Recently (cite the paper), a paper on the description of the vesicular stomatitis virus pathogenesis in pigs was released. During the early stages of infection, interleukin 6 was found to be up regulated throughout the body.
The fact that this increase was seen after an infection with a particularly virulent VSV strain raises the possibility that IL-6 levels and virus virulence in pigs are related. Findings support the idea that increased Interleukin 6 Protein levels during some viral infections may aid in virus survival and/or exacerbate clinical illness.
How IL-6 works?
Upon the binding of its particular receptor, interleukin 6 protein initiates a series of signaling events linked to the activation of the JAK/STAT3 pathway. The transcription of numerous downstream genes, including cytokines, receptors, adaptor proteins, and protein kinases, which are linked to cellular signaling events, is subsequently encouraged.
Furthermore, it manages the synthesis of proteins that are involved in the control of gene expression. The number of genes that IL-6 activity controls could be the reason for this interleukin’s pleiotropic properties. The biological effects of IL-6 production have thus been linked to both pro- and anti-inflammatory effects. This demonstrates IL-6’s critical function in both activating and controlling the immune response.
Biological Activities Affected By The Production Of Il-6
- Controlling the expression of macrophage colony-stimulating factors to govern the development of monocytes into macrophages.
- Boosting IL-2 expression to increase B-cell IgG production.
- Stimulation of the STAT3 signaling pathway, which inhibits the development of dendritic cells.
- inducing the Th2 response while preventing Th1 polarisation.
Two Mechanisms Have Been Described To Promote The Inhibition Of Th1 Polarization By Il-6:
- IL-6 directs the response to Th2 by inducing CD4 T cells to produce IL-4.
- IL-6 influences CD4 T cells’ ability to secrete IFN, a necessary interferon to support Th1 polarisation.
Together with tumor necrosis factor-alpha and interleukin 1, the interleukin 6 protein is regarded as one of the most crucial cytokines during an infection.
Increased amounts of IL-6 may have adverse effects on the cellular immune system’s ability to defend against viruses, according to experimental scientific research. The creation of a persistent viral state in infected hosts may be favored in this situation due to many potential processes involving this cytokine that may alter viral clearance.
Observed Responses That Are Caused By Il-6:
Splenocytes that had been stimulated released IL-6 in vitro. As a result of the agonist P3C’s activation of the toll-like receptor 1/2, effector CD8 T-cell responses were suppressed. When compared to equally activated and stimulated splenocytes from animals treated with IL-6, this inhibits the generation of interferon-gamma.
The synergistic interaction of interleukin 6 and 17 have been linked to virus persistence and a worsened clinical outcome. Theiler’s murine encephalomyelitis virus infection caused this to happen.
The synergistic interaction between IL-6 and IL-17 causes the production of anti-apoptotic molecules, which prevents the death of TMEV-infected cells by virus-specific CD8+ T cells. Virus survival is aided by this.
IL-6 has a significant role during viral infections, which is supported by a number of studies. The cellular immune response to viral infections, however, may suffer from disparities in IL-6 production that are caused by specific circumstances.
Elevated Interleukin 6 Protein levels may further aggravate the immunopathology after chronic infection. It achieves this by causing an increase in inflammation, which is followed by the release of cytokines and cellular recruitment, as is the case with autoimmune illnesses.