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The Importance and Control of Low-Grade Inflammation Due to Damage of Cellular Barrier Systems That May Lead to Systemic Inflammation

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The Importance and Control of Low-Grade Inflammation Due to Damage of Cellular Barrier Systems That May Lead to Systemic Inflammation

Cecilia Rönnbäck et al. Front Neurol.

Abstract

Systemic low-grade inflammation can be initiated in vivo after traumatic injury or in chronic diseases such as neurodegenerative, metabolic, and autoimmune diseases. Inducers of inflammation trigger production of inflammatory mediators, which alter the functionality of tissues and organs and leads to harmful induction of different barrier systems in the body, where the blood-brain barrier, the blood-retinal barrier, blood-nerve barrier, blood-lymph barrier and the blood-cerebrospinal fluid barrier play major roles. The different barriers are unique but structured in a similar way. They are equipped with sophisticated junctional complexes where different connexins, protein subunits of gap junction channels and hemichannels, constitute important partners. The cells involved in the various barriers are coupled in networks, are excitable but do not express action potentials and may be targets for inflammation leading to changes in several biochemical cellular parameters. During any type of inflammation barrier break-down is observed where any form of injury can start with low-grade inflammation and may lead to systemic inflammation.

Keywords: blood-brain barrier; blood-cerebrospinal fluid barrier; blood-lymph barrier; blood-nerve barrier; blood-retinal barrier; low-grade inflammation; systemic inflammation.

Figures

Figure 1
Figure 1
Schematic illustration high-lightening different barriers in the body; the blood-brain barrier, blood-retinal barrier, blood-nerve barrier, blood-lymph barrier, and blood-cerebrospinal fluid barrier. The left side demonstrates the normal physiological conditions and the right side demonstrates inflammatory conditions. The illustration is made by Pontus Andersson, ArtProduction, Gothenburg, Sweden.

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References

    1. Abbott NJ, Rönnbäck L, Hansson E. Astrocyte-endothelial interactions at the blood-brain barrier. Nat Rev Neurosci. (2006) 7:41–53. 10.1038/nrn1824 - DOI - PubMed
    1. Saunders NR, Habgood MD, Møllgård K, Dziegielewska KM. The biological signinficance of brain barrier mechanisms: help or hindrance in drug delivery to the central nervous system? F1000 Res. (2016) 5:313. 10.12688/f1000research.7378.1 - DOI - PMC - PubMed
    1. De Bock M, Vandenbroucke RE, Decrock E, Culot M, Cecchelli R, Leybaert L. A new angle on blood-CNS interfaces: a role for connexins? FEBS Lett. (2014) 588:1259–70. 10.1016/j.febslet.2014.02.060 - DOI - PubMed
    1. Ramos CJ, Antonetti DA. The role of small GTPases and EPAC-Rap signaling in the regulation of the blood-brain and blood-retinal barriers. Tissue Barriers. (2017) 5:3. 10.1080/21688370.2017.1339768 - DOI - PMC - PubMed
    1. Mizisin AP, Weerasuriya A. Homeostatic regulatoion of the endoneurial microenvironment during development, aging and in response to trauma, disease and toxic insult. Acta Neuropathol. (2011) 121:291–312. 10.1007/s00401-010-0783-x - DOI - PMC - PubMed

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