Article
Immunology
Yurong Cai, Weifeng Gao, Pu Wang, Gang Zhang, Xiaoping Wang, Lingling Jiang, Jin Zeng, Yujiong Wang, Zhiwei Wu, Yong Li
Summary: This study investigated the differential responses of bovine alveolar macrophages to Mycobacterium tuberculosis and Mycobacterium bovis infection at the protein level. The results revealed different mechanisms used by the macrophages to resist the two pathogens, and identified activated proteins and signaling pathways associated with autophagy, inflammation, and energy metabolism. These findings provide critical insights into TB pathogenesis and potential biomarkers for more effective treatment strategies. The study also supports the hypothesis of cross-species transmission of MTB.
FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY
(2023)
Review
Immunology
Victor Bonavida, Mitchell Frame, Kevin H. Nguyen, Shlok Rajurkar, Vishwanath Venketaraman
Summary: Several reports suggest that ageing negatively affects the human immune system and increases susceptibility to infections like Mycobacterium tuberculosis (M. tb). This article explores how ageing decreases T-cell immune response, reduces glutathione production, over activates the mTORC1 pathway, inhibits autophagy and mitophagy, and alters protective genes/transcription factors. It also highlights a potential defect in antigen presenting by dendritic cells and the role of inflammaging in increasing susceptibility to M. tb infection. Possible preventative strategies, such as immunomodulators and antioxidant supplementation, are proposed.
Article
Immunology
Jun Fang, Chunsheng Dong, Sidong Xiong
Summary: This study demonstrates that Rv0790c, a protein encoded by Mycobacterium tuberculosis, promotes bacterial survival by facilitating cellular autophagy at its early stage. This finding provides insights into the mechanisms through which Mycobacterium tuberculosis evades host immune responses and offers potential targets for tuberculosis treatment.
FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY
(2022)
Article
Microbiology
Xi Chen, Xiaojian Cao, Yingying Lei, Aikebaier Reheman, Wei Zhou, Bing Yang, Weipan Zhang, Weize Xu, Shuang Dong, Rohit Tyagi, Zhen F. Fu, Gang Cao
Summary: Mycobacterium tuberculosis can inhibit lysosome acidification in certain cell lines, but in others, it is targeted to acidified phagolysosomes. The gene profile analysis identified the role of ITGB3 in promoting M. tuberculosis clearance in endothelial cells, suggesting a new defense mechanism against the pathogen.
Article
Immunology
Srabasti Sengupta, Barsa Nayak, Michael Meuli, Peter Sander, Snehasish Mishra, Avinash Sonawane
Summary: This study reveals a previously unknown mechanism in which Mycobacterium tuberculosis inhibits autophagy by inducing histone hypermethylation in autophagy-related genes, promoting intracellular bacterial survival.
FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY
(2021)
Article
Immunology
Yuliang Qu, Qian Gao, Shan Wu, Tao Xu, Dan Jiang, Guangxian Xu
Summary: miR-142-3p inhibits M. tuberculosis-induced activation of autophagy, promotes H37Ra survival in macrophages, and exerts its function by targeting ATG16L1 and ATG4c.
INTERNATIONAL IMMUNOPHARMACOLOGY
(2021)
Review
Cell Biology
Anmol Raien, Sofia Davis, Michelle Zhang, David Zitser, Michelle Lin, Graysen Pitcher, Krishna Bhalodia, Selvakumar Subbian, Vishwanath Venketaraman
Summary: The phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (P13K/AKT/mTOR) pathway is crucial in tuberculosis (TB) pathogenesis and infection. Manipulating this pathway has potential benefits for host-directed therapies. The mTOR inhibitor everolimus shows promise in TB treatment by reducing glycolytic activity and mitigating lung inflammation.
Review
Immunology
Jie Zhou, Jingzhu Lv, Chelsea Carlson, Hui Liu, Hongtao Wang, Tao Xu, Fengjiao Wu, Chuanwang Song, Xiaojing Wang, Ting Wang, Zhongqing Qian
Summary: The pathogen Mycobacterium tuberculosis causes tuberculosis, which poses a significant human public health threat. Trained immunity has been found to have the capability to control and eliminate M. tuberculosis infection, providing new possibilities for vaccine development. Autophagy plays an essential role in the development of trained immunity, contributing to the prevention of M. tuberculosis infection.
EMERGING MICROBES & INFECTIONS
(2021)
Review
Infectious Diseases
Pavan Kumar Nagdev, Puja Kumari Agnivesh, Arnab Roy, Shashikanta Sau, Nitin Pal Kalia
Summary: This article discusses the current challenges of tuberculosis treatment and the potential of autophagy in improving treatment outcomes. It suggests that by inhibiting autophagy-blocking factors and mechanisms, chemotherapeutics that induce autophagy could be identified and used as adjunctive therapy for multidrug-resistant and extreme drug-resistant tuberculosis.
EUROPEAN JOURNAL OF CLINICAL MICROBIOLOGY & INFECTIOUS DISEASES
(2023)
Article
Medicine, Research & Experimental
Yiming Wu, Xue Lin, Fuyang Song, Di Xue, Yujiong Wang
Summary: This study found that vitamin D3 can activate cell autophagy signals by inhibiting the concentration of Ca2+, and effectively alleviate cellular damage caused by M.tb infection.
EXPERIMENTAL AND THERAPEUTIC MEDICINE
(2022)
Article
Oncology
Yiling Gan, Qianfang Hu, Anmao Li, Lei Gu, Shuliang Guo
Summary: Tracheobronchial tuberculosis (TBTB) is most common in young, middle-aged females. Despite adequate anti-tuberculosis therapy, tracheobronchial stenosis still occurs in most patients, leading to a high disability rate. This study investigated the role of estradiol in the development of TBTB and found that estradiol may play a key role through binding to ER alpha.
MOLECULAR MEDICINE REPORTS
(2022)
Article
Medicine, Research & Experimental
Youchao Dai, Chuanzhi Zhu, Wei Xiao, Kaisong Huang, Xin Wang, Chenyan Shi, Dachuan Lin, Huihua Zhang, Xiaoqian Liu, Bin Peng, Yi Gao, Cui Hua Liu, Baoxue Ge, Stefan H. E. Kaufmann, Carl G. Feng, Xinchun Chen, Yi Cai
Summary: Ferritin regulates iron homeostasis in macrophages and defends against Mycobacterium tuberculosis (Mtb) infection. NCOA4 is a cargo receptor involved in ferritin degradation, and Mtb infection enhances NCOA4-mediated ferritin degradation in macrophages, promoting bacterial growth. Clinical data also shows that the upregulation of FTH1 in macrophages is associated with tuberculosis (TB) disease progression. Mechanistically, Mtb infection enhances NCOA4-mediated ferritin degradation through the degradation of HERC2, an E3 ligase of NCOA4. Furthermore, NCOA4 deficiency in myeloid cells accelerates the clearance of Mtb infection in a murine model. These findings suggest that targeting host ferritin metabolism could be a potential strategy for host-directed therapy against tuberculosis.
JOURNAL OF CLINICAL INVESTIGATION
(2023)
Review
Immunology
Retsepile E. Maphasa, Mervin Meyer, Admire Dube
Summary: This review focuses on macrophage responses to Mtb infection, particularly the mechanistic aspects of autophagy and how intracellular Mtb evades autophagy. The relationship between autophagy and apoptosis is also discussed, along with known autophagy inducing compounds for Mtb infection. The use of nanoparticles to induce autophagy is explored as a potential avenue for further research into nanomedicine HDTs for TB therapy.
FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY
(2021)
Article
Immunology
SiJia Geng, PengFei Hao, Di Wang, Pengfei Zhong, Fangfang Tian, Rui Zhang, Juan Qiao, Xiaochen Qiu, Pengtao Bao
Summary: This study aimed to investigate the antibacterial mechanisms of zinc oxide nanoparticles (ZnONPs) against Mycobacterium tuberculosis (M. tb). In vitro activity assays showed that ZnONPs had minimum inhibitory concentrations (MICs) of 0.5-2 mg/L against all tested M. tb strains. The expression levels of autophagy and ferroptosis-related markers were measured in BCG-infected macrophages exposed to ZnONPs, and BCG-infected mice were used to determine the in vivo functions of ZnONPs. ZnONPs reduced the number of bacteria engulfed by macrophages in a dose-dependent manner and had varying effects on inflammation. Low doses of ZnONPs activated autophagy mechanisms, while high doses enhanced ferroptosis. Co-administration of a ferroptosis inhibitor improved the anti-Mycobacterium activity of ZnONPs in an in vivo mouse model. Based on these findings, ZnONPs have potential as antibacterial agents in future animal and clinical studies.
MICROBIAL PATHOGENESIS
(2023)
Article
Immunology
Mohammad Aqdas, Sanpreet Singh, Mohammed Amir, Sudeep Kumar Maurya, Susanta Pahari, Javed Naim Agrewala
Summary: The study observed that MSC stimulated through TLR-4 and NOD-2 (N2.T4) activated MSC and augmented the secretion of pro-inflammatory cytokines, co-localized Mtb in the lysosomes, induced autophagy, enhanced NF-kappa B activity via p38 MAPK signaling pathway, and significantly reduced the intracellular survival of Mtb in the MSC. Overall, the results suggest that triggering through N2.T4 may be a future method of immunotherapy to eliminate the Mtb concealed inside the MSC.
FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY
(2021)
Article
Cell Biology
Ke Mi, Lizhong Zeng, Yang Chen, Jingya Ning, Siyuan Zhang, Peilin Zhao, Shuanying Yang
Summary: In this study, the researchers explored the role of DHX38 in NSCLC and its underlying molecular mechanism. They found that DHX38 was overexpressed in NSCLC and patients with high DHX38 expression had poor prognosis. DHX38 promoted cell proliferation, migration, and invasion in NSCLC and activated the MAPK pathway. The researchers also identified G3BP1 as a target protein that interacted with DHX38 and showed that DHX38 regulated the expression of G3BP1. Silencing G3BP1 reversed the effects of DHX38 overexpression on tumor cell proliferation, migration, and invasion and inhibited the MAPK pathway activation.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Tiina A. Jokela, Mark A. Dane, Rebecca L. Smith, Kaylyn L. Devlin, Sundus Shalabi, Jennifer C. Lopez, Masaru Miyano, Martha R. Stampfer, James E. Korkola, Joe W. Gray, Laura M. Heiser, Mark A. Labarge
Summary: Microenvironment signals have a significant impact on cell fate and tissue homeostasis. Understanding how different microenvironment factors regulate cellular phenotype has been challenging. In this study, a high-throughput microenvironment microarray was used to identify factors that support the proliferation and maintenance of primary human mammary luminal epithelial cells. Multiple factors that modulate luminal cell number were identified and their effects were confirmed using RNA sequencing and cell-based functional studies. Hepatocyte growth factor (HGF) was found to be robust to individual variation and played a role in expanding luminal cells. Our approach demonstrates the power of high-dimensional cell-based approaches in dissecting microenvironmental signals.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Chao He, Yongfeng Ding, Yan Yang, Gang Che, Fei Teng, Haohao Wang, Jing Zhang, Donghui Zhou, Yanyan Chen, Zhan Zhou, Haiyong Wang, Lisong Teng
Summary: This study categorized gastric cancer patients into three stemness subtypes, each demonstrating distinct prognoses, components of tumor microenvironment (TME) infiltration, and varying sensitivity or resistance to treatment. A stemness risk model was constructed to predict treatment response and prognosis.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Haile Zhao, Lijuan Feng, Rui Cheng, Man Wu, Xiaozhou Bai, Lifei Fan, Yaping Liu
Summary: miR-29c-3p is overexpressed in benign and malignant ovarian carcinoma and is associated with poor prognosis. Its overexpression modulates tumorigenesis in ovarian cancer cells, including epithelial-mesenchymal transition, proliferation, migration, and invasion, through the regulation of DNMT3A, TET1, and HBP1. miR-29c-3p may serve as a potential biomarker for clinical diagnosis or co-diagnosis of ovarian carcinoma.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Haiyan Zhao, Fangfang Bi, Mengyuan Li, Yuhan Diao, Chen Zhang
Summary: This study confirmed the tumor suppressor effect of RNF180 on ovarian cancer, elucidated the mechanism of the molecule network related to RNF180 and IPO4 in ovarian cancer, and identified a new therapeutic target for ovarian cancer.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Chu Chen, Guanhua Xu, Jiajia Chen, Chunshuai Wu, Jinlong Zhang, Jiawei Jiang, Hongxiang Hong, Zhiming Cui
Summary: This study investigated the role of transcription factor FoxO1 in facet joint osteoarthritis (FJOA) and found that FoxO1 deletion led to severe osteoarthritic changes. Transcriptome sequencing and bioinformatics analysis identified differentially expressed genes (DEGs) and potential key contributors to FJOA. Additionally, over-expression of certain genes and inhibition of others were shown to counteract the impairments caused by FoxO1 deletion in chondrocyte migration and extracellular matrix synthesis. These findings help unravel the molecular mechanisms underlying FJOA and open up promising therapeutic avenues for its treatment.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Wen Deng, Ru Chen, Situ Xiong, Jianqiang Nie, Hailang Yang, Ming Jiang, Bing Hu, Xiaoqiang Liu, Bin Fu
Summary: This study demonstrates that circFSCN1 is upregulated in bladder cancer and associated with cancer-specific survival. CircFSCN1 promotes tumor progression and epithelial-mesenchymal transition in bladder cancer through enhancing MDM2-mediated silencing of p53 by sponging miR-145-5p.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Jun Wu, Weibin Hu, Wenhui Yang, Yihao Long, Kaizhao Chen, Fugui Li, Xiaodong Ma, Xun Li
Summary: Cholesterol biosynthesis and metabolism play critical roles in tumor development and microenvironmental conditions. Squalene Epoxidase (SQLE), the second rate-limiting enzyme in cholesterol synthesis, is found to be uniquely expressed in various cancers, and its expression level is closely associated with tumor mutation burden and microsatellite instability. SQLE expression is negatively correlated with immune cell infiltration. Inhibition of SQLE alters the immune response in the tumor microenvironment. Furthermore, protein metabolism and translation are identified as main binding factors with SQLE.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Zhihong Zhang, Mingyue Li, Yi Tai, Yue Xing, Hongxiang Zuo, Xuejun Jin, Juan Ma
Summary: ZNF70 plays an important role in colitis-associated colorectal cancer (CAC) by regulating macrophages IL-1 beta secretion to promote HCT116 proliferation. It may serve as a promising target for treating CAC.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Zenghong Wu, Gangping Li, Weijun Wang, Kun Zhang, Mengke Fan, Yu Jin, Rong Lin
Summary: This study comprehensively explored the role of immune checkpoints and tumor microenvironment in gastric cancer patients based on genomic data. It constructed an ICIs signature and ICI score to evaluate patient prognosis and heterogeneity.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Yantong Wan, Jieshu Zhou, Panpan Zhang, Xuemei Lin, Hao Li
Summary: This study found that Rac1 plays a role in astrocyte activation and attenuates chronic inflammatory pain by blocking the phosphorylation of NLRP3 inflammasome and NF-kappa B.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Zhen Wang, Diankun She, Lei Liu, Xianming Hua, Hao Zhu, Lingfeng Yu, Han Wang, Yan Zhu, Gentao Fan, Yicun Wang, Meng Xu, Guangxin Zhou
Summary: Circular RNAs (circRNAs) are non-coding RNAs that play a role in the regulation of various cancers, including osteosarcoma (OS). This study identified circSATB2 as a highly expressed circRNA in OS tissues and cell lines, and demonstrated its involvement in promoting OS proliferation and migration. Mechanistically, circSATB2 was found to regulate the progression of OS by sponging miR-661 and FUS to regulate ZNFX1 mRNA. These findings suggest that circSATB2 could serve as a prognostic marker and therapeutic target for osteosarcoma.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Kenichi Ogata, Masafumi Moriyama, Tatsuya Kawado, Hiroki Yoshioka, Aiko Yano, Mayu Matsumura-Kawashima, Seiji Nakamura, Shintaro Kawano
Summary: This study found that extracellular vesicles released by induced pluripotent stem cells can reduce inflammatory cell infiltration, increase saliva volume, and decrease the production of antibodies associated with Sjogren's syndrome in a mouse model. The let-7 family in these vesicles may suppress the expression of TLR4 and NF-kappa B, which leads to the inhibition of pro-inflammatory cytokine production through the MAPK pathway.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Mikayla R. Erdelsky, Sarah A. Groves, Charmi Shah, Samantha B. Delios, M. Bibiana Umana, Donald H. Maurice
Summary: Recent evidence suggests that cAMP signaling within the primary cilium plays a crucial role in promoting adipogenic differentiation of 3T3-L1 preadipocytes. In this study, the researchers identified the specific cAMP phosphodiesterases expressed by these cells and found that inhibition of PDE4 promotes FFAR4-mediated adipogenesis. This work could potentially lead to the discovery of more targeted therapeutic approaches for controlling adipogenesis and differentiation of other stem cells.
CELLULAR SIGNALLING
(2024)
Article
Cell Biology
Chun-Hui Liu, Jun-Jie Zhang, Qian-Jin Zhang, Yang Dong, Zhen-Duo Shi, Si-Hao Hong, Hou-Guang He, Wei Wu, Cong-Hui Han, Lin Hao
Summary: Bladder cancer, the most common malignant tumor in the urinary system, is associated with significantly up-regulated expression of P3H4, which is regulated by METTL3 and plays a crucial role in the proliferation, metastasis, and EMT progression of bladder cancer. Targeting this METTL3-P3H4 pathway may serve as a potential therapeutic strategy for bladder cancer.
CELLULAR SIGNALLING
(2024)