Lung Injury is One of the Primary Causes of Morbidity and Mortality in Critically Ill Patients. These Patients Will be Monitored for: 1) Immune Cell Activation 2) Blood-based Biomarkers. In Vitro Models Derived From These Samples Will be Treated With Novel Agent PIP-2 to Evaluate Its Efficacy.

ARDS (Acute Respiratory Distress Syndrome)

ROS, ARDS, PIP-2, immune cells, peripheral blood mononuclear cells

Acute Lung Injury (ALI) and Acute Respiratory Distress Syndrome (ARDS) is a condition where high levels of inflammation damage the lung. This is a highly morbid condition with no specific pharmacologic therapies. The investigators posit that ARDS is caused due to an exaggerated activation of immune cells and that blockade of this activation may reduce lung damage/injury and help in ARDS management and possibly recovery. To test this hypothesis, the investigators propose to generate an in vitro immune cell model and test a novel (reactive oxygen species) blocking agent PIP-2 on this model. The investigating team will obtain blood of ARDS patients and isolate immune cells (specifically peripheral blood mononuclear cells or PBMC) and monitor the activation of these cells and their blockade by PIP-2. This is entirely an in vitro study.

The research study is being conducted to understand the behavior of immune cells in a patient with Acute Respiratory Distress Syndrome (ARDS). Immune cells protect humans from external threats like infection. However, if these cells are overactive, they can lead to an infection progressing into ARDS. ARDS arises as a result of extensive damage possibly due to overactivated immune cells. This project aims to understand the link between immune cell activation and ARDS. To do so, the investigators will isolate immune cells specifically peripheral blood mononuclear cells (PBMC) from blood of ARDS patients. These cells will be utilized for in vitro experiments by checking for overactivation. Cells in vitro will also be treated with a novel synthetic agent PIP-2 (being developed Peroxitech Inc. a Collaborator of this study) to check if PIP-2 can reduce overactivation as monitored by the production of reactive oxygen species.

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