bims-traimu 2022-06-19 papers

Issue of 2022–06–19
six papers selected by
Yantong Wan, Southern Medical University

Front Cell Dev Biol. 2022 ;10 886086

Trained Immunity in Perivascular Adipose Tissue of Abdominal Aortic Aneurysm-A Novel Concept for a Still Elusive Disease.

Luca Piacentini, Chiara Vavassori, Gualtiero I Colombo.

Abdominal aortic aneurysm (AAA) is a chronic, life-threatening vascular disease whose only therapeutic option is a surgical repair to prevent vessel rupture. The lack of medical therapy results from an inadequate understanding of the etiopathogenesis of AAA. Many studies in animal and human models indicate a 'short-circuiting' of the regulation of the inflammatory-immune response as a major player in the AAA chronic process. In this regard, perivascular adipose tissue (PVAT) has received increasing interest because its dysfunction affects large arteries primarily through immune cell infiltration. Consistently, we have recently produced evidence that innate and adaptive immune cells present in the PVAT of AAAs contribute to sustaining a damaging inflammatory loop. However, it is still unclear how the complex crosstalk between adaptive and innate immunity can be self-sustaining. From our perspective, trained immunity may play a role in this crosstalk. Trained immunity is defined as a form of innate immune memory resulting in enhanced responsiveness to repeated triggers. Specific innate stimuli and epigenetic and metabolic reprogramming events induce and shape trained immunity in myeloid progenitor cells improving host defense, but also contributing to the progression of immune-mediated and chronic inflammatory diseases. Here we present this hypothesis with data from the literature and our observations to support it.

Keywords: abdominal aortic aneurysm; epigenetic markers; immune response; perivascular adipose tissue; trained immunity

DOI: https://doi.org/10.3389/fcell.2022.886086

Front Immunol. 2022 ;13 885782

Metabolomic Investigation of Ultraviolet Ray-Inactivated White Spot Syndrome Virus-Induced Trained Immunity in Marsupenaeus japonicus.

Shaoqing Zang, Li-Xia Lv, Chen-Fei Liu, Peng Zhang, Cang Li, Jin-Xing Wang.

Trained immunity is driven by metabolism and epigenetics in innate immune cells in mammals. The phenomenon of trained immunity has been identified in invertebrates, including shrimp, but the underlying mechanisms remain unclear. To elucidate mechanisms of trained immunity in shrimp, the metabolomic changes in hemolymph of Marsupenaeus japonicus trained by the UV-inactivated white spot syndrome virus (UV-WSSV) were analyzed using tandem gas chromatography-mass/mass spectrometry. The metabolomic profiles of shrimp trained with UV-WSSV followed WSSV infection showed significant differences comparison with the control groups, PBS injection followed WSSV infection. 16 differential metabolites in total of 154 metabolites were identified, including D-fructose-6-phosphate, D-glucose-6-phosphate, and D-fructose-6-phosphate, and metabolic pathways, glycolysis, pentose phosphate pathway, and AMPK signaling pathway were enriched in the UV-WSSV trained groups. Further study found that histone monomethylation and trimethylation at H3K4 (H3K4me1 and H3K4me3) were involved in the trained immunity. Our data suggest that the UV-WSSV induced trained immunity leads to metabolism reprogramming in the shrimp and provide insights for WSSV control in shrimp aquaculture.

Keywords: GC–MS/MS; WSSV; metabolites; shrimp; trained immunity

DOI: https://doi.org/10.3389/fimmu.2022.885782

Front Immunol. 2022 ;13 872652

Trained Immunity Enhances Human Monocyte Function in Aging and Sepsis.

P Spencer Gill, Tammy R Ozment, Nicole H Lewis, Edward R Sherwood, David L Williams.

Aging plays a critical role in the incidence and severity of infection, with age emerging as an independent predictor of mortality in sepsis. Trained immunity reprograms immunocytes to respond more rapidly and effectively to pathogens and serves as a potential approach to improve immune function in aging and/or sepsis. However, there is very little data on trained immunity in the aging immune system or in the presence of sepsis. We examined the impact of β-glucan induced innate immune training on monocytes from aging healthy humans (>60 years old) as well as sepsis patients. We observed increased metabolic capacity, upregulated cytokine secretion, increased H3K27 acetylation, and upregulation of crucial intracellular signaling pathways in trained monocytes from healthy aging subjects. The response to trained immunity in healthy aging monocytes was equivalent to the response of monocytes from younger, i.e., 18 - 59 years, individuals. Additionally, we found that trained immunity induced a unique expression pattern of cell surface markers in monocytes that was consistent across age groups. Trained monocytes from sepsis patients also displayed enhanced metabolic capacity and increased cytokine production. These results indicate that immune training can be induced in aging monocytes as well as monocytes from critically ill sepsis patients.

Keywords: aging; immunosenescence; innate immunity; monocytes; trained immunity

DOI: https://doi.org/10.3389/fimmu.2022.872652

Mol Biol Rep. 2022 Jun 13.

Immune cell metabolism and metabolic reprogramming.

Chenchen Hu, Yuxin Xuan, Xiyang Zhang, Yang Liu, Shuya Yang, Kun Yang.

Energy metabolism maintains the activation of intracellular and intercellular signal transduction, and plays a crucial role in immune response. Under environmental stimulation, immune cells change from resting to activation and trigger metabolic reprogramming. The immune system cells exhibit different metabolic characteristics when performing functions. The study of immune metabolism provides new insights into the function of immune cells, including how they differentiate, migrate and exert immune responses. Studies of immune cell energy metabolism are beginning to shed light on the metabolic mechanism of disease progression and reveal new ways to target inflammatory diseases such as autoimmune diseases, chronic viral infections, and cancer. Here, we discussed the relationship between immune cells and metabolism, and proposed the possibility of targeted metabolic process for disease treatment.

Keywords: Immune cells; Immune metabolism; Metabolic reprogramming; Targeted therapy

DOI: https://doi.org/10.1007/s11033-022-07474-2

Microbiome. 2022 Jun 14. 10(1): 91

Deletion of both Dectin-1 and Dectin-2 affects the bacterial but not fungal gut microbiota and susceptibility to colitis in mice.

Yazhou Wang, Madeleine Spatz, Gregory Da Costa, Chloé Michaudel, Alexia Lapiere, Camille Danne, Allison Agus, Marie-Laure Michel, Mihai G Netea, Philippe Langella, Harry Sokol, Mathias L Richard.

BACKGROUND: Innate immunity genes have been reported to affect susceptibility to inflammatory bowel diseases (IBDs) and colitis in mice. Dectin-1, a receptor for fungal cell wall β-glucans, has been clearly implicated in gut microbiota modulation and modification of the susceptibility to gut inflammation. Here, we explored the role of Dectin-1 and Dectin-2 (another receptor for fungal cell wall molecules) deficiency in intestinal inflammation.
DESIGN: Susceptibility to dextran sodium sulfate (DSS)-induced colitis was assessed in wild-type, Dectin-1 knockout (KO), Dectin-2KO, and double Dectin-1KO and Dectin-2KO (D-1/2KO) mice. Inflammation severity, as well as bacterial and fungal microbiota compositions, was monitored.
RESULTS: While deletion of Dectin-1 or Dectin-2 did not have a strong effect on DSS-induced colitis, double deletion of Dectin-1 and Dectin-2 significantly protected the mice from colitis. The protection was largely mediated by the gut microbiota, as demonstrated by fecal transfer experiments. Treatment of D-1/2KO mice with opportunistic fungal pathogens or antifungal agents did not affect the protection against gut inflammation, suggesting that the fungal microbiota had no role in the protective phenotype. Amplicon-based microbiota analysis of the fecal bacterial and fungal microbiota of D-1/2KO mice confirmed the absence of changes in the mycobiota but strong modification of the bacterial microbiota. We showed that bacteria from the Lachnospiraceae family were at least partly involved in this protection and that treatment with Blautia hansenii was enough to recapitulate the protection.
CONCLUSIONS: Deletion of both the Dectin-1 and Dectin-2 receptors triggered a global shift in the microbial gut environment, affecting, surprisingly, mainly the bacterial population and driving protective effects in colitis. Members of the Lachnospiraceae family seem to play a central role in this protection. These findings provide new insights into the role of the Dectin receptors, which have been described to date as affecting only the fungal population, in intestinal physiopathology and in IBD. Video Abstract.

Keywords: Dectin-1; Dectin-2; Gut inflammation; Immune response; Microbiota

DOI: https://doi.org/10.1186/s40168-022-01273-4