Christina Camell
612-625-9956
ccamell@umn.edu
Office Address

312 Church Street
Minneapolis, MN 55455
United States

Christina

Camell

Assistant Professor
Biochemistry Molecular Biology and Biophysics

Older individuals have increased vulnerability to chronic and infectious diseases. White adipose tissue is a specialized microenvironment that shows early signs of aging, including elevated levels of immune cell activation and immunosenescence. Our research focuses on the alterations in molecular and cellular interactions that drive the dysfunctional environment seen during aging.

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Research statement

Age is associated with increased inflammation, visceral adiposity and metabolic disease. Tissue resident immune cells are required for dampening inflammation and maintaining tissue homeostasis. There are changes in resident immune cells that drive the increased inflammation and metabolic impairments that are seen with increased age.
   
We are studying the cellular and molecular changes within tissue resident immune cells that drive metabolic impairments in tissues. In particular, we are focused on lipolysis, a metabolic process that is required for release of energetic substrates from stored triglycerides in adipocytes. Lipolysis is impaired in aged individuals and this impairment may contributes to a worsened ability of elderly to maintain a healthy body-weight, stay warm or exercise.
   
Our work has previously shown that adipose tissue immune cells reside in microenvironment niches and are able to inhibit lipolysis in the aged adipose tissue. There are two broad projects within the lab:

  1.    Adipose tissue macrophage-specific regulatory effects on lipolysis and inflammation during aging
  2.    Fat-associated lymphoid cluster (FALC) and lymphocyte regulation of metabolism   

Our lab focuses on mouse models of aging and uses a wide variety of techniques to investigate the changes occurring with age. We combine this in vivo approach with a complementary in vitro cell culture system to better understand a direct mechanism. Ultimately, our goal is to generate candidates that could be targets for therapeutically treating to improve health span and restore metabolism in the elderly.

Selected publications

  • Camell CD, Lee A, Günther P, Goldberg E, Spadaro O, Youm YH, Bartke A, Hubbard GB, Ikeno Y, Ruddle NH, Schultze JL, Deep VD. Aging induces Nlrp3 inflammasome dependent adipose B cell expansion to impair metabolic homeostasis. In Press. Cell Metabolism. 2019.
  • Camell CD, Sander J, Spadaro O, Lee A, Nguyen K, Wing A, Goldberg E, Youm YH, Brown CW, Elsworth J, Rodeheffer MS, Schultze JL, Dixit VD. Inflammasome-driven catecholamine catabolism in macrophages blunts lipolysis during ageing. Nature. 2017; 550 (7674): 119-23. PMID: 28953873