transforming-growth-factor-beta and Brain-Abscess

It is known that transforming growth factor beta (TGF-beta) is involved in the modulation of cell growth, differentiation, and repair following injury. We performed an immunohistochemical study of human brain autopsy and biopsy material for the expression of TGF-beta isoforms beta 1, beta 2 and beta 3, and TGF-beta receptor (T beta R) type I in different cells of necrotizing lesions such as infarction and abscess, and compared them with controls. Various cell types, both inside and in the proximity of lesions, showed immunoreactivity indicating the presence of all three isoforms. Significant values of immunoreaction for various TGF-beta s and T beta R-I were observed in cells such as astrocytes, macrophages, neurons, microvascular endothelial cells, and granulocytes. In the control cases, comprising biopsy material without necrotizing lesions, a prominent TGF-beta 2 immunoreactivity was observed in glial cells and neurons. TGF-beta 1 and TGF-beta 3 reactivity in controls, when compared with TGF-beta 2, was less. T beta R-I antiserum showed clear and distinct signals in the same type of cells as for TGF-beta s in the necrotizing lesions with varying values of significance. Our findings suggest that TGF-beta s and their receptor type I are involved in reactive processes around necrotizing human brain lesions like glial and macrophage responses, angiogenesis, and deposition of extracellular matrix.

Topics: Adult; Aged; Aged, 80 and over; Brain; Brain Abscess; Brain Chemistry; Cerebral Infarction; Female; Humans; Immunohistochemistry; Male; Middle Aged; Necrosis; Receptors, Transforming Growth Factor beta; Transforming Growth Factor beta

We correlated the histopathological findings of six human brain abscesses with the expression of basic fibroblast growth factor (bFGF), nerve growth factor (NGF), platelet-derived growth factor (PDGF) and transforming growth factor-beta (TGF beta). The clinical courses ranged from 1 month to 1 year and viridans streptococcus was the major pathogen. In early abscesses, we demonstrated strong bFGF and moderate NGF and PDGF immunoreactivities in neutrophils and monocytes/macrophages infiltrating the abscess wall and in the fibrin layer lining the abscess center. In the subacute cases, growth of capillaries and fibroblasts into the fibrin layer and deposition of collagen resulted in the formation of a mesodermal layer between the abscess center and the outer gliotic layer. The proliferative non-neural cells (endothelial cells, fibroblasts and glial cells) expressed mild to strong bFGF, NGF and PDGF immunoreactivities, while strong TGF beta staining was seen in the extracellular matrix. A loss of growth factor expression and increased fibrosis was seen in the chronic case. These findings suggest that bFGF, NGF, PDGF and TGF beta produced by the continued influx of leukocytes and by the proliferating non-neural cells may mediate various steps of defense mechanisms and wound healing such as angiogenesis, fibrogenesis and gliosis.

Topics: Antibody Specificity; Brain; Brain Abscess; Fibroblast Growth Factor 2; Fibrosis; Gliosis; Humans; Immunohistochemistry; Neovascularization, Pathologic; Nerve Growth Factors; Platelet-Derived Growth Factor; Transforming Growth Factor beta