Norlander Lab

The Norlander lab investigates immune-medicated mechanisms that contribute to the pathogenesis of inflammatory diseases including hypertension and allergy/asthma.

Hypertension, defined as blood pressure ≥ 130/80 mmHg, has become a worldwide health concern, and affects 46% of adults in the United States. Recent studies have linked the immune system to the development and pathogenesis of hypertension. Generation of tolerance to self and the promotion of anti-inflammatory pathways are potential avenues for the development of drugs to treat of hypertension.

In the last 50 years, allergic diseases such as allergic rhinitis (runny nose), asthma, food allergy, and atopic eczema (skin allergy) have been spreading rapidly. Allergen tolerance can be considered as a non-pathogenic immune response to allergen. Discovery of factors that promote tolerance to an allergy or that promote an anti-inflammatory response, are critical to reverse the increasing number and severity of allergic diseases.

Therefore, better understanding the inflammatory and immune-mediated mechanisms promoting disease pathogenesis could result in the development of drugs to treat allergy, asthma, and/or hypertension.

The Norlander Lab evaluates human cells from patients with disease and utilizes mouse models that recapitulate disease to better understand cell-type functionality, pathway alterations, and treatments of interest. Specifically, the lab is currently interested in understanding how PGI₂ or Prostaglandin I₂ is augmenting T regulatory cell and T follicular helper cell function in hypertension and allergy/asthma.

Current Research Funding

R00 HL159594 Norlander, AE (Role: PI) 01/01/2021-12/31/2025
The goals of this project are to investigate the mechanisms through which PGI₂ is augmenting Treg and DC function in hypertension.

Recent Publications

Norlander AE, Bloodworth MH, Toki S, Zhang J, Zhou W, Boyd KL, Polosukhin VV, Cephus JY, Ceneviva ZJ, Gandhi VD, Chowdhury NU, Charbonnier LM, Rogers LM, Wang J, Aronoff DM, Bastarache L, Newcomb DC, Chatila TA, Peebles RS Jr. Prostaglandin I₂ signaling licenses Treg suppressive function and prevents pathogenic reprogramming. The Journal of Clinical Investigation. 2021 February 2. PMID: 33529171

Norlander AE, Peebles RS Jr. Prostaglandin I₂ and T regulatory cell function: broader impacts. DNA and Cell Biology. Review Article. 2021 July 15. PMID: 34265210

Norlander AE, Saleh MA, Itani HA, Pandey AK, Wu J, Xiao L, Dale BL, Harrison DG, Madhur MS. T cell Specific Deletion of Serum and Glucocorticoid-Regulated Kinase 1 Attenuates Hypertension and End-Organ Inflammation. JCI Insight. 2017 July 6. PMID: 28679951.

Norlander AE, Saleh MA, Kamat N, Ko B, Gnecco J, Zhu L, Dale B, Iwakura Y, Hoover R, McDonough A, Madhur MS. Interleukin 17A Regulates Renal Sodium Transporters and Renal Injury in Angiotensin II- Induced Hypertension. Hypertension. 2016 May 2. PMID: 27141060.

Norlander AE, Madhur MS, Harrison DG. The Immunology of Hypertension. Journal of Experimental Medicine. Review Article. 2018 January 2. PMID: 29247045.