The inflammatory process is an essential immunological defence system in living organisms that has evolved to enhance species survival. Short-term, acute inflammation is a first-line defence mechanism that acts against harmful agents, such as pathogens, toxins, or allergens. Under normal conditions, the tightly coordinated actions of various defence components including immune cells, endogenous anti-inflammatory agents, and tissue remodelling processes enable the resolution of acute inflammation by facilitating the elimination of pathogens, infected cells, and repair to damaged tissues to restore body homeostasis (Freire MO et al, 2013).
However, when this intricate acute inflammatory response fails to resolve and persists, more defence components are mobilized to create a long-term unresolved immune response known as chronic inflammation. Chronic inflammation, which typically manifests itself in a low-grade manner for a prolonged period, involves macrophage- and lymphocyte-accumulated leukocytes (Chen M, et al, 2015), and various other cellular components. It is important to recognize that this chronic inflammation is causally associated with changes in the cellular redox state and cell death signalling pathways (Chung HY et al, 2006).
One of the major changes that occur during ageing is the dysregulation of the immune response, leading to a chronic systemic inflammatory state. Among the dysregulated proinflammatory mediators, cytokines and chemokines are major culprits in the development of chronic inflammation and the immunosenescence process.
For instance, interleukin (IL)-6, tumour necrosis factor (TNF)-α, and their receptors, are upregulated in aged tissues and cells (Bruunsgaard H et al, 2003). Elevated levels of chemokines and C-reactive protein (CRP) have been found to be involved in age-related pathogenesis (Gordon CJ et al, 2011).
In the ageing literature, there are currently two major hypotheses related to age-related inflammation: inflammageing (Franceschi C et al, 2000; Franceschi C et al, 2007) and molecular inflammation (Chung HY et al, 2006; Chung HY et al, 2000; Chung HY et al, 2002; Chung HY et al, 2011). These two are complementary to each other to a large extent but differ in their focus on age-related inflammatory phenomena. Chronic inflammation is so widely and deeply involved in many age-related chronic disorders such as atherosclerosis, diabetes, obesity, sarcopenia, and Alzheimer’s disease (Chung HY et al, 2011), it opens the arena for novel therapeutics, such as Carocell Bio’s novel safe and effective peptides. Skin ageing is a logical place to start.
It is now recognised that inflammation is the cause of senescence/ageing. It is hypothesised that chronic therapy with our topical peptide JEL0305, permitted because of safety as well as efficacy, could firstly prevent the recurrence of the AD, see above, and eventually lead to a delay in ageing of the skin to which it is applied. Clinical trials will help prove this exciting prospect that could open a cosmetic side or licensing opportunity for Carocell Bio.
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