Ph.D. University of Texas Medical Branch, 1981
Our studies are designed to understand (1) how sensitization of pain pathways can lead to persistent pain states and (2) how inflammatory pain can be alleviated. In response to tissue injury and pain, an amplified neurogenic drive is generated in the spinal cord dorsal horn. Nerve impulses then propagate back out to the peripheral injury site bringing neurotransmitter signals that directly impact inflammatory responses. Three neuroinflammatory models are being utilized to examine neurotransmitter activation and to promote reduction of inflammation and pain: (1) temporomandibular joint pain, (2) inflammatory pain in the knee joint, and (3) a model of visceral pain resembling chronic human pancreatitis. Treatment strategies, such as gene therapy and transdermal delivery of opioid peptides for site specific anti-nociceptive action, are being utilized to stop the activation caused by neurotransmitters for both the pancreatitis and muscle/joint inflammatory models. Information about the interface between the nervous system and the immune system is being generated, including the potential for tissue repair promoted by opioid peptides. Our investigations have led to discovery of a new visceral pain pathway and a new acid sensing G-coupled receptor in the knee joint lining. We are also developing new strategies for the treatment of chronic pain, inflammation and tissue repair after injury.
NIH RO1 NS39041-14 (Westlund, PI) “Neurogenic Amplification of Pancreatitis Pain” (04/01/00 - 03/31/15)
NIH/NCRR 2P20RR020145-06 COBRE (08/01/2010 – 7/31/2015)
PI: Ebersole, Jeffrey L. (R Danaher, PI/Trainee; K Westlund-High, Co-I/Mentor
Project 5 Gene Therapy for Orofacial Pain) “Center for the Biologic Basis of Oral/Systemic
University of Kentucky “Center for Alcohol and Drug Abuse” Pilot grant, (10/12-9/13)
Zhang LP, Ma F, Abshire SM, Westlund KN. Prolonged high fat/alcohol exposure increases TRPV4 and its functional responses in pancreatic stellate cells. Am J Physiol Regul Integr Comp Physiol. 304(9):R702-11, 2013. PMID: 2344713
Ma F, Zhang L, Lyons D, Westlund KN.Orofacial neuropathic pain mouse model induced by Trigeminal Inflammatory Compression (TIC) of the infraorbital nerve. Mol Brain 5(1):44, 2012. PMID: 23270529
Westlund KN, Zhang L, Ma F, Oz HS. Chronic inflammation and pain in a tumor necrosis factor receptor (TNFR) (p55/p75-/-) dual deficient murine model. Transl Res. 2012 Jul;160(1):84-94. PMID: 22687964
Westlund, KN and Vera-Portocarrero, LP. Rat Models of Pancreatitis Pain. Methods in Molecular Biology 851: 223-38, 2012. PMID: 22351095
Westlund, K.N. and Willis, W.D., Ch. 33 Pain System. In: THE HUMAN NERVOUS SYSTEM, Third Edition, J. Mai and G. Paxinos (ed.). Elsevier, Amsterdam, 2011.
Westlund, Karin N. Ch 3 “Animal Models of Visceral Pain” pp. 41-68. In: Animal Models of Pain, Neuromethods, Chao Ma and Jun-Ming Zhang (eds.), Springer Science+Business Media, Vol. 49, 41-68, 2011. DOI: 10.1007/978-1-60761-880-5_3
Westlund KN, Kochukov MY, Lu Y and McNearney TA. Impact of central and peripheral TRPV1 and ROS levels on proinflammatory mediators and nociceptive behavior. Molecular Pain 6:46, 2010. PMID: 20691059
Westlund KN. Gene Therapy Approach: HSV-Enkephalin Reduces Fibrosis, Inflammation, and Pain, Chronic Pancreatitis, David Sutherland (Ed.), 2012. ISBN: 978-953-51-0011-9, Available from InTech: http://www.intechopen.com/articles/show/title/gene-therapy-approach-hsv-enkephalin-reduces-fibrosis-inflammation-and-pain