Vascular Endothelium - Tissue Functioning and Remodeling in the Circulatory and Ventilatory Systems - page 543

Nanomotor myosin-2 is controlled by RhoA GTPase via MLCK and RoCK
kinases. On the other hand, the filamentous septin mesh modulates cortical rigidity,
hence lymphocyte motility [ 996 ]. 116
Leukocytes in 3D environments do not necessarily form leading edge protru-
sions that align with matrix fibers. Rather than emitting flat protrusions such as
lamellipodium, they can build cylindrical or tongue-like extensions (lobopodia) 117
between matrix fibers. In addition, they use integrins and other adhesion molecules,
such as syndecans, CD44, and discoidin domain receptors, to transmit traction
forces, but not necessarily as anchors onto the matrix [ 993 ]. Locomotion can
result from actin polymerization-driven cell deformation (ameboid-like migration).
Lobopodia pull the cell forward. Slipping cells protrude and migrate with the same
speed and shape as gripping cells.
However, in the absence of integrins, neutrophils that migrate through the
interstitium decelerate by about 30% [ 993 ]. T lymphocytes that move in lymph
nodes slow down by 10% when

β 2 integrins are lacking. Therefore, leuko-
cytes can use alternative modes of movement, switching during their displacement
from adhesion-dependent to deformation-based mode of motion, and conversely.

β 1 -and

9.7.10 Regulation of Inflammation

Inflammation is an adaptive response to tissue damage or dysfunction. Acute
inflammation triggered by infection or tissue injury caused by chemical or physical
agents is achieved by the coordinated delivery of blood components (plasma
proteins, platelets, and leukocytes) to the damaged site. 118
In the case of infection, particularly due to bacteria, inflammation is triggered
by pathogen recognition owing to receptors of the innate immune system (Toll-
like and nucleotide-binding oligomerization-domain protein-like receptors; Vol. 3 -
Chap. 11. Receptors of the Immune System), tissue-resident macrophages, and mas-
tocytes. It leads to the release of numerous inflammatory mediators: chemokines,
cytokines, vasoactive amines, eicosanoids, and products of 4 proteolytic cascades,
i.e., the kallikrein-kinin, coagulation, fibrinolytic, and complement cascades. These
mediators generate an exudate mainly across postcapillary venules.

116 Septins constitute an additional family of cytoskeletal proteins distinct from microfilaments,
microtubules, and intermediate filaments. Septin GTPases assemble in T-lymphocyte cortex and
repress protrusions, hence restricting cell migration through narrow pores.
117

: foot.
118 A cell is in a basal state when oxygen, nutrients, and growth factors are available in the
absence of abnormal change in physicochemical parameters (temperature, osmolarity, etc.) of
its environment. In noxious conditions, stressed tissues become dysfunctional. Mild dysfunction
can be cured by tissue-resident cells, mainly macrophages and mastocytes that drive para-
inflammation, i.e., a process between basal and inflammatory states, whereas extensive (sustained
or excessive) dysfunctions require the recruitment of additional types of leukocytes.

λ o β o ζ : lobe; π o δ o ζ