Opsonin-independent adherence and phagocytosis of Listeria monocytogenes by murine peritoneal macrophages

Pierce, Marcia M.; Gibson, R. E.; Rodgers, Frank G.

doi:10.1099/00222615-45-4-258

Cited by 15 publications

(7 citation statements)

References 14 publications

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“…L. monocytogenes is also efficiently internalized in the absence of serum, indicating that nonopsonic receptor-ligand interactions are also involved in host cell recognition by Listeria spp. (509). The eukaryote cell receptors used by Listeria spp.…”

Section: Internalizationmentioning

confidence: 99%

ListeriaPathogenesis and Molecular Virulence Determinants

et al. 2001

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The gram-positive bacterium Listeria monocytogenes is the causative agent of listeriosis, a highly fatal opportunistic foodborne infection. Pregnant women, neonates, the elderly, and debilitated or immunocompromised patients in general are predominantly affected, although the disease can also develop in normal individuals. Clinical manifestations of invasive listeriosis are usually severe and include abortion, sepsis, and meningoencephalitis. Listeriosis can also manifest as a febrile gastroenteritis syndrome. In addition to humans, L. monocytogenes affects many vertebrate species, including birds. Listeria ivanovii, a second pathogenic species of the genus, is specific for ruminants. Our current view of the pathophysiology of listeriosis derives largely from studies with the mouse infection model. Pathogenic listeriae enter the host primarily through the intestine. The liver is thought to be their first target organ after intestinal translocation. In the liver, listeriae actively multiply until the infection is controlled by a cell-mediated immune response. This initial, subclinical step of listeriosis is thought to be common due to the frequent presence of pathogenic L. monocytogenes in food. In normal indivuals, the continual exposure to listerial antigens probably contributes to the maintenance of anti-Listeria memory T cells. However, in debilitated and immunocompromised patients, the unrestricted proliferation of listeriae in the liver may result in prolonged low-level bacteremia, leading to invasion of the preferred secondary target organs (the brain and the gravid uterus) and to overt clinical disease. L. monocytogenes and L. ivanovii are facultative intracellular parasites able to survive in macrophages and to invade a variety of normally nonphagocytic cells, such as epithelial cells, hepatocytes, and endothelial cells. In all these cell types, pathogenic listeriae go through an intracellular life cycle involving early escape from the phagocytic vacuole, rapid intracytoplasmic multiplication, bacterially induced actin-based motility, and direct spread to neighboring cells, in which they reinitiate the cycle. In this way, listeriae disseminate in host tissues sheltered from the humoral arm of the immune system. Over the last 15 years, a number of virulence factors involved in key steps of this intracellular life cycle have been identified. This review describes in detail the molecular determinants of Listeria virulence and their mechanism of action and summarizes the current knowledge on the pathophysiology of listeriosis and the cell biology and host cell responses to Listeria infection. This article provides an updated perspective of the development of our understanding of Listeria pathogenesis from the first molecular genetic analyses of virulence mechanisms reported in 1985 until the start of the genomic era of Listeria research

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Section: Internalizationmentioning

confidence: 99%

ListeriaPathogenesis and Molecular Virulence Determinants

et al. 2001

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“…Following preliminary studies which established the ability of L. monocytogenes to bind to macrophages in a wash-resistant manner (24), the rate at which host cell receptors were saturated with listeriae was investigated. In all cases, an MOI of 1,000 resulted in high levels of organism attachment to the receptors on macrophage surface membranes; however, at this inoculum, the level of nonspecific binding of L. monocytogenes to culture plates as seen by IFA proved problematic.…”

Section: Discussionmentioning

confidence: 99%

“…However, the receptors involved in opsonin-dependent adherence may also be involved in opsonin-independent adherence, as in the case of group B streptococci (GBS), which recognize and bind to complement receptor type 3 (CR3) in the absence of opsonins (2). Direct bacterial attachment between adhesins and host cell receptors has also been reported for Legionella pneumophila (18,26) as well as for Listeria monocytogenes (5,8,24).…”

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confidence: 99%

The Role of Sialic Acid in Opsonin-Dependent and Opsonin-Independent Adhesion ofListeria monocytogenesto Murine Peritoneal Macrophages

et al. 1998

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The adhesion of listeriae to host cells employs mechanisms which are complex and not well understood. Listeria monocytogenesis a facultative intracellular pathogen responsible for meningoencephalitis, septicemia, and abortion in susceptible and immunocompromised individuals. Subsequent to colonization and penetration of the gut epithelium, the organism attaches to resident macrophages and replicates intracellularly, thus evading the humoral immune system of the infected host. The focus of these studies was to investigate the attachment of the organism to murine peritoneal macrophages in an opsonin-dependent and opsonin-independent fashion. Assessment of competitive binding experiments by immunofluorescence and enzyme-linked immunosorbent assays showed that adhesion of the organism to macrophages in the presence or absence of opsonins was inhibited (90%) by N-acetylneuraminic acid (NAcNeu). In addition, the lectin from Maackia amurensis, with affinity for NAcNeu-α(2,3)galactose, blocked binding of L. monocytogenes to host cells. Oxidation of the surface carbohydrates on the organism by using sodium metaperiodate resulted in a dose-dependent reduction (up to 98%) in adherence to macrophages. Monoclonal antibody to complement receptor 3 did not prevent listeriae from binding to mouse macrophages or from replicating within the infected cells whether or not normal mouse serum was present. Based on our results, we propose the involvement of NAcNeu, a member of the sialic acid group, in the attachment of L. monocytogenes to permissive murine macrophages.

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“…Opsonin independent adhereance and phagocytosis of microbes is often identical by murine peritoneal macrophages e.g., in case of Listeria monocytogens (Pierce et al, 1996). Attachment and entry of bacteria occurs through their apical surfaces and these processes do not appear to be actin dependent (Karunasagar et al, 1994).phagocytosis is sometimes important for lung and few other body sites,…”

Section: Ingestion Of Microbes By Phagocytementioning

confidence: 99%

Opsonin and its mechanism of action in secondary immune response

Azad¹,

Shahriyar²,

Mondal³

2016

J mol stud med res

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Opsonins are specialized biomolecules responsible for recognizing the pathogens to be crushed by our immunity which, is considered as the main precursor of undergoing any phagocytosis reaction inside the body environment. In the absence of these molecules autoimmunity and hypersensitivity may take place on regular basis. A number of research programs and projects have been launching for the opsonin research purpose, where new theories of human immunity and molecular interference in our defense mechanism are revealed from each project. Complement cascade produces opsonin as a by-product. The complement receptor 3(CR3) and Fc gammareceptor (FcgamaRs), two important phagocytic receptors, mediate phagocytosis in the cellular level. In the following passages the pathways of opsonin activity in secondary immune response, mechanism of phagocytosis reaction, role of other complement system and antibody in defense purposes, clinical aspects of opsonization and the future of opsonin research are described quite transparently. The molecular structures and proteomic modeling is the main way of revealing new technologies of drug designing both in molecular and nano-scale level.

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Opsonin-independent adherence and phagocytosis of Listeria monocytogenes by murine peritoneal macrophages

Cited by 15 publications

References 14 publications

ListeriaPathogenesis and Molecular Virulence Determinants

ListeriaPathogenesis and Molecular Virulence Determinants

The Role of Sialic Acid in Opsonin-Dependent and Opsonin-Independent Adhesion ofListeria monocytogenesto Murine Peritoneal Macrophages

Opsonin and its mechanism of action in secondary immune response

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