Dr. Tousif Sultan is an Assistant Professor in the Department of Cellular Biology & Anatomy at LSU Health Shreveport, USA, specializing in cardiovascular immunology. He completed his PhD in Biochemistry/Immunology at Calcutta University, India, in 2014, where he investigated the role of Programmed Death-1 (PD-1) in tuberculosis infection and explored the immunomodulatory effects of curcumin. His postdoctoral research at the University of KwaZulu-Natal focused on novel immunomodulatory therapies for infectious diseases such as tuberculosis and malaria, with a particular emphasis on PD-1's role in immune regulation.

Dr. Tousif's research has evolved to focus on the intersection of inflammation, immune response, and cardiac pathology. At the University of Alabama at Birmingham, he studied the role of HIPK2 in cardiovascular disease, including its influence on fibrosis and inflammation in heart failure. His work also explored the immunoregulatory roles of TKI in cardiotoxicity and the mechanisms linking immune cell dynamics to cancer.

He is currently leading multiple funded research projects, including studies on the cell-specific role of HIPK2 in cardiac pathophysiology and the role of PD-L1 in cardiac injury and heart failure. Dr. Tousif is the recipient of several prestigious awards, including the Senior Research Fellowship from ICMR and a full-time scholarship from DBT (Govt. of India) during his M.Sc. training.

His research interests also include the impact of inflammatory processes in cardiac diseases, and he continues to explore therapeutic strategies to mitigate tissue damage in heart disease and cancer.

1. Immunotherapy-Induced Cardiotoxicity and Immune Regulation in the Heart

   Immunotherapy, particularly immune checkpoint inhibitors (ICIs), represents a transformative advancement in cancer treatment, offering remarkable efficacy across various malignancies. However, this therapeutic success is accompanied by a spectrum of immune-related adverse events (IRAEs), among which ICI-associated cardiotoxicity, although rare, carries the highest mortality rate. Despite its clinical severity, the pathophysiological mechanisms driving ICI-induced cardiac toxicity remain poorly understood.

   ICIs commonly target immune regulatory pathways via monoclonal antibodies (mAbs) directed against programmed death-1 (PD-1), programmed death-ligand 1 (PD-L1), and cytotoxic T lymphocyte-associated antigen 4 (CTLA-4). Of these, PD-L1 is notably enriched in cardiac tissue, with expression found across key cardiac cell types, including myeloid cells, cardiomyocytes, fibroblasts, and endothelial cells (ECs). However, the cell type–specific contribution of PD-L1 signaling in the context of autoimmune myocarditis and immune-mediated cardiac injury during cancer immunotherapy remains poorly defined.

   The Sultan Laboratory is dedicated to investigating the cell-specific roles of PD-L1 in regulating myocardial inflammation and cardiac pathophysiology. Using genetically engineered conditional PD-L1 knockout mouse models, we aim to dissect the molecular and immunological pathways involved in immunotherapy-induced cardiotoxicity. Our goal is to advance mechanistic understanding and ultimately develop targeted strategies to mitigate the cardiac complications associated with cancer immunotherapy."

    

2. Mechanism of cardiac dysfunction and remodeling at the level of inflammation
   Heart failure (HF) development has been associated with four broad categories of risk factors: traditional risk factors (such as ischemic injury, hypertension, and metabolic syndrome), genetic predispositions, mechanical deformities, and immune-mediated factors. The latter includes both infectious and autoimmune triggers, which activate immune cells to initiate a primary immune response targeting the heart. While the inflammatory mechanisms and subsequent tissue repair processes following acute cardiac injury are well-defined, the role of these pathways in the context of chronic heart failure remains poorly understood.

   To address this gap, we utilize innovative, Cre-based genetic systems that are cell-type specific and inducible, enabling precise deletion of specific cells or genes during established chronic heart failure. This approach allows us to identify the inflammatory response components that are either protective or detrimental, with the goal of translating our findings into clinically relevant strategies to manage heart failure.

3. Inflammatory Biomarkers and Chronic Heart Failure
   Inflammatory soluble factors are a hallmark of chronic heart failure (HF), yet the role of inflammation as a primary driver of disease progression remains unclear. Studies assessing biomarkers in both HF patients and animal models show elevated levels of proinflammatory cytokines (such as TNF-α, IL-1, IL-6, galectin 3, TNFR1, and TNFR2) during HF progression, supporting the hypothesis that inflammation may contribute to the disease. Similarly, elevated serum proinflammatory cytokines have been observed in patients with heart failure with preserved ejection fraction (HFpEF). However, clinical trials aimed at inhibiting inflammation in chronic HF have largely yielded negative results. The failure of these therapeutic interventions may stem from an incomplete understanding of how inflammatory cytokines mediate cardiac remodeling. In this work, I employ both in vitro and in vivo systems to screen inflammatory biomarkers and explore whether these markers are a cause or consequence of disease progression.

4. Unresolved Inflammation and Chronic Heart Failure
   Significant advancements have been made in understanding the cardiac immune response following sterile cardiac injuries such as myocardial infarction (MI) or ischemia-reperfusion (I/R) injury. However, the immunological dynamics associated with infectious cardiac injury remain poorly understood. Emerging evidence indicates that various bacterial and viral pathogens, including influenza virus, COVID-19, Pseudomonas aeruginosa, and Streptococcus pneumoniae, can lead to cardiac damage and dysfunction even after the infection has been cleared. Yet, the underlying mechanisms remain largely unexplored.

   Damage-associated molecular patterns (DAMPs) or alarmins activate immune cells to initiate a trauma response in an autocrine fashion. This suggests that incomplete resolution of inflammation and the progression to chronic heart failure (HF) may be driven by ongoing signaling through Toll-like receptors (TLRs). The ability of infectious agents to induce acute cardiac damage is likely determined by the specific virulence factors they possess. However, the immunological mechanisms by which the host addresses this damage, and how this immune response contributes to aberrant healing and long-term cardiac dysfunction, remain entirely unknown.

   We aim to uncover the mechanisms behind bacterial and viral infection-induced cardiac dysfunction. These studies have broad implications for understanding the basic biology of infection-driven excessive cardiac inflammation (myocarditis), adverse remodeling, and long-term cardiac dysfunction during convalescence.

5. Defining the In Vivo and In Vitro Crosstalk Between Cardiac Fibroblasts, Immune Cells, and Cardiomyocytes
   Cardiac injury induces the activation of cardiac fibroblasts (FBs) through a process known as myofibroblast transformation. Myofibroblasts play a critical role in the healing phase of injury. However, their persistence after injury resolution can lead to pathological fibrotic remodeling and subsequent cardiac dysfunction. While cardiac fibroblasts are well-established contributors to fibrosis, they also play a pivotal role in inflammation by serving as a major source of inflammatory cytokines and chemokines, including IL-1, IL-6, and others. Moreover, there is a significant interplay between hypertrophic and inflammatory signaling pathways in cardiomyocytes (CMs). To further understand these interactions, our lab has developed an in vitro co-culture model involving FBs-immune cells and CMs-immune cells to investigate the signaling pathways driving cell-cell communication. Using these systems, our research aims to elucidate the mechanisms underlying the crosstalk between FBs-immune cells and CMs-immune cells, with a focus on evaluating therapeutic strategies to mitigate pathological paracrine signaling.

1. Prachi Umbarkar, Sultan Tousif, Ashish Jaiswal, Arvind Singh Bhati, Angelica Toro Cora, Rohan Sethi, Zhang Qinkun Zhang, Hind Lal. Fibroblast-    specific MyD88-dependent signaling aggravates inflammation and cardiac dysfunction in the MI heart. BBA- Molecular Basis of Disease. Volume 1871, Issue 3, March 2025, 167703. https://doi.org/10.1016/j.bbadis.2025.167703
2. Manisha Gupte, Prachi Umbarkar, Jacob Lemon, Sultan Tousif, Hind Lal. Animal models of haploinsufficiency revealed the isoform-specific role of GSK-3 in HFD-induced obesity and glucose intolerance. Am J Physiol Cell Physiol. 2024 Dec 1;327(6):C1349-C1358.10.1152/ajpcell.00552.2024
3. Mallikarjun Patil, Sarojini Singh, Praveen Kumar Dubey, Sultan Tousif, Prachi Umbarkar, Qinkun Zhang, Hind Lal, Mary Kathryn Sewell-Loftin, Channakeshava Sokke Umeshappa,     Yohannes T Ghebre, Steven Pogwizd, Jianyi Zhang, Krishnamurthy Prasanna Krishnamurthy. Fibroblast-Specific Depletion of Human Antigen R Alleviates Myocardial Fibrosis Induced by Cardiac Stress. JACC Basic Transl Sci. 2024 Jun 24;9(6):754-770. 10.1016/j.jacbts.2024.03.004
4. Kenneth P Hough, Jennifer L Trevor, Balu K Chacko, John G Strenkowski, Yong Wang, Kayla F Goliwas, Nathaniel B Bone, Young-Il Kim, Renita Holmes, Shia Vang, Alexandra Pritchard, Jay Chin, Sandeep Bodduluri, Veena B Antony, Sultan Tousif, Mohammad Athar, Diptiman Chanda, Kasturi Mitra, Jaroslaw Zmijewski, Jianhua Zhang, Steven R Duncan, Victor J Thannickal, Susanne Gabrielsson, Victor M Darley-Usmar, Jessy S Deshane. Small Extracellular Vesicle Signaling and Mitochondrial Transfer Reprograms T Helper Cell Function in Human Asthma. bioRxiv [Preprint]. 2024 May 3:2024.04.30.589227.10.1101/2024.04.30.589227
5. Prachi Umbarkar, Suma Ejantkar, Sulivette Y Ruiz Ramirez, Angelica Toro Cora, Qinkun Zhang, Sultan Tousif, Hind Lal. Cardiac fibroblast GSK-3α aggravates ischemic cardiac injury by promoting fibrosis, inflammation, and impairing angiogenesis. Basic Res Cardiol. 2023 Sep 1;118(1):35.0.1007/s00395-023-01005-1
6. Prachi Umbarkar, Sulivette Y. Ruiz Ramirez, Angelica Toro Cora,  Sultan Tousif, Hind Lal. GSK-3 at the heart of cardiometabolic diseases: Isoform-specific targeting is critical to therapeutic benefit. (BBADIS-23-89, BBA - Molecular Basis of Disease (ELS). 2023 Aug;1869(6):166724. https://pubmed.ncbi.nlm.nih.gov/37094727/
7. Sultan Tousif, Anand P Singh, Prachi Umbarkar, Cristi Galindo, Nicholas Wheeler, Angelica Toro Cora, Qinkun Zhang, Sumanth D Prabhu, Hind Lal. Ponatinib Drives Cardiotoxicity by S100A8/A9-NLRP3-IL-1β Mediated Inflammation. Circ Res. 2023 Feb 3;132(3):267-289. https://pubmed.ncbi.nlm.nih.gov/36625265/
8. Prachi Umbarkar, Sultan Tousif, Anand P Singh, Joshua C Anderson, Qinkun Zhang, Michelle D Tallquist, James Woodgett, Hind Lal. Fibroblast GSK-3α Promotes Fibrosis via RAF-MEK-ERK Pathway in the Injured Heart. Circ Res. 2022 Sep 16;131(7):620-636. https://pubmed.ncbi.nlm.nih.gov/36052698/
9. Manisha Gupte, Sultan Tousif, Jacob J Lemon, Angelica Toro Cora , Prachi Umbarkar , Hind Lal. Isoform-Specific Role of GSK-3 in High Fat Diet Induced Obesity and Glucose Intolerance. Cells. 2022 Feb 5;11(3):559. https://pubmed.ncbi.nlm.nih.gov/35159367/
10. Sultan Tousif, Joshua Jackson, Kenneth P. Hough, John G. Strenkowski, Yong Wang, Victor J. Thannickal, Robert H. McCusker, Selvarangan Ponnazhagan & Jessy S. Deshane. Indoleamine 2, 3-dioxygenase promotes differentiation of regulatory B cells in lung cancer. Front Immunol. 2021 Nov 19;12:747780. https://pubmed.ncbi.nlm.nih.gov/34867973/
11. Mallikarjun Patil, Sherin Saheera, Praveen K Dubey, Asher Kahn-Krell, Prem Kumar Govindappa, Sarojini Singh, Sultan Tousif, Qinkun Zhang, Hind Lal, Jianyi Zhang, Gangjian Qin , Prasanna Krishnamurthy. Novel Mechanisms of Exosome-Mediated Phagocytosis of Dead Cells in Injured Heart. Circ Res 2021 Nov 12;129(11):1006-1020. https://pubmed.ncbi.nlm.nih.gov/34623174/
12. Prachi Umbarkar, Suma Ejantkar, Sultan Tousif, Hind Lal. Mechanisms of Fibroblast Activation and Myocardial Fibrosis: Lessons Learned from FB-Specific Conditional Mouse Models. Cells. 2021 Sep 14;10(9):2412. https://pubmed.ncbi.nlm.nih.gov/34572061/
13. Dhiraj Kumar Singh, Sultan Tousif, Ashima Bhaskar, Annu Devi, Kriti Negi, Barnani Moitra, Anand Ranganathan, Ved Prakash Dwivedi, Gobardhan Das. Luteolin as a potential host-directed immunotherapy adjunct to isoniazid treatment of tuberculosis. PLoS Pathog. 2021 Aug 20;17(8):e1009805. https://pubmed.ncbi.nlm.nih.gov/34415976/
14. Umbarkar, P., A. P. Singh, S. Tousif, Q. Zhang, P. Sethu, and H. Lal. "Repurposing Nintedanib for Pathological Cardiac Remodeling and Dysfunction." Pharmacol Res 169 (Jul 2021): 105605. https://www.ncbi.nlm.nih.gov/pubmed/33965510
15. Wang, Y., K. F. Goliwas, P. E. Severino, K. P. Hough, D. Van Vessem, H. Wang, S. Tousif, et al. "Mechanical Strain Induces Phenotypic Changes in Breast Cancer Cells and Promotes Immunosuppression in the Tumor Microenvironment." Lab Invest 100, no. 12 (Dec 2020): 1503-16. https://www.ncbi.nlm.nih.gov/pubmed/32572176
16. Singh, A. P., P. Umbarkar, S. Tousif, and H. Lal. "Cardiotoxicity of the Bcr-Abl1 Tyrosine Kinase Inhibitors: Emphasis on Ponatinib." Int J Cardiol 316 (Oct 1 2020): 214-21. https://www.ncbi.nlm.nih.gov/pubmed/32470534
17. Singh, A. P., S. Tousif, P. Umbarkar, and H. Lal. "A Pharmacovigilance Study of Hydroxychloroquine Cardiac Safety Profile: Potential Implication in Covid-19 Mitigation." J Clin Med 9, no. 6 (Jun 15 2020). https://www.ncbi.nlm.nih.gov/pubmed/32549293
18. Pritchard, A., S. Tousif, Y. Wang, K. Hough, S. Khan, J. Strenkowski, B. K. Chacko, V. M. Darley-Usmar, and J. S. Deshane. "Lung Tumor Cell-Derived Exosomes Promote M2 Macrophage Polarization." Cells 9, no. 5 (May 24 2020). https://www.ncbi.nlm.nih.gov/pubmed/32456301. * Equal first author
19. Ahmad, S., D. Bhattacharya, N. Gupta, V. Rawat, S. Tousif, L. Van Kaer, and G. Das. "Clofazimine Enhances the Efficacy of Bcg Revaccination Via Stem Cell-Like Memory T Cells." PLoS Pathog 16, no. 5 (May 2020): e1008356. https://www.ncbi.nlm.nih.gov/pubmed/32437421
20. Sharma, N. S., G. Vestal, K. Wille, K. N. Patel, F. Cheng, S. Tipparaju, S. Tousif, et al. "Differences in Airway Microbiome and Metabolome of Single Lung Transplant Recipients." Respir Res 21, no. 1 (May 6 2020): 104. https://www.ncbi.nlm.nih.gov/pubmed/32375889
21. Gupte, M., P. Umbarkar, A. P. Singh, Q. Zhang, S. Tousif, and H. Lal. "Deletion of Cardiomyocyte Glycogen Synthase Kinase-3 Beta (Gsk-3beta) Improves Systemic Glucose Tolerance with Maintained Heart Function in Established Obesity." Cells 9, no. 5 (Apr 30 2020). https://www.ncbi.nlm.nih.gov/pubmed/32365965
22. Hough, K. P., J. L. Trevor, J. G. Strenkowski, Y. Wang, B. K. Chacko, S. Tousif, D. Chanda, et al. "Exosomal Transfer of Mitochondria from Airway Myeloid-Derived Regulatory Cells to T Cells." Redox Biol 18 (Sep 2018): 54-64. https://www.ncbi.nlm.nih.gov/pubmed/29986209
23. Wang, Y., C. C. Schafer, K. P. Hough, S. Tousif, S. R. Duncan, J. F. Kearney, S. Ponnazhagan, H. C. Hsu, and J. S. Deshane. "Myeloid-Derived Suppressor Cells Impair B Cell Responses in Lung Cancer through Il-7 and Stat5." J Immunol 201, no. 1 (Jul 1 2018): 278-95. https://www.ncbi.nlm.nih.gov/pubmed/29752311
24. Tousif, S., D. K. Singh, S. Mukherjee, S. Ahmad, R. Arya, R. Nanda, A. Ranganathan, et al. "Nanoparticle-Formulated Curcumin Prevents Posttherapeutic Disease Reactivation and Reinfection with Mycobacterium Tuberculosis Following Isoniazid Therapy." Front Immunol 8 (2017): 739. https://www.ncbi.nlm.nih.gov/pubmed/28713372
25. Bali, P., S. Tousif, G. Das, and L. Van Kaer. "Strategies to Improve Bcg Vaccine Efficacy." Immunotherapy 7, no. 9 (2015): 945-8. https://www.ncbi.nlm.nih.gov/pubmed/26310608 * Equal first author
26. Tousif, Sultan, Shaheer Ahmad, Kuhulika Bhalla, P. Moodley, and G. Das. "Challenges of Tuberculosis Treatment with Dots: An Immune Impairmentperspective." Journal of Cell Science and Therapy 6 (2015): 1-6.
27. Bhalla, K., M. Chugh, S. Mehrotra, S. Rathore, S. Tousif, V. Prakash Dwivedi, P. Prakash, et al. "Host Icams Play a Role in Cell Invasion by Mycobacterium Tuberculosis and Plasmodium Falciparum." Nat Commun 6 (Jan 14 2015): 6049. https://www.ncbi.nlm.nih.gov/pubmed/25586702
28. Samuchiwal, S. K., S. Tousif*, D. K. Singh, A. Kumar, A. Ghosh, K. Bhalla, P. Prakash, et al. "A Novel Peptide Interferes with Mycobacterium Tuberculosis Virulence and Survival." FEBS Open Bio 4 (2014): 735-40. https://www.ncbi.nlm.nih.gov/pubmed/25349777* Equal first author
29. Tousif, S., D. K. Singh, S. Ahmad, P. Moodley, M. Bhattacharyya, L. Van Kaer, and G. Das. "Isoniazid Induces Apoptosis of Activated CD4+ T Cells: Implications for Post-Therapy Tuberculosis Reactivation and Reinfection." J Biol Chem 289, no. 44 (Oct 31 2014): 30190-95. https://www.ncbi.nlm.nih.gov/pubmed/25202011
30. Samuchiwal, S. K., S. Tousif*, D. K. Singh, A. Kumar, A. Ghosh, K. Bhalla, P. Prakash, et al. "A Peptide Fragment from the Human Cox3 Protein Disrupts Association of Mycobacterium Tuberculosis Virulence Proteins Esat-6 and Cfp10, Inhibits Mycobacterial Growth and Mounts Protective Immune Response." BMC Infect Dis 14 (Jul 1 2014): 355. https://www.ncbi.nlm.nih.gov/pubmed/24985537 * Equal first author
31. Ghosh, A., S. Tousif, D. Bhattacharya, S. K. Samuchiwal, K. Bhalla, M. Tharad, S. Kumar, et al. "Expression of the Arpc4 Subunit of Human Arp2/3 Severely Affects Mycobacterium Tuberculosis Growth and Suppresses Immunogenic Response in Murine Macrophages." PLoS One 8, no. 7 (2013): e69949. https://www.ncbi.nlm.nih.gov/pubmed/23894563
32. Thakur, R. S., S. Tousif, V. Awasthi, A. Sanyal, P. K. Atul, P. Punia, and J. Das. "Mesenchymal Stem Cells Play an Important Role in Host Protective Immune Responses against Malaria by Modulating Regulatory T Cells." Eur J Immunol 43, no. 8 (Aug 2013): 2070-7. https://www.ncbi.nlm.nih.gov/pubmed/23670483
33. Singh, Y., V. Kaul, A. Mehra, S. Chatterjee, S. Tousif, V. P. Dwivedi, M. Suar, et al. "Mycobacterium Tuberculosis Controls Microrna-99b (Mir-99b) Expression in Infected Murine Dendritic Cells to Modulate Host Immunity." J Biol Chem 288, no. 7 (Feb 15 2013): 5056-61. https://www.ncbi.nlm.nih.gov/pubmed/23233675
34. Dwivedi, V. P., S. Tousif*, D. Bhattacharya, D. V. Prasad, L. Van Kaer, J. Das, and G. Das. "Transforming Growth Factor-Beta Protein Inversely Regulates in Vivo Differentiation of Interleukin-17 (Il-17)-Producing Cd4+ and Cd8+ T Cells." J Biol Chem 287, no. 5 (Jan 27 2012): 2943-7. https://www.ncbi.nlm.nih.gov/pubmed/22170065 * Equal first author
35. Khan, M. M., S. Chatterjee, V. P. Dwivedi, N. K. Pandey, Y. Singh, S. Tousif, N. S. Bhavesh, et al. "Cd4+ T Cell-Derived Novel Peptide Thp5 Induces Interleukin-4 Production in Cd4+ T Cells to Direct T Helper 2 Cell Differentiation." J Biol Chem 287, no. 4 (Jan 20 2012): 2830-5. https://www.ncbi.nlm.nih.gov/pubmed/22130674
36. Tousif, S., Y. Singh, D. V. Prasad, P. Sharma, L. Van Kaer, and G. Das. "T Cells from Programmed Death-1 Deficient Mice Respond Poorly to Mycobacterium Tuberculosis Infection." PLoS One 6, no. 5 (May 12 2011): e19864. https://www.ncbi.nlm.nih.gov/pubmed/21589883
    
    Communicated/ Under Review
37. Sultan Tousif, Prachi Umbarkar, Rohan Sethi, Angelica Tora Cora, Yunxi Chen, Jin He, Praveen Dubey, Qinkun Zhang, Min Xie, Prasanna Krishnamurthy, Hind Lal. HIPK2 regulates cardiac Inflammation and function through Purinergic signaling (Circulation Research, CIRCRES/2024/324811) *Corresponding author
38. Sultan Tousif, Daniel Minassian, Prachi Umbarkar, Mohammed Mohasin, Chao He, Nathan Erdmann, Min Xie, Palaniappan Sethu, Carlos J Orihuela, and Hind Lal. S100A8/9-NLRP3 mediated chronic unresolved inflammation drives Cardiac pathologies following Invasive Pneumococcal Disease (Submitted to Experimental & Molecular Medicine, EMM20241639R) *Corresponding author
39. Cara C.  Schafer, Sultan Tousif, and Jessy S.  Deshane.  Indoleamine 2,3-dioxygenase   pathway: Relevance in cancer progression and tumor cell escape.  Laboratory investigation; (18-0097-BF, under revision).
    
    Book Chapter
40. *Tousif S, Singh AP, Umbarkar P, Lal H. Cardiovascular Complications of Immune Checkpoint    Inhibitors. “Immune Cells, Inflammation and Heart Diseases.” CRC Press/Taylor & Francis. *Corresponding author

Postdoctoral Position Available - Sultan Laboratory

The Sultan Laboratory at LSUHS is currently seeking a highly motivated postdoctoral fellow to join our research team. Our work is at the intersection of cardio-oncology, cardio-immunology, and immune-mediated mechanisms of heart failure, with a particular emphasis on cancer immunotherapy–induced cardiotoxicity and the crosstalk between immune cells and cardiac cell subsets in the context of heart failure. Interested candidates are encouraged to contact Dr. Sultan directly for more information at tousif.sultan@lsuhs.edu.

Graduate Research Opportunity - Sultan Laboratory

Graduate students with an interest in cardio-immunology are encouraged to explore research opportunities in the Sultan Laboratory. Interested students should contact Dr. Sultan at tousif.sultan@lsuhs.edu.

Undergraduate Students Position Available – Sultan Laboratory

The Sultan Laboratory at LSUHS is currently accepting applications for a student worker position. This opportunity is ideal for students interested in gaining hands-on experience in biomedical research, particularly in the areas of cardio-oncology, cardio-immunology, and immune-mediated mechanisms of heart failure. Interested candidates should contact Dr. Sultan directly for more information at tousif.sultan@lsuhs.edu.

Contact the Sultan Lab

LSU Health Shreveport
Department of Cellular Biology & Anatomy
1501 Kings Hwy
Shreveport, LA 71103

Office: (318) 675-5594 
Lab: (318) 675-5595 
Email: tousif.sultan@lsuhs.edu