Ischemic stroke is one of the most common causes of death and disability worldwide. Neuroinflammation is a major pathological event involved in the process of ischemic injury and repair. In particular, microglia play a dual role in neuroinflammation. During the acute phase of stroke onset, M2 microglia are the dominant phenotype and exert protective effects on neuronal cells, whereas permanent M1 microglia contribute to prolonged inflammation and are detrimental to brain tissue. Emerging evidence indicates that microRNAs (miRNAs) may have regulatory effects on microglia-associated inflammation. Thus, we briefly reviewed the dynamic response of microglia after a stroke and assessed how specific miRNAs affect the behavior of reactive microglia. We concluded that miRNAs may be useful novel therapeutic targets to improve stroke outcomes and modulate neuroinflammation.

Colorectal cancer (CRC) is one of the most common cancer worldwide. Chronic inflammation contributes to CRC development and progression. Emodin, is a natural anthraquinone derivative with anti-oxidant, anti-inflammatory, and anti-tumor activities. We used the AOM/DSS model of colitis-associated intestinal tumorigenesis to characterize the effect of Emodin on inflammation and tumorigenesis at weeks 3, 5, and 14 after initiation with AOM. At all three time points, Emodin (50 mg/kg) reduced inflammatory cell (i.e. CD11b+ and F4/80+) recruitment, cytokine (i.e. TNFα, IL1α/β, IL6, CCL2, CXCL5) and pro-inflammatory enzymes (i.e. COX-2, NOS2) expression in the tumor microenvironment, while promoting recruitment of CD3+ T lymphocytes at 14 weeks. Emodin decreased the incidence of premalignant lesions (adenoma) at week 3, the incidence of dysplastic lesions and carcinomas at week 5, and the incidence, size and the invasiveness of carcinomas at week 14. Emodin also reduced the acute clinical intestinal symptoms (i.e. bleeding and diarrhea) during DSS treatment. In vitro, Emodin inhibited the expression of pro-inflammatory mediators by LPS-stimulated RAW 264.7 macrophages, and reduced viability, adhesion, migration, and fibroblasts-induced invasion of SW620 and HCT116 colon cancer cells. In conclusion, this work demonstrates that Emodin suppresses carcinogenesis-associated intestinal inflammation and prevents AOM/DSS-induced intestinal tumorigenesis and progression. These results instigate further studies on Emodin as a natural agent for the prevention or treatment of colorectal cancer.

is considered as an essential pathophysiologic factor and target in the context of MI. However, numerous clinical trials of post-MI immunomodulating/anti-inflammatory targets have shown inconclusive and controversial results. [3] Hence, studies are needed to understand what, how, and in what time frame the immune system is activated, providing a basis for modulating the immune-inflammatory mechanisms underlying the myocardial healing process.Cardiac immune cells are highly heterogeneous, and their activation in the progression of MI is distinct. [4] Some cell types such as macrophages and monocytes, which play a central role in multiple pathophysiological processes of MI, are comprised of diverse subsets because of their different origins and functions. [5] However, much less is known about the complex diversity of cardiac immunity. Recently, an innovative high-throughput technology, single-cell RNA sequencing (scRNA-seq), has increased our understanding of the major immune cell types in the mammalian heart and their dynamics during disease progression. Dick et al. [6] identified functionally distinct cardiac macrophage subsets that are hierarchically replaced by monocytes after infarction. Vafadarnejad et al. [7] revealed temporal diversity and local transition of neutrophils within the ischemic tissue. Moreover, Farbehi et al. [8] described the heterogeneity and dynamics of several cardiac immune Myocardial infarction (MI) is strongly associated with the temporal regulation of cardiac immunity. However, a variety of current clinical trials have failed because of the lack of post-MI immunomodulating/anti-inflammatory targets. Single-cell RNA sequencing analysis of the cardiac Cd45 + immune cell at 0, 3, 7, and 14 d after injury in a mouse left anterior descending coronary artery ligation model is performed. Major immune cell populations, distinct subsets, and dynamic changes are identified. Macrophages (Mø) are most abundant, peaking at 3 d after infarction. Mø-5 and Mø-6 are the predominant infiltrated subsets at this time point, with strong expression of inflammatory factors. Further analysis demonstrates that suppressing these sets attenuated pathological MI progression by preventing subsequent leukocyte extravasation and adverse remodeling. Abundant apoptotic neutrophils and a profibrotic macrophage subset on days 7 and 14, respectively, are also detected. These results provide a basis for developing cell type-and time-specific interventions in MI.The ORCID identification number(s) for the author(s) of this article can be found under https://doi.org/10.1002/smtd.202100752.

Communication between microglia and other cells has recently been at the forefront of research in central nervous system (CNS) disease. In this review, we provide an overview of the neuroinflammation mediated by microglia, highlight recent studies of crosstalk between microglia and CNS resident and infiltrating cells in the context of ischemic stroke (IS), and discuss how these interactions affect the course of IS. The in-depth exploration of microglia-intercellular communication will be beneficial for therapeutic tools development and clinical translation for stroke control.