Steroids freely penetrate cell membranes and bind to a specific steroid-binding
protein receptor in the cytoplasm, forming a steroid-receptor complex.
This complex then moves into the nucleus and binds to chromatin, signaling
production of messenger RNA and coding for enzymes and proteins that
determine the response of that particular cell to the hormone.
Constriction of blood vessels and reduction of vascular permeability induced
by acute inflammation. This minimizes leakage into the target site of fluid,
proteins, and inflammatory cells.
Stabilization of intracellular lysosomal membranes and inhibition
of the expression of various damaging enzymes; inhibition of polymorphonuclear
(PMN) cell degranulation is also significantly inhibited.
Stabilization of mast cell and basophil membranes is important in inhibiting
the process of degranulation and subsequent release of histamine (vasoactive
amines), bradykinin, platelet-activating factor (PAF), proteases, and eosinophilic
chemotactic factors (ECF).
Mobilization of PMNs from the bone marrow results in neutrophilic leukocytosis.
Steroids simultaneously prevent adherence of PMNs to the vascular endothelium,
making them less mobile and less accessible to the site of inflammation.
Suppression of lymphocyte proliferation and lymphopenia. In small- to moderate-sized
doses, corticosteroids more significantly affect T lymphocytes. In larger
doses, B lymphocytes are affected as well, and, thus, antibody production.Steroids
do not destroy T lymphocytes but rather affect their redistribution into
circulation, concentrating them in the bone marrow
Reduction of circulating eosinophils and monocytes.
Inhibition of macrophage recruitment and migration.Steroids also interfere
with the ability of macrophages to process antigens.
Suppression of fibroplasia.
Depression of the bactericidal activity of monocytes and macrophages.
Via a protein called macrocortin, steroids inhibit phospholipase A2, resulting
in inhibition of arachidonic acid degradation and subsequent synthesis
of prostaglandins and leukotrienes by cyclooxygenase and lipoxygenase pathways