Adhesins and ligands involved in the interaction of Candida spp. with epithelial and endothelial surfaces

Hostetter, Margaret K.

doi:10.1128/cmr.7.1.29

Cited by 198 publications

(140 citation statements)

References 106 publications

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“…Hence fungal infections of the cornea begin via adhesion of fungi to the damaged cornea. Fungal pathogens display a variety of adhesins that are capable of adhering to various cell types and interact with a variety of host proteins and glycoproteins present in host cells [68]. The outer fibrillar layer of yeast and filamentous fungal cell wall is composed of mannan or mannoprotein [75,195].…”

Section: Adhesionmentioning

confidence: 99%

Pathogenesis of microbial keratitis

Lakhundi

Siddiqui

Khan

2017

Microbial Pathogenesis

171

121

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Microbial keratitis is a sight-threatening ocular infection caused by bacteria, fungi, and protist pathogens. Epithelial defects and injuries are key predisposing factors making the eye susceptible to corneal pathogens. Among bacterial pathogens, the most common agents responsible for keratitis include Staphylococcus aureus, Pseudomonas aeruginosa, Streptococcus pneumonia and Serratia species. Fungal agents of corneal infections include both filamentous as well as yeast, including Fusarium, Aspergillus, Phaeohyphomycetes, Curvularia, Paecilomyces, Scedosporium and Candida species, while in protists, Acanthamoeba spp. are responsible for causing ocular disease. Clinical features include redness, pain, tearing, blur vision and inflammation but symptoms vary depending on the causative agent. The underlying molecular mechanisms associated with microbial pathogenesis include virulence factors as well as the host factors that aid in the progression of keratitis, resulting in damage to the ocular tissue. The treatment therefore should focus not only on the elimination of the culprit but also on the neutralization of virulence factors to minimize the damage, in addition to repairing the damaged tissue. A complete understanding of the pathogenesis of microbial keratitis will lead to the rational development of therapeutic interventions. This is a timely review of our current understanding of the advances made in this field in a comprehensible manner. Coupled with the recently available genome sequence information and high throughput genomics technology, and the availability of innovative approaches, this will stimulate interest in this field.

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Section: Adhesionmentioning

confidence: 99%

Pathogenesis of microbial keratitis

Lakhundi

Siddiqui

Khan

2017

Microbial Pathogenesis

171

121

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“…Candida albicans adhere to EC in large numbers within 1 hour and rapidly penetrate them without phagocytosis (reviewed in Hostetter, 1994). Listeria monocytogenes is similarly capable of rapid binding to and invasion of EC (Drevets et al, 1995;Greiffenberg et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

Association of Mycobacterium Leprae with Human Endothelial Cells In Vitro

Scollard

2000

Laboratory Investigation

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SUMMARY:Endothelial cell infection by Mycobacterium leprae has long been described histologically in all types of leprosy and in some of the acute reactions occurring in this disease. Recent evidence from experimental lepromatous neuritis indicates that M. leprae colonizes endothelial cells of epineural blood vessels even in sites of minimal infection, suggesting that interaction between these cells and M. leprae may play an important role in the selective localization of this organism to peripheral nerve. To begin to study the mechanisms involved, we have examined the interaction between M. leprae and human umbilical vein endothelial cells (HUVEC) in vitro using light microscopy, scanning and transmission electron microscopy, and confocal laser scanning microscopy. When M. leprae were added to confluent monolayers of HUVEC, uptake increased slowly to a maximum at 24 hours. Maximal percentages of infected cells were similar at ratios of organisms:cell over a range of 25:1 to 100:1. The bacilli appeared to lie within membrane-bound vacuoles at all time points. The kinetics of association of M. leprae with HUVEC are much slower than has previously been observed with macrophages, possibly due to differences in the binding of M. leprae. Compared with other pathogens that infect endothelial cells, M. leprae also appear to be ingested more slowly, and to a more limited degree. The receptors involved in M. leprae binding to endothelial cells and the impact of intracellular infection by M. leprae on these cells remain to be determined. (Lab Invest 2000, 80:663-669).I nfection of endothelial cells (EC) by Mycobacterium leprae was repeatedly noted in the early histopathologic descriptions of leprosy (Hansen and Looft, 1895;Klingmü ller, 1930). The extent of EC infection in this disease was reported in detail in a large study by Fite in 1941, who noted focal infection of blood vessels in 42% of skin lesions of all types, "usually with bacilli in the lining endothelial cells." Later studies further described EC infection by M. leprae at the light microscopic and ultrastructural levels (Boddingius, 1984;Burchard and Bierther, 1985;Coruh and McDougall, 1979;Fite, 1941;Mukherjee et al, 1987;Turkel et al, 1982). The remarkable extent of these descriptions, compared with other diseases, was emphasized in a review of the phagocytic properties of EC (Ryan, 1988). The pathogenesis of leprosy is now widely understood from the perspective of its unique immunologic spectrum, and EC involvement has not been widely appreciated among students of leprosy. However, the current cellular and molecular knowledge of immunologic mechanisms in leprosy do not obviate the longstanding observation of EC infection; rather, infection of EC appears to have been largely overlooked because, for over four decades, it had no apparent role in the immunological issues that dominated research on leprosy. Recent observations on the localization of M. leprae to peripheral nerves have indicated that EC play an important role in this process (Scollard et al, 199...

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“…The cell wall of Candida is primarily made up of three polysaccharides, mannan, glucan and chitin. Candida attaches to oral tissues and dentures with the help of adhesins such as Als1p, Als5p, Int1p and Hwp1p (Chaffin, et al, 1998, Hostetter, 1994. These glycoproteins bind to the extracellular matrix of mammalian cells such as fibrinogen, laminin and collagen (Chaffin, et al, 1998).…”

Section: Pathogenesismentioning

confidence: 99%