SAQ3: Describe the likely molecular events in the leukocytes that have led to this
increased strength of adhesion. (3 marks)

Question

BlackTom AI · Accepted Answer

The prompt asks to describe the likely molecular events in leukocytes that have led to an increased strength of adhesion, so we should map out the adhesion cascade and how intracellular signaling changes enhance adhesion.
First, consider the initial contact: leukocytes roll along the endothelium mediated by selectins (E- and P-selectin) binding to their ligands. An increased strength of adhesion implies not just more rolling but a transition to firm adhesion, which requires inside-out activation of integrins on the leukocyte surface.
Next, chemokine signaling on the endothelial surface (for example CXCL8/IL-8 or C5a) binds chemokine receptors on leukocytes, triggering intracellular signaling cascades. This signaling leads to rapid conformational changes (activation) of integrins such as LFA-1 (αLβ2) and Mac-1 (αMβ2), changing them from low- to high-affinity states.
Concurrently, outside-in signaling promotes cytoskeletal rearrangements. Actin polymerization and linkage to integrins via adaptor proteins (like talin, kindlin, and paxillin) stabilize the high-affinity integrin–ligand interactions, strengthening adhesion to ICAM-1 and VCAM-1 on the endothelium.
Increased adhesion strength can also involve upregulation or increased clustering of adhesion ligands on leukocytes and endothelial cells. Endothelial cells may express higher levels of ICAM-1 and VCAM-1 in response to inflammatory cytokines (e.g., TNF-α, IL-1β), providing more binding sites for integrins and amplifying adhesion.
Signal transduction pathways implicated include activation of small GTPases (Rac, Rho, and Cdc42) that regulate the actin cytoskeleton, as well as kinases such as Src family kinases, focal adhesion kinase (FAK), and MAP kinases that propagate signals to strengthen cytoskeletal contacts and integrin–ligand bonds.
Calcium flux within leukocytes also contributes to adhesion by promoting conformational changes in integrins and activating calmodulin-dependent processes that support cytoskeletal remodeling and adhesion stabilization.
Therefore, the combined picture is: chemokine-triggered inside-out signaling → integrin activation and clustering (LFA-1, Mac-1) → stronger leukocyte–endothelial adhesion via ICAM-1/VCAM-1 interactions → cytoskeletal rearrangements and focal adhesion complex formation — all of which yield increased adhesion strength during an inflammatory response.
If we were to expand on experimental indicators, we would expect increased expression or activation (not just surface density) of integrin heterodimers, enhanced affinity states of integrins observed via ligand-binding assays, and upregulated endothelial adhesion molecule expression in inflamed tissues, all correlating with tighter adhesion.

BIOM20001_2025_SM1 Practise EOS exam in classic quiz format

SAQ3: Describe the likely molecular events in the leukocytes that have led to this increased strength of adhesion. (3 marks)

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