Inflammasome Activation and Function During Infection with Mycobacterium Tuberculosis

The development of effective innate and subsequent adaptive host immune responses is highly dependent on the production of proinflammatory cytokines that increase the activity of immune cells. The key role in this process is played by inflammasomes, multimeric protein complexes serving as a platform for caspase-1, an enzyme responsible for proteolytic cleavage of IL-1βand IL-18 precursors. Inflammasome activation, which triggers the multifaceted activity of these two proinflammatory cytokines, is a prerequisite for developing an efficient inflammatory response against pathogenicMycobacterium tuberculosis(M.tb). This review focuses on the role of NLRP3 and AIM2 inflammasomes inM.tb-driven immunity.

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The thick waxy coat of mycobacteria, a protective layer against antibiotics and the host's immune system

Biochemical Journal ◽

10.1042/bcj20200194 ◽

2020 ◽

Vol 477 (10) ◽

pp. 1983-2006 ◽

Cited By ~ 1

Author(s):

Sarah M. Batt ◽

David E. Minnikin ◽

Gurdyal S. Besra

Keyword(s):

Infectious Disease ◽

Cell Wall ◽

Mycobacterium Tuberculosis ◽

Immune System ◽

Mortality Rate ◽

Cell Envelope ◽

Protective Layer ◽

Structure And Function ◽

Complex Lipids ◽

And Function

Tuberculosis, caused by the pathogenic bacterium Mycobacterium tuberculosis (Mtb), is the leading cause of death from an infectious disease, with a mortality rate of over a million people per year. This pathogen's remarkable resilience and infectivity is largely due to its unique waxy cell envelope, 40% of which comprises complex lipids. Therefore, an understanding of the structure and function of the cell wall lipids is of huge indirect clinical significance. This review provides a synopsis of the cell envelope and the major lipids contained within, including structure, biosynthesis and roles in pathogenesis.

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Helminth Coinfection Alters Monocyte Activation, Polarization, and Function in Latent Mycobacterium tuberculosis Infection

The Journal of Immunology ◽

10.4049/jimmunol.1901127 ◽

2020 ◽

Vol 204 (5) ◽

pp. 1274-1286

Author(s):

Anuradha Rajamanickam ◽

Saravanan Munisankar ◽

Chandrakumar Dolla ◽

Pradeep A. Menon ◽

Thomas B. Nutman ◽

...

Keyword(s):

Mycobacterium Tuberculosis ◽

Tuberculosis Infection ◽

Monocyte Activation ◽

Mycobacterium Tuberculosis Infection ◽

And Function

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Mutual Interplay of Host Immune System and Gut Microbiota in the Immunopathology of Atherosclerosis

International Journal of Molecular Sciences ◽

10.3390/ijms21228729 ◽

2020 ◽

Vol 21 (22) ◽

pp. 8729 ◽

Cited By ~ 1

Author(s):

Chih-Fan Yeh ◽

Ying-Hsien Chen ◽

Sheng-Fu Liu ◽

Hsien-Li Kao ◽

Ming-Shiang Wu ◽

...

Keyword(s):

Immune System ◽

Immune Responses ◽

Cytokine Production ◽

Current Knowledge ◽

Inflammatory Diseases ◽

Inflammasome Activation ◽

Host Immune System ◽

Gut Permeability ◽

And Function ◽

Progression Of Atherosclerosis

Inflammation is the key for the initiation and progression of atherosclerosis. Accumulating evidence has revealed that an altered gut microbiome (dysbiosis) triggers both local and systemic inflammation to cause chronic inflammatory diseases, including atherosclerosis. There have been some microbiome-relevant pro-inflammatory mechanisms proposed to link the relationships between dysbiosis and atherosclerosis such as gut permeability disruption, trigger of innate immunity from lipopolysaccharide (LPS), and generation of proatherogenic metabolites, such as trimethylamine N-oxide (TMAO). Meanwhile, immune responses, such as inflammasome activation and cytokine production, could reshape both composition and function of the microbiota. In fact, the immune system delicately modulates the interplay between microbiota and atherogenesis. Recent clinical trials have suggested the potential of immunomodulation as a treatment strategy of atherosclerosis. Here in this review, we present current knowledge regarding to the roles of microbiota in contributing atherosclerotic pathogenesis and highlight translational perspectives by discussing the mutual interplay between microbiota and immune system on atherogenesis.

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Characterization and function of Mycobacterium tuberculosis H37Rv Lipase Rv1076 (LipU)

Microbiological Research ◽

10.1016/j.micres.2016.12.005 ◽

2017 ◽

Vol 196 ◽

pp. 7-16 ◽

Cited By ~ 10

Author(s):

Chunyan Li ◽

Qiming Li ◽

Yuan Zhang ◽

Zhen Gong ◽

Sai Ren ◽

...

Keyword(s):

Mycobacterium Tuberculosis ◽

Tuberculosis H37rv ◽

Mycobacterium Tuberculosis H37rv ◽

And Function

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Mycobacterium tuberculosis Prevents Inflammasome Activation

Cell Host & Microbe ◽

10.1016/j.chom.2008.03.003 ◽

2008 ◽

Vol 3 (4) ◽

pp. 224-232 ◽

Cited By ~ 265

Author(s):

Sharon S. Master ◽

Silvana K. Rampini ◽

Alexander S. Davis ◽

Christine Keller ◽

Stefan Ehlers ◽

...

Keyword(s):

Mycobacterium Tuberculosis ◽

Inflammasome Activation

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The interplay of the type II TA system with other processes

10.7287/peerj.preprints.27770v2 ◽

2019 ◽

Author(s):

Wei Wen-ping ◽

Jia Wan Zhong ◽

Yang Min

Keyword(s):

Mycobacterium Tuberculosis ◽

Environmental Stress ◽

Regulatory Mechanism ◽

Phage Infection ◽

Type Ii ◽

System Research ◽

Cellular Processes ◽

The Stability ◽

And Function ◽

Insight Into

The type II toxin antitoxin (TA) system is the most well-studied TA system and is widely distributed in bacteria, especially pathogens such as Mycobacterium tuberculosis. Type II TA system plays an important role in many cellular processes, including maintaining the stability of mobile genetic elements, and bacterial altruistic suicide in response to nutritional starvation, environmental stress and phage infection. Interactions between toxin proteins and antitoxin proteins are critical for the regulation and function of type II TA systems; indeed, the understanding of their function is mainly derived from interaction and regulation of paired TA system proteins. Nonetheless, investigating interaction between unpaired TA system proteins, and the interaction between TA system proteins and other functional proteins, are becoming more common and have provided new insight into the complexity of its regulatory mechanism. In this review, we outlined the cross-interaction between TA system proteins, and the interaction between TA system proteins and other functional proteins, and we are trying to explain novel mechanism of TA system in the regulation of cellular activities. On this basis, we further discussed the knowledge and physiological implications of the relevant aspects of TA system research.

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Immunometabolic modulation of retinal inflammation by CD36 ligand

Scientific Reports ◽

10.1038/s41598-019-49472-8 ◽

2019 ◽

Vol 9 (1) ◽

Cited By ~ 7

Author(s):

Katia Mellal ◽

Samy Omri ◽

Mukandila Mulumba ◽

Houda Tahiri ◽

Carl Fortin ◽

...

Keyword(s):

Mononuclear Phagocytes ◽

Inflammasome Activation ◽

Peroxisome Proliferator ◽

Dependent Manner ◽

Peroxisome Proliferator Activated Receptor ◽

Pyrin Domain ◽

Ppar Γ ◽

Injury Characteristic ◽

And Function ◽

Cluster Of Differentiation

Abstract In subretinal inflammation, activated mononuclear phagocytes (MP) play a key role in the progression of retinopathies. Little is known about the mechanism involved in the loss of photoreceptors leading to vision impairment. Studying retinal damage induced by photo-oxidative stress, we observed that cluster of differentiation 36 (CD36)-deficient mice featured less subretinal MP accumulation and attenuated photoreceptor degeneration. Moreover, treatment with a CD36-selective azapeptide ligand (MPE-001) reduced subretinal activated MP accumulation in wild type mice and preserved photoreceptor layers and function as assessed by electroretinography in a CD36-dependent manner. The azapeptide modulated the transcriptome of subretinal activated MP by reducing pro-inflammatory markers. In isolated MP, MPE-001 induced dissociation of the CD36-Toll-like receptor 2 (TLR2) oligomeric complex, decreasing nuclear factor-kappa B (NF-κB) and NLR family pyrin domain containing 3 (NLRP3) inflammasome activation. In addition, MPE-001 caused an aerobic metabolic shift in activated MP, involving peroxisome proliferator-activated receptor-γ (PPAR-γ) activation, which in turn mitigated inflammation. Accordingly, PPAR-γ inhibition blocked the cytoprotective effect of MPE-001 on photoreceptor apoptosis elicited by activated MP. By altering activated MP metabolism, MPE-001 decreased immune responses to alleviate subsequent inflammation-dependent neuronal injury characteristic of various vision-threatening retinal disorders.

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