ArticleThe Journal of experimental medicine1991
Phenolic glycolipid-1 of Mycobacterium leprae binds complement component C3 in serum and mediates phagocytosis by human monocytes.
Article in The Journal of experimental medicine, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
31 citing papers in PubMed, 84 citations in OpenAlex.
- The effects of prednisolone treatment on serological responses and lipid profiles in Ethiopian leprosy patients with Erythema Nodosum Leprosum reactions.PLoS neglected tropical diseases · 2018Trial
- Article
- Leprosy.Nature reviews. Disease primers · 2024Review
- Biophysical Interaction Landscape of Mycobacterial Mycolic Acids and Phenolic Glycolipids with Host Macrophage Membranes.ACS applied bio materials · 2023Article
- Review
- Complement C3 and Activated Fragment C3a Are Involved in Complement Activation and Anti-Bacterial Immunity.Frontiers in immunology · 2022Article
- Adding MASP1 to the lectin pathway-Leprosy association puzzle: Hints from gene polymorphisms and protein levels.PLoS neglected tropical diseases · 2020Article
- Expression of NLRP3 inflammasome in leprosy indicates immune evasion of Mycobacterium leprae.Memorias do Instituto Oswaldo Cruz · 2020Observational
- Cell Biology of Intracellular Adaptation ofMicrobiology spectrum · 2019Review
- Intrinsic activation of the vitamin D antimicrobial pathway by M. leprae infection is inhibited by type I IFN.PLoS neglected tropical diseases · 2018Article
- Identification of OprF as a complement component C3 binding acceptor molecule on the surface of Pseudomonas aeruginosa.Infection and immunity · 2015Article
- Binding of CXCL8/IL-8 to Mycobacterium tuberculosis Modulates the Innate Immune Response.Mediators of inflammation · 2015Article
- Mycobacterium marinum MgtC plays a role in phagocytosis but is dispensable for intracellular multiplication.PloS one · 2014Article
- Modulation of the cytokine response in human monocytes by mycobacterium leprae phenolic glycolipid-1.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2012Article
- Leprosy and the human genome.Microbiology and molecular biology reviews : MMBR · 2010Review
- Mycobacterium leprae phenolglycolipid-1 expressed by engineered M. bovis BCG modulates early interaction with human phagocytes.PLoS pathogens · 2010Article
- Deciphering the genetic bases of the structural diversity of phenolic glycolipids in strains of the Mycobacterium tuberculosis complex.The Journal of biological chemistry · 2008Article
- Intact pks15/1 in non-W-Beijing Mycobacterium tuberculosis isolates.Emerging infectious diseases · 2006Article
- The continuing challenges of leprosy.Clinical microbiology reviews · 2006Review
- Mycobacterial protein HbhA binds human complement component C3.Infection and immunity · 2001Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Previous studies from this laboratory have demonstrated that Mycobacterium leprae, an obligate intracellular bacterial parasite, enters human mononuclear phagocytes via complement receptors on these host cells and bacterium-bound C3. The present study investigates the role of M. leprae surface molecules in C3 fixation and phagocytosis. By enzyme-linked immunosorbent assay, C3 binds selectively to phenolic glycolipid-1 (PGL-1), a major surface molecule of the leprosy bacillus. C3 fixation to PGL-1 is serum concentration dependent and is abolished in heat-inactivated serum or serum containing ethylenediaminetetraacetic acid. C3 fixation is also abolished in serum containing ethyleneglycol-bis (beta-aminoethyl ether)N,N,N'-tetraacetic acid and MgCl2 indicating that isolated PGL-1 fixes C3 via the classical complement pathway. The capacity of PGL-1 to fix C3 is dependent upon its terminal trisaccharide since sequential removal of monosaccharide units of the trisaccharide results in a stepwise reduction in C3 fixation. Deacylation of PGL-1 also abolishes C3 fixation. C3 fixes to the trisaccharide of PGL-1 that is chemically linked to bovine serum albumin via the chemical carrier, 8-methoxycarbonyloctanol. PGL-1 mediates C3 fixation to polystyrene microspheres, and PGL-1 and C3 together mediate ingestion of polystyrene microspheres by human monocytes, wherein these inert test particles reside in membrane-bound phagosomes. Thus, complement receptors on mononuclear phagocytes, complement component C3, and PGL-1 comprise a three-component receptor-ligand-acceptor molecule system for mediating phagocytosis of M. leprae.
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