Publications by authors named "Danen Mootoosamy Cunoosamy"

Article Synopsis
  • The airway epithelium plays a crucial role in fighting respiratory infections, primarily via the interferon regulatory factor-3 (IRF3), which promotes type I and type III interferon signaling.
  • A small-molecule inhibitor targeting the MEK pathway was tested to understand its effect on the interferon response in human primary airway epithelial cells when exposed to rhinovirus (RV2), respiratory syncytial virus (RSVA2), and a TLR3 agonist.
  • Results showed that inhibiting the MEK pathway enhances the IRF3-driven interferon response, activates the PI3K-AKT pathway, and reduces STAT3 activation, leading to increased production of antiviral signals.
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Human rhinovirus is frequently seen as an upper respiratory tract infection but growing evidence proves the virus can cause lower respiratory tract infections in patients with chronic inflammatory lung diseases including chronic obstructive pulmonary disease (COPD). In addition to airway epithelial cells, macrophages are crucial for regulating inflammatory responses to viral infections. However, the response of macrophages to HRV has not been analyzed in detail.

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Rationale: B cell-activating factor (BAFF) plays a major role in activation of B cells and in adaptive humoral immune responses. In chronic obstructive pulmonary disease (COPD), lymphoid follicles have been associated with disease severity, and overexpression of BAFF has been demonstrated within lymphoid follicles of patients with severe COPD.

Objectives: To investigate expression and localization of BAFF in the lungs of patients with COPD and to study the role of BAFF in COPD by antagonizing BAFF in a mouse model of chronic cigarette smoke (CS) exposure.

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Rationale: The B cell-attracting chemokine CXCL13 is an important mediator in the formation of tertiary lymphoid organs (TLOs). Increased numbers of ectopic lymphoid follicles have been observed in lungs of patients with severe chronic obstructive pulmonary disease (COPD). However, the role of these TLOs in the pathogenesis of COPD remains unknown.

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