Filamentous proteophosphoglycan secreted by Leishmania promastigotes forms gel-like three-dimensional networks that obstruct the digestive tract of infected sandfly vectors

Stierhof, York‐Dieter; Bates, Paul A.; Jacobson, Raymond L.; Rogers, Matthew E.; Schlein, Yosef; Handman, Emanuela; Ilg, Thomas

doi:10.1016/s0171-9335(99)80036-3

Cited by 87 publications

(71 citation statements)

References 45 publications

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“…This promastigote secretory gel (PSG) is formed by the parasites and has been shown to enhance cutaneous infections when deposited onto the skin with sand fly saliva (Rogers et al 2004, Titus 1998. A major component of PGS is a filamentous glycoprotein, proteophosphoglycan (fPPG) (Ilg et al 1996), which forms the 3D matrix of the plug that blocks the gut (Stierhof et al 1999) and keeps the valve open. The production of PSG has been shown to occur is several Leishmania-sand fly combinations (Stierhof et al 1999).…”

Section: Changes In Biting and Probing Behaviourmentioning

confidence: 99%

“…A major component of PGS is a filamentous glycoprotein, proteophosphoglycan (fPPG) (Ilg et al 1996), which forms the 3D matrix of the plug that blocks the gut (Stierhof et al 1999) and keeps the valve open. The production of PSG has been shown to occur is several Leishmania-sand fly combinations (Stierhof et al 1999). It has been suggested that the plug facilitates regurgitation and, by restricting blood flow into the fly, prolongs feeding time and causes flies to bite more, a concept known as 'the blocked fly hypothesis' .…”

Section: Changes In Biting and Probing Behaviourmentioning

confidence: 99%

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Olfaction in vector-host interactions

Takken¹,

Knols²

2010

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Section: Changes In Biting and Probing Behaviourmentioning

confidence: 99%

Section: Changes In Biting and Probing Behaviourmentioning

confidence: 99%

Olfaction in vector-host interactions

Takken¹,

Knols²

2010

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“…The phytopathogen Xylella fastidiosa forms a biofilm of polarly attached cells in the foregut of its vectors, which are sap-feeding insects in the leafhopper family (Newman et al 2004;Purcell et al 1979); and transmission of Leishmania depends on blockage of the anterior midgut of the sandfly vector by parasites embedded in a polysaccharide-containing secretory gel. (Rogers et al 2002;Stierhof et al 1999). The body of evidence that has accumulated in support of the biofilm model of plague transmission is presented in the following sections.…”

Section: The Biofilm Model Of Proventricular Infectionmentioning

confidence: 99%

Yersinia pestis Biofilm in the Flea Vector and Its Role in the Transmission of Plague

Hinnebusch¹,

Erickson²

2008

Current Topics in Microbiology and Immunology

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Transmission by fleabite is a relatively recent evolutionary adaptation of Yersinia pestis, the bacterial agent of bubonic plague. To produce a transmissible infection, Y. pestis grows as an attached biofilm in the foregut of the flea vector. Biofilm formation both in the flea foregut and in vitro is dependent on an extracellular matrix (ECM) synthesized by the Yersinia hms gene products. The hms genes are similar to the pga and ica genes of Escherichia coli and Staphylococcus epidermidis, respectively, that act to synthesize a poly-β-1,6-N-acetyl-dglucosamine ECM required for biofilm formation. As with extracellular polysaccharide production in many other bacteria, synthesis of the Hms-dependent ECM is controlled by intracellular levels of cyclic-di-GMP. Yersinia pseudotuberculosis, the food-and water-borne enteric pathogen from which Y. pestis evolved recently, possesses identical hms genes and can form biofilm in vitro but not in the flea. The genetic changes in Y. pestis that resulted in adapting biofilm-forming capability to the flea gut environment, a critical step in the evolution of vector-borne transmission, have yet to be identified. During a flea bite, Y. pestis is regurgitated into the dermis in a unique biofilm phenotype, and this has implications for the initial interaction with the mammalian innate immune response.

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“…Infection of mammals is initiated by metacyclic promastigotes, which are regurgitated in a plug of promastigote secretory gel (PSG) when the sand fly takes a blood meal [43,44]. The parasites first pass through neutrophils [45] before infecting macrophages and differentiating to amastigotes.…”

Section: Parasite-derived Vesicles For Long-range Communication With mentioning

confidence: 99%

The languages of parasite communication

Roditi

2016

Molecular and Biochemical Parasitology

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Although it is regarded as self-evident that parasites interact with their hosts, with the primary aim of enhancing their own survival and transmission, the extent to which unicellular parasites communicate with each has been severely underestimated.Recent publications show that information is commonly exchanged between parasites of the same species and that this can govern their decisions to divide, to differentiate or to migrate as a group. Communication can take the form of soluble secreted factors, extracellular vesicles or contact between cells. Extracellular parasites can do this directly, while intracellular parasites use the infected host cell -or components derived from it -as an intermediary. By emitting signals that can be dispersed within the host, parasites can also have long-distance effects on the course of an infection and its pathology. This article presents an overview of recent developments in this field and draws attention to some older work that merits re-examination. 3 Most readers of this article will not need to be told that diseases such as sleeping sickness, malaria, Leishmaniasis, Trichomoniasis and Chagas Disease are caused by unicellular parasites. This knowledge might come with the tacit assumption that singlecelled organisms are completely self-sufficient and have no need to interact, much less cooperate, with members of their own species. In recent years, however, it has become apparent that a number of decisions are group decisions that rely on parasites communicating with each other. Just as animals can exchange information in different ways, be it vocally, visually, chemically or by body language, parasites have also developed a range of mechanisms for communicating with each other. This sometimes occurs directly, from parasite to parasite, or by using the infected host cell -or components derived from it -as an intermediary. By emitting signals that can be dispersed within the host, parasites can also have wide-ranging effects on the course of an infection and its pathology. This article presents an overview of recent developments in this field and draws attention to some older work that merits re-examination. Owing to space constraints, it will not cover molecules used by intracellular parasites to reprogram the cells that they infect. Quorum sensing and differentiationDifferent subspecies of Trypanosoma brucei, the pathogens responsible for human sleeping sickness and Nagana in domestic animals, are extracellular throughout their life cycle. In the mammalian host the parasites use a quorum sensing mechanism to maintain a balance between slender bloodstream forms, which are capable of dividing every 6-8 hours, and stumpy bloodstream forms, which cannot divide and have a lifespan of a few days. When trypanosomes ingested by a tsetse fly, the slender form is killed while the stumpy form survives and differentiates to the next life stage, the procyclic form, in the insect midgut [1,2]. If slender forms were to proliferate unchecked, this would result in rapid death of th...

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Filamentous proteophosphoglycan secreted by Leishmania promastigotes forms gel-like three-dimensional networks that obstruct the digestive tract of infected sandfly vectors

Cited by 87 publications

References 45 publications

Olfaction in vector-host interactions

Olfaction in vector-host interactions

Yersinia pestis Biofilm in the Flea Vector and Its Role in the Transmission of Plague

The languages of parasite communication

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