Background
Bronchial epithelial cells (BEC) are primary target for Rhinovirus infection through attaching to cell membrane proteins. OM-85, a bacterial extract, improves recovery of asthma and COPD patients after viral infections, but only part of the mechanism was addressed, by focusing on defined immune cells.
Conclusion
The OM-85-induced increased of C1q-R and β-defensin, both important for antigen presentation and phagocytosis, supports its activity in host cell's defence against Rhinovirus infection.
Methods
BEC were treated with OM-85 alone (24 hours) or infected with Rhinovirus. BEC survival was monitored by manual cell counting and Rhinovirus replication by lytic activity. Immuno-blotting and ELISA were used to determine the expression of Rhinovirus interacting proteins: intracellular adhesion molecule (ICAM), major histocompatibility complex class II (MHC-2), complement component C1q receptor (C1q-R), inducible T-Cell co-stimulator (ICOS), its ligand ICOSL, and myeloid differentiation primary response gene 88 (Myd88); as well as for signal transducers Erk1/2, p38, JNK mitogen activated protein kinases MAPK), and cAMP.
Objective
We therefore determined the effect of OM-85 on isolated primary human BEC of controls (n = 8), asthma patients (n = 10) and COPD patients (n = 9).
Results
OM-85 significantly reduced Rhinovirus-induced BEC death and virus replication. OM-85 significantly increased the expression of virus interacting proteins C1q-R and β-defensin in all 3 probes and groups, which was prevented by either Erk1/2 MAPK or cAMP inhibition. In addition, OM-85 significantly reduced Rhinovirus induced expression of ICAM1 involving p38 MAPK. In BEC OM-85 had no significant effect on the expression of ICOS, ICOSL and MHC-2 membrane proteins nor on the adaptor protein MyD88.