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Review
. 2021 May 12;8(5):380.
doi: 10.3390/children8050380.

Perinatal Inflammation: Could Partial Blocking of Cell Adhesion Molecule Function Be a Solution?

Nikolaos Vrachnis  1   2   3 , Dimitrios Zygouris  3 , Dionysios Vrachnis  4 , Nikolaos Roussos  3 , Nikolaos Loukas  5 , Nikolaos Antonakopoulos  1 , Georgios Paltoglou  6 , Stavroula Barbounaki  7 , Georgios Valsamakis  6 , Zoi Iliodromiti  8
Affiliations
Review

Perinatal Inflammation: Could Partial Blocking of Cell Adhesion Molecule Function Be a Solution?

Nikolaos Vrachnis et al. Children (Basel). .

Abstract

In spite of the great advances made in recent years in prenatal and perinatal medicine, inflammation can still frequently result in injury to vital organs and often constitutes a major cause of morbidity. It is today well established that in neonates-though vulnerability to infection among neonates is triggered by functional impairments in leukocyte adhesion-the decreased expression of cell adhesion molecules also decreases the inflammatory response. It is also clear that the cell adhesion molecules, namely, the integrins, selectins, and the immunoglobulin (Ig) gene super family, all play a crucial role in the inflammatory cascade. Thus, by consolidating our knowledge concerning the actions of these vital cell adhesion molecules during the prenatal period as well as regarding the genetic deficiencies of these molecules, notably leukocyte adhesion deficiency (LAD) I, II, and III, which can provoke severe clinical symptoms throughout the first year of life, it is anticipated that intervention involving blocking the function of cell adhesion molecules in neonatal leukocytes has the potential to constitute an effective therapeutic approach for inflammation. A promising perspective is the potential use of antibody therapy in preterm and term infants with perinatal inflammation and infection focusing on cases in which LAD is involved, while a further important scientific advance related to this issue could be the combination of small peptides aimed at the inhibition of cellular adhesion.

Keywords: Ig superfamily; cell adhesion molecules; integrins; neonatal inflammation; perinatal; prenatal; selectins.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
The integrin family. Integrins are heterodimers composed of 18 α subunits and 8 β subunits. β1 subunits participate in all three kinds of receptors: collagen, laminin, and leukocyte, while β2 and β7 participate in leukocyte receptors and β4 in laminin receptors.
Figure 2
Figure 2
Mechanism of leukocyte transendothelial migration. Initially, there is loose adhesion, which gradually becomes firmer, resulting in diapedesis and emigration. Endothelial cell stimulation leads to ICAM-1 and JAM-1 up-regulation, thus enhancing the adhesion, while selectins enhance the attachment of the free-flowing leukocytes. ICAM-1: Intercellular Adhesion Molecule 1; JAM-1: junctional adhesion molecule-1; CD99: Cluster of differentiation 99; PECAM-1: Platelet endothelial cell adhesion molecule-1.
Figure 3
Figure 3
In the model of oligodendrocyte cell damage and death, Ig superfamily have a pivotal role leading in neurodevelopment problems. Macrophages and microglia adhere to oligodendrocytes through ICAM1 and LFA-1. Additionally, high levels of inflammatory cytokines shown in the figure enhance this interaction, thus accelerating cell damage and death. IFN-γ: Interferon gamma; TNF: Tumor necrosis factor; IL-1β: Interleukin 1β; ICAM-1: Intercellular Adhesion Molecule 1.
See this image and copyright information in PMC

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