Narayanan Parameswaran, BVSc., Ph.D.

Overall research focus of Parameswaran’s laboratory is to understand the cellular and molecular mechanisms that regulate inflammation and inflammatory diseases. In particular, the lab is interested in mechanisms of signal transduction in physiology and disease. There are two major focus areas that the lab is working on:

  1. A long-standing interest for the lab is studying the role of “arrestins” and “G-protein coupled receptor kinases (GRKs)" in inflammatory signaling. Arrestins are scaffolding proteins that can bind to receptors as well as signaling proteins and have a broad role in cell signaling. GRKs are serine/threonine kinases that can bind to and phosphorylate receptors and other intracellular substrates. Recent studies indicate that members of these two protein families have important functions in innate immune cells. Research in Parameswaran’s lab is currently focused towards understanding the biochemical and signaling mechanisms of arrestins and GRKs in immune cell types such as macrophages. How these functions of arrestins and GRKs are translated in disease pathogenesis is also another important area that is being pursued. Also in collaboration with Dr. McCabe’s lab (a bone and gut physiologist), we are looking at the role of arrestins and GRKs in intestinal inflammation and how this influences inflammation in other organs including bone.
  2. In an effort to further understand how gut as an organ can influence other organs in the body, we are working with Drs. McCabe and Britton (a Microbial geneticist) to modulate gut environment to test the effects on bone. Initial observations by Drs. McCabe and Britton set out the fundamental idea that oral treatment of probiotic L. reuteri can increase bone in mice. This quickly evolved into testing the effects of probiotics in clinically relevant models of bone loss including menopause and diabetes. Through collaborative and team-based efforts of the three labs (Drs. McCabe, Britton and Parameswaran), we identified that oral probiotics treatment in estrogen deficient mice (menopause model) not only prevents bone loss, but also alters bone marrow immune cells in a favorable manner. We are currently testing how estrogen deficiency and diabetes induces gut and bone inflammation, whether they are linked, and if so, whether probiotics are acting at the level of gut inflammation and/or bone inflammation.


Selected papers:

Note: For a complete list of published work please visit:

  1. Lactobacillus reuteri 6475 Increases Bone Density in Intact Females Only under an Inflammatory Setting.

Collins FL, Irwin R, Bierhalter H, Schepper J, Britton RA, Parameswaran N, McCabe LR.
PloS one. 2016; 11(4):e0153180.
PubMed [journal]PMID: 27058036 PMCID: PMC4825993


  1. Non-Hematopoietic β-Arrestin1 Confers Protection Against Experimental Colitis.

Lee T, Lee E, Arrollo D, Lucas PC, Parameswaran N.
Journal of cellular physiology. 2016; 231(5):992-1000. NIHMSID: NIHMS732540
PubMed [journal]PMID: 26479868 PMCID: PMC4728047


  1. Bacterial Dose-Dependent Role of G Protein-Coupled Receptor Kinase 5 in Escherichia coli-Induced Pneumonia.

Packiriswamy N, Steury M, McCabe IC, Fitzgerald SD, Parameswaran N.
Infection and immunity. 2016; 84(5):1633-41.|
PubMed [journal]PMID: 26975990


  1. Protective Role of β-arrestin2 in Colitis Through Modulation of T-cell Activation.

Sharma D, Malik A, Steury MD, Lucas PC, Parameswaran N.
Inflammatory bowel diseases. 2015; 21(12):2766-77. NIHMSID: NIHMS705107
PubMed [journal]PMID: 26296063 PMCID: PMC4654649


  1. Multifaceted role of β-arrestins in inflammation and disease.

Sharma D, Parameswaran N.
Genes and immunity. 2015; 16(8):499-513. NIHMSID: NIHMS712809
PubMed [journal]PMID: 26378652 PMCID: PMC4670277


  1. Prebiotic and Probiotic Regulation of Bone Health: Role of the Intestine and its Microbiome.

McCabe L, Britton RA, Parameswaran N.
Current osteoporosis reports. 2015; 13(6):363-71. NIHMSID: NIHMS727225
PubMed [journal]PMID: 26419466 PMCID: PMC4623939


  1. G-protein-coupled receptor kinases in inflammation and disease.

Packiriswamy N, Parameswaran N.
Genes and immunity. 2015; 16(6):367-77. NIHMSID: NIHMS701896
PubMed [journal]PMID: 26226012 PMCID: PMC4560643


  1. Probiotic L. reuteri treatment prevents bone loss in a menopausal ovariectomized mouse model.

Britton RA, Irwin R, Quach D, Schaefer L, Zhang J, Lee T, Parameswaran N, McCabe LR.
Journal of cellular physiology. 2014; 229(11):1822-30. NIHMSID: NIHMS585754
PubMed [journal]PMID: 24677054 PMCID: PMC4129456


  1. Nonhematopoietic β-Arrestin-1 inhibits inflammation in a murine model of polymicrobial sepsis.

Sharma D, Packiriswamy N, Malik A, Lucas PC, Parameswaran N.
The American journal of pathology. 2014; 184(8):2297-309.
PubMed [journal]PMID: 24946011 PMCID: PMC4116700


  1. Colitis-induced bone loss is gender dependent and associated with increased inflammation.

Irwin R, Lee T, Young VB, Parameswaran N, McCabe LR.
Inflammatory bowel diseases. 2013; 19(8):1586-97. NIHMSID: NIHMS485249
PubMed [journal]PMID: 23702805 PMCID: PMC4127911


  1. β-Arrestin-1 deficiency protects mice from experimental colitis.

Lee T, Lee E, Irwin R, Lucas PC, McCabe LR, Parameswaran N.
The American journal of pathology. 2013; 182(4):1114-23.
PubMed [journal]PMID: 23395087 PMCID: PMC3620400


  1. Tumor necrosis factor-α signaling in macrophages.

Parameswaran N, Patial S.
Critical reviews in eukaryotic gene expression. 2010; 20(2):87-103. NIHMSID: NIHMS281055
PubMed [journal]PMID: 21133840 PMCID: PMC3066460


  1. G-protein-coupled-receptor kinases mediate TNFα-induced NFκB signalling via direct interaction with and phosphorylation of IκBα.

Patial S, Luo J, Porter KJ, Benovic JL, Parameswaran N.
The Biochemical journal. 2009; 425(1):169-78. NIHMSID: NIHMS185736
PubMed [journal]PMID: 19796012 PMCID: PMC2856098


  1. Adenovirus vector-induced innate inflammatory mediators, MAPK signaling, as well as adaptive immune responses are dependent upon both TLR2 and TLR9 in vivo.

Appledorn DM, Patial S, McBride A, Godbehere S, Van Rooijen N, Parameswaran N, Amalfitano A.
Journal of immunology 2008; 181(3):2134-44.
PubMed [journal]PMID: 18641352


  1. Toll-like receptors differentially regulate GPCR kinases and arrestins in primary macrophages.

Loniewski K, Shi Y, Pestka J, Parameswaran N.
Molecular immunology. 2008; 45(8):2312-22.
PubMed [journal]PMID: 18180038