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Review
. 2019 Dec 10;11(1):1-16.
doi: 10.1007/s13167-019-00195-w. eCollection 2020 Mar.

The greater inflammatory pathway-high clinical potential by innovative predictive, preventive, and personalized medical approach

Maria Giovanna Maturo  1 , Marzia Soligo  2 , Greg Gibson #  3 , Luigi Manni #  2 , Christine Nardini #  4   5
Affiliations
Review

The greater inflammatory pathway-high clinical potential by innovative predictive, preventive, and personalized medical approach

Maria Giovanna Maturo et al. EPMA J. .

Abstract

Background and limitations: Impaired wound healing (WH) and chronic inflammation are hallmarks of non-communicable diseases (NCDs). However, despite WH being a recognized player in NCDs, mainstream therapies focus on (un)targeted damping of the inflammatory response, leaving WH largely unaddressed, owing to three main factors. The first is the complexity of the pathway that links inflammation and wound healing; the second is the dual nature, local and systemic, of WH; and the third is the limited acknowledgement of genetic and contingent causes that disrupt physiologic progression of WH.

Proposed approach: Here, in the frame of Predictive, Preventive, and Personalized Medicine (PPPM), we integrate and revisit current literature to offer a novel systemic view on the cues that can impact on the fate (acute or chronic inflammation) of WH, beyond the compartmentalization of medical disciplines and with the support of advanced computational biology.

Conclusions: This shall open to a broader understanding of the causes for WH going awry, offering new operational criteria for patients' stratification (prediction and personalization). While this may also offer improved options for targeted prevention, we will envisage new therapeutic strategies to reboot and/or boost WH, to enable its progression across its physiological phases, the first of which is a transient acute inflammatory response versus the chronic low-grade inflammation characteristic of NCDs.

Keywords: Autonomic nervous system; Big data analysis; Epigenetics; Genetics; Individualized patient profile; Inflammation; Machine learning; Mechanotransduction; Multi-omics; Network science; Neuro-immuno modulation; Non-communicable diseases; Patient stratification; Phenotyping; Predictive; Risk; Wound healing; and personalized medicine; modifiable; preventable factors; preventive.

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Conflict of interest statement

Conflict of interestThe authors declare that they have no conflict of interest.

Figures

Fig. 1
Fig. 1
Different effector pathways controlling inflammation are coordinated by brain activity. Circulation delivers inflammatory cells and diffusible factors (such as cytokines and anti-inflammatory hormones) to and from the inflammatory site, establishing slow and concentration gradient–dependent anti-inflammatory response. The local, fast neural anti-inflammatory regulation is exerted by cholinergic and noradrenergic neurons, releasing their neurotransmitters and predominately inhibiting pro-inflammatory cytokine release from immune cells. Sensory neurons are instead effective in stimulating cytokine synthesis and release, amplifying the local inflammatory response
Fig. 2
Fig. 2
Adapted with permission from [132]. The integration of multi-omic information to represent the RA molecular network. Panel a shows the density of the new multi-omic integrated network (grey nodes) versus the original transcriptomic network (red and orange nodes). Red and orange nodes are classified based on their topological characteristics (number of edges, connectivity) as climbers if the number of edges increases after integration in the new network, or accomplished if the number is stable. Panel b shows the same information at the functional level (i.e., which functions are altered by modifying the topology). This operation joined to biomedical considerations enabled the identification of IRK4 as a relevant molecule with potential side and adverse effects
See this image and copyright information in PMC

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