FibroGenesis Identifies Mechanism Responsible for Blocking COVID19-Like Lung Inflammation

Regenerative Medicine Company Advances Development of Fibroblast-Based Product as an "Off the Shelf" Cell-Treatment for Coronavirus Acute Respiratory Distress Syndrome (ARDS)

HOUSTON, July 1, 2020 /PRNewswire/ -- FibroGenesis announced today identification of molecular mechanisms associated with the potent reduction of lung inflammation previously reported by the Company in an animal model of COVID-19 lung failure. 

The Company disclosed data demonstrating that administration of PneumoBlast resulted in dramatic alterations of immunological signaling molecules called "cytokines".  The studies showed that PneumoBlast reduced concentrations of the inflammatory cytokines interleukin-1 beta, interleukin-6, interleukin-8, interleukin-17, interleukin-18, and Tumor Necrosis Factor alpha, TNFa.  Supporting the inflammation-inhibiting properties of PneumoBlast, Company scientists observed an increase in anti-inflammatory cytokines interleukin-4, interleukin-10, interleukin-13 and interleukin-35, as well as regeneration-associated cytokines FGF-2 and HGF-1.  The cytokines found to be manipulated by PneumoBlast are known to be associated with survival and recuperation from COVID-19. 

Interleukin-1 beta (IL-1β): Mortality from acute respiratory distress syndrome (ARDS), is associated with increased IL-1β.  Studies have shown that administration of Anakinra, a drug specifically designed to block IL-1β, reduces mortality in patients with a COVID-19 associated cytokine storm, one of the other causes of death.

Interleukin-6 (IL-6):  In a review of 1,426 COVID-19 patients in nine separated studies, interleukin-6 levels were more than three times higher in patients with complicated COVID-19 compared with those with a non-complicated disease.  Furthermore, it was shown that higher levels of interleukin-6 correlated with death.   Supporting a causative role of interleukin-6 in pathology of COVID-19, studies have shown that administration of blocking antibodies to interleukin-6 reduces pathology of this disease.

Interleukin-8 (IL-8): Patients with ARDS show that elevated levels of IL-8 are associated with higher mortality.  IL-8 is known to recruit and activate neutrophils in the lung. Under normal circumstances, neutrophils serve to fight infections.  In the case of COVID-19, excessive neutrophils in the lung are believed to be associated with lethality.