<i>Mycobacterium abscessus</i>: an emerging rapid‐growing potential pathogen

Petrini, Björn

doi:10.1111/j.1600-0463.2006.apm_390.x

Cited by 198 publications

(205 citation statements)

References 81 publications

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“…In other clinical situations, lung infection is progressive and refractory to antibiotic therapy, necessitating lung resection for cure (Griffith et al, 1993;Daley & Griffith, 2002;Sherwood et al, 2005). This latter clinical scenario has resulted in the view that M. abscessus is the most virulent of the rapidly growing mycobacteria that cause invasive lung infection (Petrini, 2006). One of our laboratories has focused their studies on three well-characterized isogenic M. abscessus variants; 390R (rough colony morphology), 390S (smooth colony morphology) and 390V (rough colony morphology).…”

Section: Introductionmentioning

confidence: 99%

Deletion of the mmpL4b gene in the Mycobacterium abscessus glycopeptidolipid biosynthetic pathway results in loss of surface colonization capability, but enhanced ability to replicate in human macrophages and stimulate their innate immune response

et al. 2011

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Mycobacterium abscessus is considered to be the most virulent of the rapidly growing mycobacteria. Generation of bacterial gene knockout mutants has been a useful tool for studying factors that contribute to virulence of pathogenic bacteria. Until recently, the optimal genetic approach to generation of M. abscessus gene knockout mutants was not clear. Based on the recent identification of genetic recombineering as the preferred approach, a M. abscessus mutant was generated in which the gene mmpL4b, critical to glycopeptidolipid synthesis, was deleted. Compared to the previously well-characterized parental strain 390S, the mmpL4B deletion mutant had lost sliding motility and the ability to form biofilm, but acquired the ability to replicate in human macrophages and stimulate macrophage Toll-like receptor 2. This study demonstrates that deletion of a gene associated with expression of a cell-wall lipid can result in acquisition of an immunostimulatory, invasive bacterial phenotype and has important implications for the study of M. abscessus pathogenesis at the cellular level.

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Section: Introductionmentioning

confidence: 99%

Deletion of the mmpL4b gene in the Mycobacterium abscessus glycopeptidolipid biosynthetic pathway results in loss of surface colonization capability, but enhanced ability to replicate in human macrophages and stimulate their innate immune response

et al. 2011

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“…Mycobacterium abscessus is a rapidly growing mycobacterium that is ubiquitously present in the soil and in both natural and potable water (1). Although most individuals are able to resist infection with M. abscessus, this organism can cause skin, soft tissue, and chronic lung infections that are often difficult to treat (1,2).…”

mentioning

confidence: 99%

“…Although most individuals are able to resist infection with M. abscessus, this organism can cause skin, soft tissue, and chronic lung infections that are often difficult to treat (1,2). Patients with cystic fibrosis may be chronically infected with M. abscessus, and the presence of this bacterium has been associated with a decline in lung function (3).…”

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confidence: 99%

“…Immunocompromised individuals are also more susceptible to M. abscessus infection. These infections are typically difficult to eradicate because the organism has an inherently high level of drug resistance (1). Indeed, the only class of oral drugs that has in vitro activity against M. abscessus is the second generation macrolides, clarithromycin and azithromycin (1).…”

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confidence: 99%

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The Antioxidant Mimetic, MnTE-2-PyP, Reduces Intracellular Growth of Mycobacterium abscessus

Oberley‐Deegan

Lee

Morey

et al. 2009

Am J Respir Cell Mol Biol

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Mycobacterium abscessus is a rapidly growing environmental mycobacterium that can cause severe skin, soft tissue, and lung infections. M. abscessus grows inside macrophages, and these cells release a vast number of proinflammatory cytokines in response to infections. The metalloporphyrin, MnTE-2-PyP, is a broad antioxidant that reduces inflammatory cell signaling. Macrophage-like THP-1 cells were infected with M. abscessus in the presence or absence of MnTE-2-PyP. MnTE-2-PyP significantly decreased, in a dose-dependent manner, the number of M. abscessus organisms recovered from infected THP-1 cells 4 and 8 days after infection. Furthermore, when combined with clarithromycin, MnTE-2-PyP additively reduced the number of cells associated with M. abscessus. A mechanism of bacterial growth inhibition by MnTE-2-PyP was then elucidated. It was found that MnTE-2-PyP promoted the survival of infected THP-1 cells and increased fusion of M. abscessus-containing phagosomes with lysosomes.

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“…It is considered to be the most virulent rapidly growing mycobacterium and is responsible for most pulmonary infections due to rapidly growing mycobacteria (1). M. abscessus has also been identified as an important pulmonary pathogen in patients with cystic fibrosis (2).…”

mentioning

confidence: 99%

Mycobacterium abscessus Glycopeptidolipids Mask Underlying Cell Wall Phosphatidyl-myo-Inositol Mannosides Blocking Induction of Human Macrophage TNF-α by Preventing Interaction with TLR2

Rhoades

Archambault²,

Greendyke³

et al. 2009

The Journal of Immunology

128

132

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Mycobacterium abscessus causes disease in patients with structural abnormalities of the lung, and it is an emerging pathogen in patients with cystic fibrosis. Colonization of the airways by nontuberculous mycobacteria is a harbinger of invasive lung disease. Colonization is facilitated by biofilm formation, with M. abscessus glycopeptidolipids playing an important role. M. abscessus can transition between a noninvasive, biofilm-forming, smooth colony phenotype that expresses glycopeptidolipid, and an invasive rough colony phenotype that expresses minimal amounts of glycopeptidolipid and is unable to form biofilms. The ability of this pathogen to transition between these phenotypes may have particular relevance to lung infection in cystic fibrosis patients since the altered pulmonary physiology of these patients makes them particularly susceptible to colonization by biofilm-forming bacteria. In this study we demonstrate that rough variants of M. abscessus stimulate the human macrophage innate immune response through TLR2, while smooth variants do not. Temperature-dependent loss or physical removal of glycopeptidolipid from the cell wall of one of the smooth variants leads to TLR2 stimulation. This response is stimulated in part through phosphatidyl-myo-inositol mannosides that are present in the cell wall of both rough and smooth variants. Mannose-binding lectins bind to rough variants, but lectin binding to an isogenic smooth variant is markedly reduced. This suggests that glycopeptidolipid in the outermost portion of the M. abscessus cell wall masks underlying cell wall lipids involved in stimulating the innate immune response, thereby facilitating colonization. Conversely spontaneous “unmasking” of cell wall lipids may promote airway inflammation.

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Mycobacterium abscessus: an emerging rapid‐growing potential pathogen

Cited by 198 publications

References 81 publications

Deletion of the mmpL4b gene in the Mycobacterium abscessus glycopeptidolipid biosynthetic pathway results in loss of surface colonization capability, but enhanced ability to replicate in human macrophages and stimulate their innate immune response

Deletion of the mmpL4b gene in the Mycobacterium abscessus glycopeptidolipid biosynthetic pathway results in loss of surface colonization capability, but enhanced ability to replicate in human macrophages and stimulate their innate immune response

The Antioxidant Mimetic, MnTE-2-PyP, Reduces Intracellular Growth of Mycobacterium abscessus

Mycobacterium abscessus Glycopeptidolipids Mask Underlying Cell Wall Phosphatidyl-myo-Inositol Mannosides Blocking Induction of Human Macrophage TNF-α by Preventing Interaction with TLR2

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