General Information of MIC (ID: MIC00845)
MIC Name Mycobacteroides abscessus (actinobacteria)
MIC Synonyms Mycobacterium chelonei
Body Site Skin
Lineage Kingdom: Bacteria
Phylum: Actinobacteria
Class: Actinobacteria
Order: Corynebacteriales
Family: Mycobacteriaceae
Genus: Mycobacteroides
Species: Mycobacteroides abscessus
Oxygen Sensitivity Aerobe
Microbial Metabolism Respiratory
Gram Positive
Host Relationship Pathogen
Genome Size (bp) 4826045
Description Mycobacterium abscessus is an aerobic, Gram positive bacterium. It is the most pathogenic and chemotherapy-resistant rapidly growing mycobacteria. Mycobacterium abscessus causes severe, chronic pulmonary infections in susceptible hosts.
External Links Taxonomy ID
36809
Genome Assembly ID
ASM167721v1
GOLD Organism ID
Go0519494
Disease Relevance
          Chronic obstructive pulmonary disease  [ICD-11: CA22]
             Description Mycobacterium abscessus is an emerging pathogen capable of causing invasive pulmonary infections in patients with chronic lung diseases. [1]
          Cystic fibrosis  [ICD-11: CA25]
             Description Lung infections with Mycobacterium abscessus, a species of multidrug-resistant nontuberculous mycobacteria, are emerging as an important global threat to individuals with cystic fibrosis (CF), in whom M. abscessus accelerates inflammatory lung damage, leading to increased morbidity and mortality. [2]
          Tuberculosis  [ICD-11: 1B10]
             Description Tuberculosis is a contagious, infectious disease, due to Mycobacterium. [3]
Host Genetic Factors (HGFs)
          hsa-miR-146a-5p
             HGF ID HGF0252 HGF Info       Class Non-coding RNA: Micro (ncRNA-miRNA)
             Description The level of miR-146a expression is increased by Mycobacterium infection. [4]
          hsa-miR-21-5p
             HGF ID HGF0204 HGF Info       Class Non-coding RNA: Micro (ncRNA-miRNA)
             Description The level of miR-21 expression was induced by Mycobacterium species, leading to excessive immune responses. [5]
          rs77665588
             HGF ID HGF1434 HGF Info       Class Single Nucleotide Polymorphism: Intron variant (SNP-IV)
             Description The rs77665588 SNP in mucosal immunity pathways influences the abundance of Mycobacterium in the upper airway (p-value=1.30E-06). [6]
          rs1802665
             HGF ID HGF1930 HGF Info       Class Single Nucleotide Polymorphism: Prime UTR variant (SNP-PV)
             Description The rs1802665 SNP in mucosal immunity pathways influences the abundance of Mycobacterium in the upper airway (p-value=8.73E-08). [6]
Host Immune Factors (HIFs)
          Tumor necrosis factor
             HIF ID HIFM0226 HIF Info       Class Cytokine (Cyt)
             Description Mycobacterium abscessus could induce TNF-Alpha production through TLR2 and myeloid differentiation 88 signaling pathways. [7]
          Interferon gamma
             HIF ID HIFM0260 HIF Info       Class Cytokine (Cyt)
             Description IFN-Gamma is essential against Mycobacterium abscessus in the murine model. [7]
          Low affinity immunoglobulin gamma Fc region receptor II-a
             HIF ID HIFM0099 HIF Info       Class Fc Receptor (FCR)
             Description The FcgRIIA-R131 polymorphism increases susceptibility to a number of infections and that IgG and FcgRs promote defense against Mycobacterial infection. [8]
          Neutrophils
             HIF ID HIFC0029 HIF Info       Class Granulocytes (Gra)
             Description Neutrophils were important components in the host defense against Mycobacterium abscessus infection. [7]
          Macrophages
             HIF ID HIFC0020 HIF Info       Class Macrophages (Mac)
             Description Macrophages can polarize into two subtypes (M1 and M2) in response to Mycobacterium infections. [9]
          Dectin-1 signaling pathway
             HIF ID HIFP0006 HIF Info       Class Signaling pathway (SP)
             Description Mycobacterium abscessus activates the macrophage innate immune response via a physical and functional interaction between TLR2 and dectin-1. [7]
          T cells
             HIF ID HIFC0002 HIF Info       Class T cells (TCs)
             Description T cells were important components in the host defense against Mycobacterium abscessus infection. [7]
          Toll-like receptor 2
             HIF ID HIFM0217 HIF Info       Class Toll-like receptor (TLR)
             Description Mycobacterium abscessus induced TNF- production through TLR2 and myeloid differentiation 88 signaling pathways. [7]
References
1 Synergistic Efficacy of -Lactam Combinations against Mycobacterium abscessus Pulmonary Infection in Mice. Antimicrob Agents Chemother. 2019 Jul 25;63(8):e00614-19. doi: 10.1128/AAC.00614-19. Print 2019 Aug.
2 Emergence and spread of a human-transmissible multidrug-resistant nontuberculous mycobacterium. Science. 2016 Nov 11;354(6313):751-757. doi: 10.1126/science.aaf8156.
3 The history of tuberculosis: from the first historical records to the isolation of Koch's bacillus. J Prev Med Hyg. 2017 Mar;58(1):E9-E12.
4 miRNAs reshape immunity and inflammatory responses in bacterial infection. Signal Transduct Target Ther. 2018 May 25;3:14. doi: 10.1038/s41392-018-0006-9. eCollection 2018.
5 Commensal microbiota-induced microRNA modulates intestinal epithelial permeability through the small GTPase ARF4. J Biol Chem. 2017 Sep 15;292(37):15426-15433. doi: 10.1074/jbc.M117.788596. Epub 2017 Jul 31.
6 Host genetic variation in mucosal immunity pathways influences the upper airway microbiome.Microbiome. 2017 Feb 1;5(1):16. doi: 10.1186/s40168-016-0227-5.
7 Host immune response to rapidly growing mycobacteria, an emerging cause of chronic lung disease. Am J Respir Cell Mol Biol. 2010 Oct;43(4):387-93. doi: 10.1165/rcmb.2009-0276TR. Epub 2010 Jan 15.
8 Anti-commensal IgG Drives Intestinal Inflammation and Type 17 Immunity in Ulcerative Colitis. Immunity. 2019 Apr 16;50(4):1099-1114.e10. doi: 10.1016/j.immuni.2019.02.006. Epub 2019 Mar 12.
9 Mycobacterium marinum: a potential immunotherapy for Mycobacterium tuberculosis infection. Drug Des Devel Ther. 2013 Jul 29;7:669-80. doi: 10.2147/DDDT.S45197. Print 2013.

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