bims-traimu 2024-01-28 papers

Issue of 2024‒01‒28
five papers selected by
Yantong Wan, Southern Medical University

Adv Sci (Weinh). 2024 Jan 26. e2308978

Innate Immune Training Initiates Efferocytosis to Protect against Lung Injury.

Yoon-Young Kang, Dong-Young Kim, Sang-Yong Lee, Hee-Joong Kim, Taehawn Kim, Jeong A Cho, Taewon Lee, Eun Young Choi.

Innate immune training involves myelopoiesis, dynamic gene modulation, and functional reprogramming of myeloid cells in response to secondary heterologous challenges. The present study evaluates whether systemic innate immune training can protect tissues from local injury. Systemic pretreatment of mice with β-glucan, a trained immunity agonist, reduces the mortality rate of mice with bleomycin-induced lung injury and fibrosis, as well as decreasing collagen deposition in the lungs. β-Glucan pretreatment induces neutrophil accumulation in the lungs and enhances efferocytosis. Training of mice with β-glucan results in histone modification in both alveolar macrophages (AMs) and neighboring lung epithelial cells. Training also increases the production of RvD1 and soluble mediators by AMs and efferocytes. Efferocytosis increases trained immunity in AMs by stimulating RvD1 release, thus inducing SIRT1 expression in neighboring lung epithelial cells. Elevated epithelial SIRT1 expression is associated with decreased epithelial cell apoptosis after lung injury, attenuating tissue damage. Further, neutrophil depletion dampens the effects of β-glucan on macrophage accumulation, epigenetic modification in lung macrophages, epithelial SIRT1 expression, and injury-mediated fibrosis in the lung. These findings provide mechanistic insights into innate immune training and clues to the potential ability of centrally trained immunity to protect peripheral organs against injury-mediated disorders.

Keywords: alveolar macrophages; efferocytosis; inflammation; lung injury; trained immunity

DOI: https://doi.org/10.1002/advs.202308978

Int Immunopharmacol. 2024 Jan 23. pii: S1567-5769(24)00076-6. [Epub ahead of print]128 111558

Association between periodontitis and inflammatory comorbidities: The common role of innate immune cells, underlying mechanisms and therapeutic targets.

Qibing Wu, Weijia Zhang, Yaqiong Lu, Hongxia Li, Yaru Yang, Fengxue Geng, Jinwen Liu, Li Lin, Yaping Pan, Chen Li.

Periodontitis, which is related to various systemic diseases, is a chronic inflammatory disease caused by periodontal dysbiosis of the microbiota. Multiple factors can influence the interaction of periodontitis and associated inflammatory disorders, among which host immunity is an important contributor to this interaction. Innate immunity can be activated aberrantly because of the systemic inflammation induced by periodontitis. This aberrant activation not only exacerbates periodontal tissue damage but also impairs systemic health, triggering or aggravating inflammatory comorbidities. Therefore, innate immunity is a potential therapeutic target for periodontitis and associated inflammatory comorbidities. This review delineates analogous aberrations of innate immune cells in periodontitis and comorbid conditions such as atherosclerosis, diabetes, obesity, and rheumatoid arthritis. The mechanisms behind these changes in innate immune cells are discussed, including trained immunity and clonal hematopoiesis of indeterminate potential (CHIP), which can mediate the abnormal activation and myeloid-biased differentiation of hematopoietic stem and progenitor cells. Besides, the expansion of myeloid-derived suppressor cells (MDSCs), which have immunosuppressive and osteolytic effects on peripheral tissues, also contributes to the interaction between periodontitis and its inflammatory comorbidities. The potential treatment targets for relieving the risk of both periodontitis and systemic conditions are also elucidated, such as the modulation of innate immunity cells and mediators, the regulation of trained immunity and CHIP, as well as the inhibition of MDSCs' expansion.

Keywords: CHIP; Innate immunity; MDSCs; Periodontitis; Systemic inflammation; Trained immunity

DOI: https://doi.org/10.1016/j.intimp.2024.111558

Front Immunol. 2023 ;14 1356400

Editorial: Exploring the health of aquatic organisms through an immune viewpoint.

Antonio Figueras, Lingling Wang, Simon MacKenzie, Jorge Galindo-Villegas.

Keywords: AF10 cells; CRISPR; arthropods; crustacea; germ-free; medaka; receptor interacting 9 protein 2; trained immunity

DOI: https://doi.org/10.3389/fimmu.2023.1356400

Hum Vaccin Immunother. 2024 Dec 31. 20(1): 2306675

From defense to offense: Modulating toll-like receptors to combat arbovirus infections.

Rafidah Lani, Ilya Maisarah Thariq, Nuramira Syazreen Suhaimi, Pouya Hassandarvish, Sazaly Abu Bakar.

Arboviruses are a significant threat to global public health, with outbreaks occurring worldwide. Toll-like receptors (TLRs) play a crucial role in the innate immune response against these viruses by recognizing pathogen-associated molecular patterns and initiating an inflammatory response. Significantly, TLRs commonly implicated in the immune response against viral infections include TLR2, TLR4, TLR6, TLR3, TLR7, and TLR8; limiting or allowing them to replicate and spread within the host. Modulating TLRs has emerged as a promising approach to combat arbovirus infections. This review summarizes recent advances in TLR modulation as a therapeutic target in arbovirus infections. Studies have shown that the activation of TLRs can enhance the immune response against arbovirus infections, leading to increased viral clearance and protection against disease. Conversely, inhibition of TLRs can reduce the excessive inflammation and tissue damage associated with arbovirus infection. Modulating TLRs represents a potential therapeutic strategy to combat arbovirus infections.

Keywords: Infectious disease; adjuvant; agonist; antagonist; arboviruses; modulation; toll-like receptors

DOI: https://doi.org/10.1080/21645515.2024.2306675

Nat Commun. 2024 Jan 23. 15(1): 680

An IL-10/DEL-1 axis supports granulopoiesis and survival from sepsis in early life.

Eleni Vergadi, Ourania Kolliniati, Ioanna Lapi, Eleftheria Ieronymaki, Konstantina Lyroni, Vasileia Ismini Alexaki, Eleni Diamantaki, Katerina Vaporidi, Eleftheria Hatzidaki, Helen A Papadaki, Emmanouil Galanakis, George Hajishengallis, Triantafyllos Chavakis, Christos Tsatsanis.

The limited reserves of neutrophils are implicated in the susceptibility to infection in neonates, however the regulation of neutrophil kinetics in infections in early life remains poorly understood. Here we show that the developmental endothelial locus (DEL-1) is elevated in neonates and is critical for survival from neonatal polymicrobial sepsis, by supporting emergency granulopoiesis. Septic DEL-1 deficient neonate mice display low numbers of myeloid-biased multipotent and granulocyte-macrophage progenitors in the bone marrow, resulting in neutropenia, exaggerated bacteremia, and increased mortality; defects that are rescued by DEL-1 administration. A high IL-10/IL-17A ratio, observed in newborn sepsis, sustains tissue DEL-1 expression, as IL-10 upregulates while IL-17 downregulates DEL-1. Consistently, serum DEL-1 and blood neutrophils are elevated in septic adult and neonate patients with high serum IL-10/IL-17A ratio, and mortality is lower in septic patients with high serum DEL-1. Therefore, IL-10/DEL-1 axis supports emergency granulopoiesis, prevents neutropenia and promotes sepsis survival in early life.

DOI: https://doi.org/10.1038/s41467-023-44178-y