Isolation of mycolic acid-containing glycolipids in Nocardia rubra and their granuloma forming activity in mice.

Yano, Ikuya; Tomiyasu, Ikuko; Kaneda, Kenji; Kato, Yoshiko; Sumi, Yukie; Kurano, Satoko; Sugimoto, Nobuko; Sawai, Hirofumi

doi:10.1248/bpb1978.10.113

Cited by 22 publications

(21 citation statements)

References 33 publications

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“…The amino acid side chains consist of diamidated L-alanine-D-ct-glutamine-meso-DAP tripeptides and L-alanine-D-ct-glutaminemeso-DAP-D-alanine tetrapeptides (29,688 333-336, 412, 469, 614). This trehalose-6,6'-dimycolate (cord factor) has specific biologic activity; it is toxic, it inhibits calcium-dependent membrane fusion, it inhibits phagosome-lysosome fusion in macrophages, and it appears to be associated with nocardial virulence (336,615,629,630,661,729). Furthermore, there are specific additional fatty acids and mycolic acids firmly linked to the cell wall.…”

Section: Mechanisms Of Nocardl4 Pathogenesismentioning

confidence: 99%

Nocardia species: host-parasite relationships

1994

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The nocardiae are bacteria belonging to the aerobic actinomycetes. They are an important part of the normal soil microflora worldwide. The type species, Nocardia asteroides, and N. brasiliensis, N. farcinica, N. otitidiscaviarum, N. nova, and N. transvalensis cause a variety of diseases in both normal and immunocompromised humans and animals. The mechanisms of pathogenesis are complex, not fully understood, and include the capacity to evade or neutralize the myriad microbicidal activities of the host. The relative virulence of N. asteroides correlates with the ability to inhibit phagosome-lysosome fusion in phagocytes; to neutralize phagosomal acidification; to detoxify the microbicidal products of oxidative metabolism; to modify phagocyte function; to grow within phagocytic cells; and to attach to, penetrate, and grow within host cells. Both activated macrophages and immunologically specific T lymphocytes constitute the major mechanisms for host resistance to nocardial infection, whereas B lymphocytes and humoral immunity do not appear to be as important in protecting the host. Thus, the nocardiae are facultative intracellular pathogens that can persist within the host, probably in a cryptic form (L-form), for life. Silent invasion of brain cells by some Nocardia strains can induce neurodegeneration in experimental animals; however, the role of nocardiae in neurodegenerative diseases in humans needs to be investigated.

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Section: Mechanisms Of Nocardl4 Pathogenesismentioning

confidence: 99%

Nocardia species: host-parasite relationships

1994

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“…Figure 1 shows the chemical structure of GaGM (27). Trehalose 6,6'dimycolate was also isolated from Nocardia rubra (NrTDM) as described in our previous reports (12,28,29). Liposome preparation.…”

Section: Methodsmentioning

confidence: 71%

Induction of Interferons (IFNs) and Tumor Necrosis Factor (TNF) in Mice by a Novel Glycolipid Trehalose 2,3,6′‐Trimycolate from Rhodococcus aurantiacus (Gordona aurantiaca)

Fujita¹,

Sugimoto²,

Yokoi³

et al. 1990

Microbiology and Immunology

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“…the main components are phthiocerol-containing lipids, phosphatidylinositol mannosides (PIM), lipomannan (LM), lipoarabinomannan (LAM), trehalose dimycolates (TDM or cord factor), trehalose monomycolates, glycopeptidolipids (GPL), and sulfolipids (11,15,16). For Nocardia spp., trehalose-containing lipids, glycolipids, diethyl ether-soluble lipids, tuberculostearic acid, nocobactin, and nocardones have been identified (2,33,35,48).…”

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confidence: 99%

Nocardia brasiliensis Cell Wall Lipids Modulate Macrophage and Dendritic Responses That Favor Development of Experimental Actinomycetoma in BALB/c Mice

et al. 2012

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Nocardia brasiliensis is a Gram-positive facultative intracellular bacterium frequently isolated from human actinomycetoma. However, the pathogenesis of this infection remains unknown. Here, we used a model of bacterial delipidation with benzine to investigate the role of N. brasiliensis cell wall-associated lipids in experimental actinomycetoma. Delipidation of N. brasiliensis with benzine resulted in complete abolition of actinomycetoma without affecting bacterial viability. Chemical analyses revealed that trehalose dimycolate and an unidentified hydrophobic compound were the principal compounds extracted from N. brasiliensis with benzine. By electron microscopy, the extracted lipids were found to be located in the outermost membrane layer of the N. brasiliensis cell wall. They also appeared to confer acid-fastness. In vitro, the extractable lipids from the N. brasiliensis cell wall induced the production of the proinflammatory cytokines interleukin-1␤ (IL-1␤), IL-6, and CCL-2 in macrophages. The N. brasiliensis cell wall extractable lipids inhibited important macrophage microbicidal effects, such as tumor necrosis factor alpha (TNF-␣) and nitric oxide (NO) production, phagocytosis, bacterial killing, and major histocompatibility complex class II (MHC-II) expression in response to gamma interferon (IFN-␥). In dendritic cells (DCs), N. brasiliensis cell wall-associated extractable lipids suppressed MHC-II, CD80, and CD40 expression while inducing tumor growth factor ␤ (TGF-␤) production. Immunization with delipidated N. brasiliensis induced partial protection preventing actinomycetoma. These findings suggest that N. brasiliensis cell wall-associated lipids are important for actinomycetoma development by inducing inflammation and modulating the responses of macrophages and DCs to N. brasiliensis.

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Isolation of mycolic acid-containing glycolipids in Nocardia rubra and their granuloma forming activity in mice.

Cited by 22 publications

References 33 publications

Nocardia species: host-parasite relationships

Nocardia species: host-parasite relationships

Induction of Interferons (IFNs) and Tumor Necrosis Factor (TNF) in Mice by a Novel Glycolipid Trehalose 2,3,6′‐Trimycolate from Rhodococcus aurantiacus (Gordona aurantiaca)

Nocardia brasiliensis Cell Wall Lipids Modulate Macrophage and Dendritic Responses That Favor Development of Experimental Actinomycetoma in BALB/c Mice

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