Tissue injury results in an initiation of inflammation. Acute mucosal inflammation developed in response to an infection is beneficial to host, as it helps in eradicating the infectious pathogen. However, the inflammation that persists (chronic inflammation) in mucosal tissue for longer time-period is detrimental to host because it prevents an effective healing and the normal functioning of the tissue. Depending upon the tissue that gets inflamed, chronic inflammation could cause morbidity or mortality to the host. The goal of our lab is to understand the cellular and molecular pathways involved in regulating sterile inflammation and viral infection induced chronic inflammation.
Awards & Honors
- Received - Faculty Recognition award" for Research at Oakland University, 2014
- Awarded - Junior Faculty Travel Award to attend American Association of Immunologists (AAI) annual meeting held at Boston, MA, 2012
- Awarded National Eye Institute (NEI) travel grant to attend Association for Research in Vision and Ophthalmology (ARVO) annual meeting held at Fort Lauderdale, FL, 2011
- Awarded Junior Faculty Travel Award to attend AAI annual meeting held at Baltimore, MD, 2009
- Awarded Junior Faculty Travel Award to attend AAI annual meeting held at Seattle, WA, 200
- Awarded Prestigious Bill and Melinda Gates Foundation Global Health Travel award to attend Keystone Symposium on Immunologic Memory at Santa Fe, NM, 2007
- nvited to give a talk in minisymposium on The Untapped Immunomodulating Potential of Neuropeptides at 2013 ARVO (The Association for Research in Vision and Ophthalmology) meeting held at Seattle, Washington from May 5-9 2013
- Invited to give a talk on Rediscovering the pathogenesis of herpetic stromal keratitis at Allergan Pharmaceuticals, Irvin, CA, 2011
- Invited to give a talk on Substance P, a double edge sword in herpes viral infection at Neuroimmunology lecture series of The University of Michigan School of Medicine, Ann Arbor, MI, 2011
Role of peripheral nervous system (PNS) in regulating immunity and immunopathology to herpes simplex virus (HSV) infection: HSV-1 and HSV-2 are neurotropic viruses. HSV-1 is well known to establish latency in trigeminal ganglia (TG). Recurrent reactivation of HSV-1 in TG followed by an anterograde trafficking of virus to the corneal tissue could cause the development of herpes stromal keratitis (HSK). The later is virus-induced chronic immunoinflammatory condition and the most common cause of infection-induced blindness in the United States. We recently demonstrated the role of sensory neuropeptides in pathogenesis of HSK. While using mouse model of ocular herpes simplex virus-1 infection, we are now determining the role of neuropeptides and neurotransmitters in HSV-1 latency and immunopathogenesis to HSK.
Role of hypoxia and oxygenation pathways in regulating pathogenesis of HSK: Massive influx of neutrophils and the development of angiogenesis in inflamed cornea are the hallmark of HSK. We recently showed the development of hypoxia in progressing HSK lesions in a mouse model. Development of inflammatory hypoxia was associated with the predominance of glycolysis in inflamed corneal tissue. The goal of this study is to understand how metabolic pathways in inflamed corneal tissue change under hypoxic and oxygenated condition.
Role of peripheral nervous system in regulating inflammaging: Inflammaging is low-grade chronic inflammation, which is reported to develop with healthy aging. Inflammaging could significantly affect the immunity of elderly individual. The lab is trying to understand the relative contribution of PNS in the development of inflammaging and the effect of inflammaging on immune system homeostasis and the immunity to elderly host.
Links of Interest
- Gaddipati S, Estrada K, Rao P, Jerome A and Suvas S (2015). IL-2/anti-IL-2 complex treatment inhibits the development but not the progression of herpetic stromal keratitis. J Immunol. 194 (1): 273-82.
- Alazabi FA, Zohdy, MA and Suvas S (2013). Parameter estimation from experimental laboratory data of HSV-1 by using alternative regression method. Systems and Synthetic Biology. 7(14): 151-60.
- Channappanavar R, Twardy BS and Suvas S (2012). Blocking of PDL-1 interaction enhances primary and secondary CD8 T cell response to herpes simplex virus-1 infection. PLoS One. 7(7): e39757.
- Twardy BS, Channappanavar R, Suvas S (2011). Substance P in the corneal stroma regulates the severity of herpetic stromal keratitis lesions. Invest Ophthalmol Vis Sci. 4; 52(12): 8604-13.
- Channappanavar R, Twardy BS, Krishna P and Suvas S (2009). Advancing age leads to predominance of inhibitory receptor expressing CD4 T cells. Mech Ageing Dev 130 (10): 709-12.
- Susmit Suvas (2008). Advancing age and immune cell dysfunction: is it reversible or not? Expert Opinion on Biological Therapy 8 (5): 657-68.