Functional and Antigenic Maturation of Brugia malayi Microfilariae

Fuhrman, Juliet A.; Urioste, Sandy S.; Hamill, Bruce; Spielman, Andrew; Piessens, Willy F.

doi:10.4269/ajtmh.1987.36.70

Cited by 31 publications

(22 citation statements)

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“…Despite the high proportion of seemingly filarial wormrestricted or uninformative genes that lack functional sequence-based clues, we observed several differences in abundance for transcripts identified with certain functional gene categories. Most notably, the transcriptome of mature mf is enriched for transcripts identified with the microfilarial cuticle and sheath, providing support for the hypothesis that surface changes during maturation of mf might determine their infectivity for the mosquito vector (Fuhrman et al 1987).…”

Section: Discussionmentioning

confidence: 65%

“…Within the mosquito, infective mf quickly penetrate the midgut and resume development in the hemocoel. The sheath, a remnant of the eggshell membrane, is cast from the worm during or after midgut penetration in a successful infection (Fuhrman et al 1987;Yamamoto et al 1983). The sheath is acellular and insoluble, and is composed of chitin Simpson and Laurence 1974;Paulson et al 1988;Fuhrman and Piessense 1985), matrix proteins (elastin, fibronectin, collagen type IV, laminin), and shp2, an insoluble and cross-linking protein (Hirzmann et al 2002); as well 25 as sulfur-containing proteins, proteoglycans, phospholipids and acidic mucopolysaccharides Simpson and Laurence 1974;Araujo et al 1993;Araujo et al 1994).…”

Section: Discussionmentioning

confidence: 99%

“…There is evidence that the microfilarial sheath is modified during maturation; for example, immature mf differ from mature mf in that they cannot be chemically exsheathed with calcium, the sheaths of immature and mature mf differ in their ability to bind various lectins (Furman and Ash 1983 a and b;Paulson et al 1988;Fuhrman and Piessens 1989) and a sheath-directed monoclonal antibody (Fuhrman et al 1987;Canlas et al 1984), and unlike mature mf, immature mf do not bind complement factors and promote granulocyte adherence in vitro (Johnson et al 1981). Chitinase activity in the sheath increases during maturation and coincides with mf infectivity for mosquitoes (Fuhrman et al 1987;Fuhrman et al 1992).…”

Section: Discussionmentioning

confidence: 99%

“…mf that have not 'matured' cannot successfully penetrate the midgut of the mosquito, subsequently cannot develop to the L3 stage; apparently requiring at least mammalian host to mature (Fuhrman et al 1987). Glycosidic changes occur to the with maturation, an observation of great interest because the sheath malayi is sequenced and though not yet mapped, has been karyotyped to show 4 autosomes and 1 sex determining pair (XY) (Sakaguchi et al 1983), with a projected size of ~90 Mb with ~11,500 protein coding genes (Ghedin et al 2007).…”

mentioning

confidence: 99%

“…aegypti (de Hollanda et al 1982;Fuhrman et al 1987 (Brehm et al 2003;Buckingham et al 2003;Paba et al 2004;Storey 2003;Yamazaki and Saito 2002). In the present study, we used microarray analysis to examine gene expression changes that occur with maturation of mf in the mammalian host.…”

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confidence: 99%

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Use of microarray hybridization to identify Brugia genes involved in mosquito infectivity

et al. 2009

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Filarial nematodes are a family of insect-borne parasitic worms that cause a number of diseases in man and animals. The most widespread filarial disease of humans is lymphatic filariasis, caused by worms in the genera Wuchereria and Brugia. Lymphatic filariasis is an economic and social burden in endemic countries and affects approximately 119 million people worldwide. Brugia malayi and B. pahangi microfilariae (mf) require a maturation period of at least five days in the mammalian host before they can infect mosquito vectors. This maturation process correlates with changes in the surface composition of mf that likely are associated with changes in gene expression. To test this hypothesis, we verified the differential infectivity of immature (<3 day) and mature (>30 day) Brugia mf for black-eyed Liverpool strain of Aedes aegypti (LVP), and then assessed transcriptome changes associated with microfilarial maturation by competitively hybridizing microfilarial cDNAs to the B. malayi oligonucleotide microarray. We identified transcripts that were more abundant in immature (94 in B. pahangi and 29 in B. malayi) and mature (64 in B. pahangi and 14 in B. malayi) mf. In each case, >40% of Brugia transcripts shared no similarity to known genes, or were similar to genes with unknown function; the remaining transcripts were categorized by putative function based on sequence similarity to known genes/proteins. Microfilarial maturation was not associated with demonstrable changes in the abundance of transmembrane or secreted proteins; however, differences in transcript abundance were observed for many that have predicted functions. For example, immature mf were enriched for transcripts putatively associated with immune modulation, neurotransmission, transcription and cellular cytoskeleton elements. In mature mf, there was an increase in transcripts potentially encoding hypodermal/muscle and surface molecules, i.e., cuticular collagens and sheath components. These finding lend support to the underlying hypothesis that changes in microfilarial gene expression drive surface modifications that influence the parasite to begin development in compatible vectors. Brugia malayi genes corresponding to differentially abundant transcripts were identified, and transcript abundance validated by quantitative polymerase chain reaction. These studies serve as a starting point towards gaining a better understanding of the parasite side of the intricate parasite/mosquito relationship.

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Section: Discussionmentioning

confidence: 65%