Progress in DNA-sensing pathways in Epstein-Barr virus infection / 中华微生物学和免疫学杂志

Epstein-Barr virus (EBV) is generally susceptible in human beings and multi-organ systems can be involved in EBV infection, such as blood, respiratory, urinary, digestive and nervous systems. EBV infection also plays an important role in the pathogenesis of related tumors, autoimmune diseases and other diseases, posing a great threat to human health. As a DNA virus, EBV can be sensed by DNA recognition receptors to trigger a series of downstream immune responses. A DNA-sensing pathway consists of DNA sensors, adaptor molecules and downstream effector signals. Double-stranded DNA sensors mainly include absent in melanoma 2-like receptors (ALRs) and cyclic GMP-AMP synthase (cGAS). Adaptors were mainly stimulator of interferon genes (STING) and apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC). Downstream immune responses mainly involve typeⅠIFN, inflammasomes and proinflammatory cytokines. As a double-stranded DNA virus of the Herpesviridae family, EBV triggers complex innate and adaptive immune responses in the host, especially the sensing pathways mediated by a variety of DNA recognition receptors, which play a key role in host immune defense and pathogen immune evasion. This review made the DNA sensor as the clue to comprehensively summarize the progress in the activation, regulatory mechanism and clinical relevance of DNA-sensing pathways in EBV infection in recent years, aiming to achieve a better understanding of the host innate immune responses during EBV infection and provide an immunological basis for the prevention and treatment of EBV infection-related diseases.

Lonicerin targets EZH2 to alleviate ulcerative colitis by autophagy-mediated NLRP3 inflammasome inactivation

Aberrant activation of NLRP3 inflammasome in colonic macrophages strongly associates with the occurrence and progression of ulcerative colitis. Although targeting NLRP3 inflammasome has been considered to be a potential therapy, the underlying mechanism through which pathway the intestinal inflammation is modulated remains controversial. By focusing on the flavonoid lonicerin, one of the most abundant constituents existed in a long historical anti-inflammatory and anti-infectious herb

Significance of expression of AIM2, IL / 中南大学学报(医学版)

OBJECTIVES@#Inflammation especially the overexpression of inflammasome and inflammatory cytokines, is one of the important reasons that affect the occurrence and development of acute cerebral infarction, including the initiation of cerebral infarction, the progress and recovery of post-infarction injury. This study aims to explore expressions of absent in melanoma 2 (AIM2), interleukin-1β (IL-1β), and interleukin-18 (IL-18) in plasma of patients with acute cerebral infarction and its significance.@*METHODS@#A total of 85 patients with acute cerebral infarction were enrolled in the cerebral infarction group. They were assigned into mild, moderate, and severe groups according to the severity of neurological deficits. They were assigned into small, middle, and large cerebral infarction groups according to the area of cerebral infarction. They were assigned into a good prognosis group and a poor prognosis group according to the Modified Rankin Scale (mRS) score on the 90th day after the onset. A total of 85 healthy controls were selected as a control group. The levels of AIM2, IL-1β, and IL-18 in plasma of the cerebral group and the control group were detected by enzyme-linked immunosorbent assay (ELISA).@*RESULTS@#The levels of plasma AIM2, IL-1β, and IL-18 in the cerebral infarction group were significantly higher than those in the control group (all @*CONCLUSIONS@#Expressions of AIM2, IL-1β, and IL-18 are up-regulated in the plasma of patients with acute cerebral infarction, and they are closely related to the severity of neurological deficit, cerebral infarction area, and prognosis in patients with acute cerebral infarction, suggesting that AIM2, IL-1β, and IL-18 may play an important role in the occurrence and development of acute cerebral infarction.

Research advances of absent in melanoma 2 in the development of cancer / 医学研究生学报

Absent in melanoma 2 (AIM2) is a cytoplasmic protein, which can identify and combine with the cytoplasmic dsDNA to activate caspase-1, and promote the maturation and release of IL-1β and IL-18, or induce pyroptosis.AIM2 belongs to the innate immune system and is the first line of defense to protect the body against the invasion of alien microbes.After identifying the pathogenic microorganisms, the activation of the host signal caused the reaction, which started microorganisms.The activation of the host signal caused the reaction, which started the innate immune and acquired immune response.Research also suggests that AIM2 plays an important role in the occurrence and development of tumor, which was abnormally expressed in many malignant tumors such as prostatic cancer, colorectal cancer, breast cancer, nasopharyngeal carcinoma, oral squamous cell carcinoma, non small cell lung cancer, and AIM2 plays different roles in the progression of different tumor.This article will summarize the research progress of AIM2 in innate immunity and tumor development.

Research progress on absent in melanoma 2 in defending pathogenic microorganism invasion / 中华临床感染病杂志

Innate immunity is on the frontline of fight against pathogenic microorganism invasion .As a DNA sensor, absent in melanoma 2 (AIM2) is an important member of innate immune system.It can recognize dsDNA of pathogenic microbes to form AIM 2 inflammasomes , which facilitates defending and clearing the invasion of pathogens by activating caspase-1 dependent pyroptosis and the mature of IL-18 and IL-1β.AIM2 inflammasomes play an important part in responding to Listeria monocytogenes, Francisella tularensis, Streptococcus pneumoniae, Mycobacterium tuberculosis, Aspergillus fumigatus, vaccinia virus , murine cytomegalovirus , and hepatitis B virus infections .This paper introduces the components of AIM 2 inflammasomes and summarizes its function in defending the invasion of pathogenic microorganisms .

Molecular mechanisms of absent in melanoma AIM2 inducing breast cancer cell apoptosis / 医学研究生学报

Objective The human IFN-inducible protein absent in melanoma 2 (AIM2) has been regarded as a tumour sup-pressor, however, the molecular mechanisms of its antitumor activity still remain unclear.This research is to study the molecular mech-anisms of AIM2 inducing breast cancer cell apoptosis. Methods Tet-Off induction model system was established to induce AIM2 ex-pression in great quantities, MCF-7 tTA-AIM2 cells as the experimental group and MCF-7 tTA-Luc cells as control group.Western blotting was used to detect AIM2 expression in breast cancer cell lines and subcellular localization.XTT assay was applied to analyze the effects of AIM2 on cell proliferation.Apoptosis were detected by Annexin V-FITC and propidium iodide staining, and the apoptosis mechanism were investigated by west blot. Results The established Tet-off guidance system could combine tTA to TRE, thereby promoting AIM2 gene transcription and inducing great expression of AIM2 protein.4 days after induction, the expression of AIM2 could be detected in cytoplasm and nucleus, and AIM2 expression increased with the increasing days.XTT assay detected the growth speed of MCF-7 tTA-AIM2 cell lines slowed down 6 days after induction.After abundant expression of induced AIM2, the percentage of FITC fluorescence apoptosis increased significantly (2.36%vs 14.45%, P<0.01) .Increased AIM2 expression inhibited the expression of the anti-apoptotic protein Bcl-xL, increased the expression of the apoptosis proteins Bad and Bax, and activated caspases, resulting in the cleavage of DNA repair protein PARP. Conclusion In breast cancer Tet-off induction system, AIM2 will express in cytoplasm and nucleus, influence cell proliferation, and stimulate the mitochondria to cell apoptosis.