What is the role of PGL?
What is the role of PGL?
PGL-I has also been implicated in the tropism of M. leprae for Schwann cells, through specific binding to laminin, and to play an important role in downregulation of the inflammatory immune response and inhibition of dendritic cell maturation and activation, thereby facilitating the persistence of M. leprae/leprosy.
What is PGL in microbiology?
Phenolic glycolipids (PGLs) are polyketide-derived virulence factors produced by Mycobacterium tuberculosis, Mycobacterium leprae, and other mycobacterial pathogens.
What property of Mycobacterium leprae is an important factor in it’s pathogenicity?
A key aspect of M. leprae pathogenesis is its capacity to exploit host cell lipid metabolism, leading to the accumulation of cholesterol-enriched lipid droplets in the cytoplasm of infected cells (Virchow, 1863; Mattos et al., 2010; Mattos et al., 2011a; Mattos et al., 2014).
How do you get Mycobacterium leprae?
Leprosy is transmitted during close and frequent contacts with untreated cases, transmission being mainly via droplets, usually from the nose but also the mouth, but it is not highly infectious. Most people in leprosy-endemic populations have been exposed to M.
What is Lepromin test?
A lepromin skin test is used to determine the type of leprosy a person has contracted. The lepromin skin test is also called the leprosy skin test. Leprosy is a long-term (chronic) condition caused by the bacteria Mycobacterium leprae.
Are phenolic glycolipids hydrophobic?
The hydrophobic hydrocarbon chains of these lipids comprise the OMs which may be the thickest of all biological membranes yet identified. The asymmetric OM consists largely of long-chain mycolic acids comprising most of the inner leaflet with a diversity of other lipids contributing to the outer leaflet.
Is Mycobacterium leprae aerobic or anaerobic?
Mycobacterium leprae is an aerobic, rod-shaped, Gram-positive bacterium in the Mycobacteriaceae family. Infections with this bacterium lead to leprosy.
Where is Mycobacterium leprae commonly found?
Leprosy is most commonly found in developing countries. The countries with the highest numbers of new cases annually include Nigeria, Brazil, Indonesia, and India. Transmission has not been fully elucidated, but likely occurs person-to-person via respiratory secretions.
How do I identify Mycobacterium leprae?
leprae can be rapidly detected and identified using PCR-RFLP. The new PCR/restriction enzyme pattern would help to arrive at the differentiation between leprosy and other mycobacterial infectious cases. It also had shown an advantage to detect the clinical samples from paraffin-embedded skin biopsy and fresh tissues.
How do you test for Mycobacterium leprae?
Depending on the form of leprosy suspected by the treating physician, the following specimens may be collected:
- Skin smears from the earlobes, elbows, and knees.
- Skin biopsy from edges of active patches.
- Nerve biopsy from thickened nerves.
How is Mycobacterium leprae diagnosed?
To confirm the diagnosis, your doctor will take a sample of your skin or nerve (through a skin or nerve biopsy) to look for the bacteria under the microscope and may also do tests to rule out other skin diseases.
Is PGL-1 involved in the pathogenesis of Mycoplasma leprae?
PGL-1 is involved in the M. leprae invasion of Schwann cells through the basal lamina in a laminin-2-dependent pathway. The results indicate a novel role of a bacterial glycolipid in determining the nerve predilection of a human pathogen.
Can purpurified PGL-1 and dpgl prevent bacterial infection?
Purified PGL-1 and dPGL from M. leprae can prevent bacterial killing by intact phagocytes and cell-free antimicrobial systems. Both glycolipids completely abolished the antimicrobial effect of the acetaldehyde-XO-Fe2+ system.
How does PGL-1 bind to laminin 2?
PGL-1 binds specifically to the native laminin-2 in the basal lamina of Schwann cell-axon units. This binding is mediated by the alpha (2LG1, alpha2LG4, and alpha2LG5 modules present in the naturally cleaved fragments of the peripheral nerve laminin alpha2 chain, and is inhibited by the synthetic terminal trisaccharide of PGL-1.
Can PGL-1 scavenge reactive oxygen species in the phagosome?
These results, suggesting that PGL-1 can scavenge reactive oxygen species and prevent microbial death within the phagosome, may in part explain the intracellular survival of M. leprae in certain cell types. Research Support, U.S. Gov’t, P.H.S.