic control using naïve primary microglia derived from newborn wild-type mice, PI3Kγ-deficient mice and mice carrying a targeted mutation causing loss of lipid kinase activity. We found that ULP-induced IIM triggered an enhancement of oxygen consumption and ATP production. In contrast, HP was followed by suppressed oxygen consumption and glycolytic activity indicative of immune tolerance. PI3Kγ inhibited glycolysis due to modulation of cAMP-dependent pathways. However, no impact of specific PI3Kγ signaling on immunometabolic rewiring due to dose-dependent LPS priming was detected. In conclusion, immunometabolic reprogramming of microglia is involved in IIM in a dose-dependent manner via the glycolytic pathway, oxygen consumption and ATP production: ULP (ultra-low-dose priming) increases it, while HP reduces it.

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