Magic™ Anti-RSV Monoclonal antibody, Clone N04042232

Respiratory syncytial virus (RSV) is the most common viral pathogen causing acute lower respiratory tract infections (LRTI) in infants. Airway epithelial cells, including Club cells, are primary targets of RSV infection. The "Club cell 10-kDa protein" (CC10), produced mainly by Club cells, possesses anti-inflammatory and immunoregulatory properties that are relevant in infection, injury, and allergic reactions. However, its role in the RSV infection is not fully understood. In the clinic, we found that levels of CC10 in the nasopharyngeal aspirates (NPA) of infants, hospitalized with RSV bronchiolitis, were significantly lower than those without LRTI, and were also negatively correlated with the severity of the disease. In BALB/c mice, the CC10 levels in the bronchoalveolar lavage fluid (BALF) were also decreased at the 5th day after infection. When recombinant CC10 was administrated in the mice, RSV-induced airway inflammation and airway hyperresponsiveness (AHR) were alleviated. Similarly, inhibition of cytosolic phospholipase A2 (cPLA2) or cyclooxygenase 2 (COX2), which is a downstream signaling molecule for cPLA2, both alleviated RSV-induced airway inflammation and AHR. Administration of CC10 reduced the phosphorylation of cPLA2 and protein levels of COX-2 in mouse lungs, resulting from infection, thus providing a molecular mechanism for previous reports that CC10 plays a protective role, partly through inhibiting the activity of cPLA2. We conclude that CC10 inhibits the cPLA2/COX2 pathway to alleviate RSV-induced lung airway inflammation and AHR.

A preliminary observation about resveratrol (RSV) dependent normalization of inflammatory and apoptotic factors in the cortex of hyperammonemic rat model of moderate grade hepatic encephalopathy (MoHE) led us to evaluate whether RSV is ultimately able to confer neuroprotection against MoHE pathogenesis and that it does so by activating its bonafide molecular target SIRT1. The present study compared the profile of relevant neurobehavioral pattern vs neuromorphometry of hippocampal CA1 neurons and SIRT1 activity in the hippocampus of the chronic liver failure (CLF) model of moderate grade HE (MoHE) rats induced by administration of 100 mg/kg body weight of thioacetamide i.p. for 10 days and in the CLF/MoHE rats treated with 10 mg/kg body weight RSV i.p. for 7 days. As compared to the control group rats, the MoHE rats showed significantly deranged pattern of memory and motor functions on MWM and rota rod tests, respectively. These behavioural deficits were associated with a significant reduction in apical dendrite length and number of branching points in the CA1 pyramidal neurons. Interestingly, all these parameters were found to be recovered back to their normal levels in the MoHE rats treated with RSV. Concordantly, MoHE associated declined SIRT1 activity in the hippocampus could be normalized back due to RSV treatment to those MoHE rats. Our findings suggest that RSV is able to normalize MoHE associated memory impairments and motor deficits vis a vis reversal of CA1 dendritic atrophy via SIRT1 activation.