- Inflammasome and immune disorders
- Neonatal Respiratory Health Research
- Pulmonary Hypertension Research and Treatments
- Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Respiratory Support and Mechanisms
- Immune Response and Inflammation
- Mitochondrial Function and Pathology
- RNA modifications and cancer
- Autophagy in Disease and Therapy
- Heme Oxygenase-1 and Carbon Monoxide
- MicroRNA in disease regulation
- Cardiac Ischemia and Reperfusion
- Chronic Obstructive Pulmonary Disease (COPD) Research
- interferon and immune responses
- Epigenetics and DNA Methylation
- Eicosanoids and Hypertension Pharmacology
- Circular RNAs in diseases
- S100 Proteins and Annexins
- Cancer, Hypoxia, and Metabolism
- Redox biology and oxidative stress
- Eosinophilic Esophagitis
- RNA Research and Splicing
- Medical Imaging and Pathology Studies
- Ion channel regulation and function
- Asthma and respiratory diseases
University of South Florida
2016-2025
Massachusetts General Hospital
2008-2010
Harvard University
2008-2010
Brigham and Women's Hospital
2010
Pulmonary and Critical Care Associates
2009
Oklahoma State University
2005-2006
Inspiration of a high concentration oxygen, therapy for acute lung injury (ALI), could unexpectedly lead to reactive oxygen species (ROS) production and hyperoxia-induced (HALI). Nucleotide-binding domain leucine-rich repeat PYD-containing protein 3 (NLRP3) senses the ROS, triggering inflammasome activation interleukin-1β (IL-1β) secretion. However, role NLRP3 in HALI is unclear. The main aim this study determine effect gene deletion on inflammatory response epithelial cell death. Wild-type...
Pulmonary Arterial Hypertension (PAH) is a progressive devastating disease characterized by excessive proliferation of the Smooth Muscle Cells (PASMCs). Studies suggest that PAH and cancers share an apoptosis-resistant state featuring cell proliferation. MicroRNA-206 (miR-206) known to regulate implicated in various types cancers. However, role miR-206 has not been studied. In this study, it hypothesized could play PASMCs. present expression patterns were investigated normal hypertensive...
Soluble angiotensin-converting enzyme 2 (sACE2) could be a therapeutic option to treat coronavirus disease 2019 (COVID-19) infection. Severe acute respiratory syndrome (SARS-CoV-2) utilizes ACE2 receptors on cell surfaces gain intracellular entry, making them an ideal target for therapy. High-affinity variants of sACE2, engineered using high-throughput mutagenesis, are capable neutralizing COVID-19 infection as decoy receptors. These compete with native present cells by binding spike (S)...
A hallmark of hyperoxic acute lung injury is the influx inflammatory cells to tissue and production proinflammatory cytokines, such as IL-1beta; however, mechanisms connecting hyperoxia response damage not clear. The inflammasome protein complex activates caspase-1 promote processing secretion cytokines. We hypothesized that hyperoxia-induced K(+) efflux via purinergic P2X7 receptor cause inflammation injury. To test this hypothesis, we characterized expression activation components in...
OPINION article Front. Physiol., 21 March 2013Sec. Redox Physiology Volume 4 - 2013 | https://doi.org/10.3389/fphys.2013.00050
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Disproportionately high incidence and mortality of respiratory infection such as influenza A virus (IAV) SARS-CoV-2 have been evidenced in the elderly, but role mechanism age-associated immune deregulation disease exacerbation are not well defined. Using a late generation mice deficient telomerase RNA (Terc-/- ), we herein demonstrated that aged were exquisitely susceptible to viral infection, with excessive inflammation increased mortality. Furthermore, identified cGAS/STING pathway, which...
Overexpression of IL-6 markedly diminishes hyperoxic lung injury, hyperoxia-induced cell death, and DNA fragmentation, enhances Bcl-2 expression. We hypothesized that changes in the interactions between family members play an important role IL-6-mediated protective response to oxidative stress. Consistent with this hypothesis, we found induced expression, both vivo vitro, disrupted proapoptotic antiapoptotic factors, suppressed H(2)O(2)-induced loss mitochondrial membrane potential vitro. In...
Type II alveolar epithelial cells (AEC II) proliferate and transdifferentiate into type I I) when the normal AEC population is damaged in lung alveoli. We hypothesized that signaling by transforming growth factor beta1 (TGF beta1), through its downstream Smad proteins, involved keeping quiescent altered may be trans-differentiation of to I. In lung, TGF Smad4 were highly expressed II. Using an vitro cell culture model, we demonstrated I-like began with a proliferative phase, followed...
The hallmark of acute lung injury (ALI) is the influx proinflammatory cytokines into tissue and alveolar permeability that ultimately leads to pulmonary edema. However, mechanisms involved in inflammatory cytokine production are unclear. Recent studies suggest excessive ceramide has clinical relevance as a mediator edema ALI. Our earlier indicate activation inflammasome promotes processing secretion causes role underlying mechanism relation not known. We hypothesized activates epithelial...
Background Sensitisation with Aspergillus fumigatus ( Af ) is known to be associated severe allergic lung inflammation, but the mechanism remains clarified. Phosphoinositide 3-kinase (PI3K)-δ and endoplasmic reticulum (ER) stress are suggested involved in steroid-resistant inflammation. We aimed elucidate role of PI3K-δ its relationship ER fungus-induced Methods Using -exposed vivo vitro experimental systems, we examined whether regulates stress, thereby contributing steroid resistance...
We report that S100 proteins were reduced in patients with chronic rhinosinusitis (CRS). S100A8/9, which is important epithelial barrier function, was particularly decreased elderly CRS. Epithelial expression of S100A8/9 partly regulated by the IL-6 trans-signaling pathway. The goal this study to investigate whether or not age-related reduction CRS associated blunting trans-signaling. levels IL-6, soluble receptor (sIL-6R), gp130 (sgp130), and from control subjects (n = 10), without nasal...
// Lakshmi Galam 1 , Athena Failla Ramani Soundararajan Richard F. Lockey and Narasaiah Kolliputi Division of Allergy Immunology, Department Internal Medicine, Morsani College University South Florida, Tampa, FL, USA Correspondence to: Kolliputi, email: Keywords : acute lung injury, hyperoxia, ROS, 4-HNE, mitochondrial dysfunction, Immunology Microbiology Section, Immune response, Immunity Received August 10, 2015 Accepted September 24, Published October 15, Abstract Prolonged exposure to...
Idiopathic Pulmonary Fibrosis (IPF) is a progressive and chronic lung disorder characterized by the fibrosis of parenchyma, resulting in gradual decline function eventual respiratory failure. Despite advancements understanding IPF, its exact cause remains elusive. Environmental pollutants—particularly cadmium carbon black—have gained attention due to their widespread prevalence. This paper delves into unique perspective on this interaction examining epigenetic modifications induced these...
IL-6 overexpression protects mice from hyperoxic acute lung injury in vivo, and treatment with cells oxidant-mediated death vitro. The mechanisms of protection, however, are not clear. We characterized the expression, localization, regulation Bax, a proapoptotic member Bcl-2 family, wild-type (WT) lung-specific transgenic (Tg(+)) exposed to 100% O(2) human umbilical vein endothelial (HUVEC) treated H(2)O(2) IL-6. In control HUVEC or WT O(2), marked induction Bax translocation dimerization...
Increasing evidence shows that hyperoxia is a serious complication of oxygen therapy in acutely ill patients causes excessive production free radicals leading to hyperoxia-induced acute lung injury (HALI). Our previous studies have shown P2X7 receptor activation required for inflammasome during HALI. However, the role HALI unclear. The main aim this study was determine effect gene deletion on Wild-type (WT) and knockout (P2X7 KO) mice were exposed 100% O 2 72 h. KO treated with had enhanced...