Grant: Project Grant
University of Manitoba
$1,005,976.00
The Role of Long Pentraxin-3 (PTX3) in Regulation of Immunity to Cutaneous Leishmaniasis
EF 2023-24
Résumé
Leishmaniasis is a spectral disease caused by protozoan parasites belonging to the genus Leishmania. The disease affects over 12 million people globally with an estimated 350 million people at risk of infection. Depending on the species of the parasite and host genetics, the disease manifestation ranges from self-healing skin ulcers to large disfiguring scars and involvement of the visceral organs that results in death. Despite this significant health and societal burden, there is no vaccine against the disease and current treatments either have major side effects or are only minimally effective. The lack of effective vaccine and new therapies is mainly due to poor understanding of how the parasite subverts the host immunity. My laboratory recently found that Leishmania infection leads to the induction of a pattern recognition molecule, called Pentraxin 3 (PTX3) in infected the host. PTX3 in turn suppresses a major arm of immunity, (called Th17 cells) that contributes to optimal resistance against the parasite. These seminal findings suggest that targeting PTX3 molecule may be a viable option for developing novel drug therapy against leishmaniasis. Using experimental animal model of the disease, we will address if this
molecule may be a good target for drug therapy and provide a rational strategy for treatment of the disease. Our studies will aims to establish a role for PTX3 in the pathogenesis of cutaneous leishmaniasis and could provide important information on treatment approach against the disease.
Programme
Project Grant
Bénéficiaire
Emplacement
Manitoba, Canada
Type de bénéficiaire
Academia
Type
Grant
Source
CIHR Funding Decisions Database
Tel que publié
Id
501814
Name
Uzonna Jude E
Region
Manitoba
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Infection and Immunity
Theme2
Biomedical
Prcname2
Microbiology & Infectious Diseases
Projecttitle
The Role of Long Pentraxin-3 (PTX3) in Regulation of Immunity to Cutaneous Leishmaniasis
Programtype2
Operating Grants
Orgnameinp2
University of Manitoba
Cihramount2
$1,005,976
Cihrequipment2
$0
Programname2
Project Grant
Keyworddelim
Host Defense; Immunity; Induction Of Long Pentraxin-3; Leishmania; Leishmania Surface Molecules; Protozoan Parasite
Abstract
Leishmaniasis is a spectral disease caused by protozoan parasites belonging to the genus Leishmania. The disease affects over 12 million people globally with an estimated 350 million people at risk of infection. Depending on the species of the parasite and host genetics, the disease manifestation ranges from self-healing skin ulcers to large disfiguring scars and involvement of the visceral organs that results in death. Despite this significant health and societal burden, there is no vaccine against the disease and current treatments either have major side effects or are only minimally effective. The lack of effective vaccine and new therapies is mainly due to poor understanding of how the parasite subverts the host immunity. My laboratory recently found that Leishmania infection leads to the induction of a pattern recognition molecule, called Pentraxin 3 (PTX3) in infected the host. PTX3 in turn suppresses a major arm of immunity, (called Th17 cells) that contributes to optimal resistance against the parasite. These seminal findings suggest that targeting PTX3 molecule may be a viable option for developing novel drug therapy against leishmaniasis. Using experimental animal model of the disease, we will address if this
molecule may be a good target for drug therapy and provide a rational strategy for treatment of the disease. Our studies will aims to establish a role for PTX3 in the pathogenesis of cutaneous leishmaniasis and could provide important information on treatment approach against the disease.
Competitiondate
202403
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Uzonna, Jude E
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $1,005,976~ $0~