Grant: Project Grant
Centre hospitalier de l'Université de Montréal (CHUM)
$1,980,055.00
IL-32, a new biomarker and potential therapeutic target for chronic inflammation and residual reservoirs in HIV-infected individuals
EF 2015-16
Résumé
HIV-infected individuals are aging and present increased risks for age-associated health complications such as cardiovascular diseases (CVD). Inflammation plays a critical role in HIV-associated premature aging phenotypes. HIV infection induces a state of chronic activation of the immune system, which persists even in the presence of antiretroviral therapy (ART) as indicated by increased levels of proinflammatory cytokines such as IL-6 and TNF-a. IL-32 is a novel proinflammatory cytokine expressed in response to HIV infection, which induces the expression of IL-6, TNF-¿ as well as other inflammatory mediators such as IL-1¿ and IL-8. IL-32 is involved in the pathophysiology of age-related inflammatory disorders such as arthritis and atherosclerosis. We propose to study a model which suggests that in aging HIV-infected ART-treated individuals, residual viral replication and intestinal dysbiosis induce IL-32 proinflammatory isoforms that exacerbate inflammation-mediated CVD and that IL-32 may be an important therapeutic target.
Programme
Project Grant
Emplacement
Quebec, Canada
Type de bénéficiaire
Not-for-profit organization or charity
Type
Grant
Source
CIHR Funding Decisions Database
Tel que publié
Id
344296
Name
Tremblay Cécile L
Region
Québec
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Infection and Immunity
Theme2
Biomedical
Prcname2
Project Grant Competition
Projecttitle
IL-32, a new biomarker and potential therapeutic target for chronic inflammation and residual reservoirs in HIV-infected individuals
Programtype2
Operating Grants
Orgnameinp2
Centre hospitalier de l'Université de Montréal (CHUM)
Cihramount2
$1,980,055
Cihrequipment2
$0
Programname2
Project Grant
Keyworddelim
Biomarker; Dysbiosis; Hiv Immune Activation; Hiv Reservoirs; Il-32; Inflammation; Microbiota; Th17 Lymphocytes; Therapeutic Target
Abstract
HIV-infected individuals are aging and present increased risks for age-associated health complications such as cardiovascular diseases (CVD). Inflammation plays a critical role in HIV-associated premature aging phenotypes. HIV infection induces a state of chronic activation of the immune system, which persists even in the presence of antiretroviral therapy (ART) as indicated by increased levels of proinflammatory cytokines such as IL-6 and TNF-a. IL-32 is a novel proinflammatory cytokine expressed in response to HIV infection, which induces the expression of IL-6, TNF-¿ as well as other inflammatory mediators such as IL-1¿ and IL-8. IL-32 is involved in the pathophysiology of age-related inflammatory disorders such as arthritis and atherosclerosis. We propose to study a model which suggests that in aging HIV-infected ART-treated individuals, residual viral replication and intestinal dysbiosis induce IL-32 proinflammatory isoforms that exacerbate inflammation-mediated CVD and that IL-32 may be an important therapeutic target.
Competitiondate
201603
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Tremblay, Cécile L
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $1,980,055~ $0~
