Omar Tliba, Ph.D.

Omar Tliba, Ph.D.

Associate Professor, Division of Pulmonary and Critical Care Medicine Robert Wood Johnson Medical School, Rutgers Institute for Translational Medicine and Science, Child Health Institute of New Jersey

Rutgers Institute for Translational Medicine and Science
Child Health Institute of New Jersey
Rutgers, The State University of New Jersey
89 French Street
New Brunswick, NJ 08901
Fax: (732) 235-7178


Ms, Biomedical Sciences, University of Rennes I, France
Ms, Immunology, Institut pasteur, Paris
Ph.D., Immunology, University of Francois Rabellais, Tours, France

Postdoctoral Fellowship

University of Pennsylvania, Philadelphia, PA

The recent therapeutic benefit in severe asthmatics provided by bronchial thermoplasty, a therapy that attenuates bronchoconstriction via reduction of airway smooth muscle (ASM) mass, has strongly supported the notion that ASM is a key player in the pathogenesis of asthma. ASM could also participate in the progression of asthma by secreting pro-inflammatory mediators reported both in cultured cells and in bronchial biopsies. My research interest includes airway smooth muscle biology, glucocorticoid signaling, and glucocorticoid resistance. Current research efforts are focused in four major areas:

  • Use ASM cells as a model to gain mechanistic insight in the development of steroid insensitivity in severe asthma. While much research aimed at understanding the basis of insensitivity to glucocorticoid therapy in severe asthmatics focused on the role of immune cells, little has been done to clarify the role of ASM cells. Recent studies performed on bronchial biopsies from asthmatics treated with inhaled or oral glucocorticoids showed a persistent expression of chemokines in ASM bundles. The expression of these genes correlated with the severity of asthma. Our previous studies replicated this finding in vitro using cultured human ASM cells. The induction of pro-asthmatic genes is less sensitive to inhibition by glucocorticoids when such induction was triggered by TNF and IFN combination. We will use ASM as a model to further define the mechanisms involved in steroid insensitivity.
  •   Characterize the mechanisms that regulate glucocorticoid receptor phosphorylation with a primary focus on the role of Mitogen-Activated Protein Kinase (MAPK) pathways and serine/threonine protein phosphatases (PPs). Phosphorylation of glucocorticoid receptor (GR) on various residues such as serine 203 (S203), S211, and S226 plays a key role in determining the strength and duration of GR actions. At present, uncertainty still exists about the nature of the GR phosphorylation-dependent mechanisms regulating the overall cellular responsiveness to glucocorticoid and which particular GR phosphorylation profile is associated with steroid insensitive conditions. We are using various molecular, biochemical, and cellular strategies to better characterize the role of Mitogen-Activated Protein Kinase (MAPK) pathways and serine/threonine protein phosphatases (PPs) that regulate GR phosphorylation, and thus function, in airway cells with a long-term goal of providing new insight into therapies aiming at restoring steroid responsiveness in patients with severe asthma.
  • Expression and function of glucocorticoid-target genes in airway cells. These studies involve collaborations with a number of investigators and are focused on evaluating the biological role of steroid-target genes in airway cells both in vivo and in vitro using endobronchial tissues isolated from asthmatics with varying degrees of disease severity. Our long-term goal is to integrate the biological effects of such genes in the evaluation of inhaled glucocorticoids efficacy in asthmatic patients.
  • Transcriptional regulation of cytokine functions in airway cells. ASM cells respond to many cytokines, growth factors and lipid mediators to produce a wide array of immuno-modulatory molecules which may in turn orchestrate and perpetuate the disease process in asthma. Our goals are to identify intracellular signaling pathways by which cytokines modulate or induce these cellular responses. A focus of this project is to investigate the transcriptional and post-transcriptional mechanisms regulating cytokine functions in ASM cells.


Selected publications

  1. Adiponectin/AdipoR1 Axis Promotes IL-10 Release by Human Regulatory T Cells Ramos-Ramírez P, Malmhäll C, Tliba O, Rådinger M, Bossios A. Front Immunol. 2021 May 18;12:677550. doi: 10.3389/fimmu.2021.677550. eCollection 2021. PMID: 34084174 Free PMC article.
  2. Potential Role of Mast Cells in Regulating Corticosteroid Insensitivity in Severe Asthma Alzahrani A, Hussain A, Alhadian F, Hakeem J, Douaoui S, Tliba O, Bradding P, Amrani Y. Adv Exp Med Biol. 2021 April 1;1303:1-12.
  3. Glucocorticoid Receptor β (GRβ): Beyond Its Dominant-Negative Function Ramos-Ramírez P, Tliba O. Int J Mol Sci. 2021 Mar 31;22(7):3649.
  4. Important lessons learned from studies on the pharmacology of glucocorticoids in human airway smooth muscle cells: Too much of a good thing may be a problem. Amrani Y, Panettieri RA, Ramos-Ramírez P, Schaafsma D, Kaczmarek K, Tliba O. Pharmacol Ther. 2020 May 27:107589. Epub ahead of print.
  5. Glucocorticoids rapidly activate cAMP production via G<sub>αs</sub> to initiate non-genomic signaling that contributes to one-third of their canonical genomic effects Nuñez FJ, Johnstone TB, Corpuz ML, Kazarian AG, Mohajer NN, Tliba O, Panettieri RA Jr, Koziol-White C, Roosan MR, Ostrom RS. FASEB J. 2020 Feb;34(2):2882-2895. Epub 2019 Dec 27.
  6. Budesonide enhances agonist-induced bronchodilation in human small airways by increasing cAMP production in airway smooth muscle Koziol-White C, Johnstone TB, Corpuz ML, Cao G, Orfanos S, Parikh V, Deeney B, Tliba O, Ostrom RS, Dainty I, Panettieri RA Jr. Am J Physiol Lung Cell Mol Physiol. 2020 Feb 1;318(2):L345-L355. Epub 2019 Nov 20.
  7. Glucocorticoids regulate pentraxin-3 expression in human airway smooth muscle cells Zhang J, Koussih L, Shan L, Halayko AJ, Tliba O, Gounni AS. PLoS One. 2019 Aug 22;14(8):e0220772.
  8. Airway smooth muscle cells are insensitive to the anti-proliferative effects of corticosteroids: The novel role of insulin growth factor binding Protein-1 in asthma Bui H, Amrani Y, Deeney B, Panettieri RA, Tliba O. Immunobiology. 2019 Jul;224(4):490-496. doi: 10.1016/j.imbio.2019.05.006. Epub 2019 May 23. PMID: 31133345 Free PMC article.
  9. Paucigranulocytic asthma: Uncoupling of airway obstruction from inflammation Tliba O, Panettieri RA Jr. J Allergy Clin Immunol. 2019 Apr;143(4):1287-1294. Epub 2018 Jun 19.
  10. Non genomic Effects of Glucocorticoids: An Updated View Panettieri RA, Schaafsma D, Amrani Y, Koziol-White C, Ostrom R, Tliba O. Trends Pharmacol Sci. 2019 Jan;40(1):38-49. Epub 2018 Nov 26.