Soluble transforming growth factor beta-1 enhances murine mast cell release of Interleukin 6 in IgE-independent and Interleukin 13 in IgE-dependent settings in vitro

The pleiotropic immunoregulatory cytokine transforming growth factor beta (TGF-beta) potently suppresses production of the human immunodeficiency virus (HIV), the causative agent of the acquired immunodeficiency syndrome, in the chronically infected promonocytic cell line U1. TGF-beta significantly (50-90%) inhibited HIV reverse transcriptase production and synthesis of viral proteins in U1 cells stimulated with phorbol myristate acetate (PMA) or interleukin 6 (IL-6). Furthermore, TGF-beta suppressed PMA induction of HIV transcription in U1 cells. In contrast, TGF-beta did not significantly affect the expression of HIV induced by tumor necrosis factor alpha (TNF-alpha). These suppressive effects were not mediated via the induction of interferon alpha (IFN-alpha). TGF-beta also suppressed HIV replication in primary monocyte-derived macrophages infected in vitro, both in the absence of exogenous cytokines and in IL-6-stimulated cultures. In contrast, no significant effects of TGF-beta were observed in either a chronically infected T cell line (ACH-2) or in primary T cell blasts infected in vitro. Therefore, TGF-beta may play a potentially important role as a negative regulator of HIV expression in infected monocytes or tissue macrophages in infected individuals.

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Role of peripheral inflammatory biomarkers, transforming growth factor-beta and interleukin 6 in predicting peritoneal adhesions following repeat cesarean delivery

Irish Journal of Medical Science (1971 -) ◽

10.1007/s11845-021-02878-8 ◽

2022 ◽

Author(s):

Elif Ciler Eren ◽

Pelin Basım

Keyword(s):

Growth Factor ◽

Cesarean Delivery ◽

Transforming Growth Factor Beta ◽

Interleukin 6 ◽

Transforming Growth Factor ◽

Inflammatory Biomarkers ◽

Peritoneal Adhesions ◽

Growth Factor Beta ◽

Repeat Cesarean Delivery

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Transforming growth factor beta 1 (TGF-beta 1) induced neutrophil recruitment to synovial tissues: implications for TGF-beta-driven synovial inflammation and hyperplasia.

Journal of Experimental Medicine ◽

10.1084/jem.173.5.1121 ◽

1991 ◽

Vol 173 (5) ◽

pp. 1121-1132 ◽

Cited By ~ 129

Author(s):

R A Fava ◽

N J Olsen ◽

A E Postlethwaite ◽

K N Broadley ◽

J M Davidson ◽

...

Keyword(s):

Growth Factor ◽

Synovial Tissue ◽

Transforming Growth Factor Beta ◽

Transforming Growth Factor ◽

Biologically Active ◽

Tgf Beta ◽

Histological Techniques ◽

Growth Factor Beta

We have studied the consequences of introducing human recombinant transforming growth factor beta 1 (hrTGF-beta 1) into synovial tissue of the rat, to begin to better understand the significance of the fact that biologically active TGF-beta is found in human arthritic synovial effusions. Within 4-6 h after the intra-articular injection of 1 microgram of hrTGF-beta 1 into rat knee joints, extensive recruitment of polymorphonuclear leukocytes (PMNs) was observed. Cytochemistry and high resolution histological techniques were used to quantitate the influx of PMNs, which peaked 6 h post-injection. In a Boyden chamber assay, hrTGF-beta 1 at 1-10 fg/ml elicited a chemotactic response from PMNs greater in magnitude than that evoked by FMLP, establishing that TGF-beta 1 is an effective chemotactic agent for PMNs in vitro as well as in vivo. That PMNs may represent an important source of TGF-beta in inflammatory infiltrates was strongly suggested by a demonstration that stored TGF-beta 1 was secreted during phorbol myristate acetate-stimulated degranulation in vitro. Acid/ethanol extracts of human PMNs assayed by ELISA contained an average of 355 ng of TGF/beta 1 per 10(9) cells potentially available for secretion during degranulation of PMNs. [3H]Thymidine incorporation in vivo and autoradiography of tissue sections revealed that widespread cell proliferation was triggered by TGF-beta 1 injection. Synovial lining cells and cells located deep within the subsynovial connective tissue were identified as sources of at least some of the new cells that contribute to TGF-beta 1-induced hyperplasia. Our results demonstrate that TGF-beta is capable of exerting pathogenic effects on synovial tissue and that PMNs may represent a significant source of the TGF-beta present in synovial effusions.

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Interleukin-6, Transforming Growth Factor-Beta 1, and Bone Markers After Kidney Transplantation

Calcified Tissue International ◽

10.1007/s00223-004-0044-x ◽

2004 ◽

Vol 75 (1) ◽

pp. 1-6 ◽

Cited By ~ 4

Author(s):

V. Kusec ◽

R. Smalcelj ◽

Z. Puretic ◽

T. Szekeres

Keyword(s):

Kidney Transplantation ◽

Growth Factor ◽

Transforming Growth Factor Beta ◽

Interleukin 6 ◽

Bone Markers ◽

Transforming Growth Factor ◽

Growth Factor Beta

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Expression and secretion of transforming growth factor-beta by bleomycin-stimulated rat alveolar macrophages

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.1993.264.1.l36 ◽

1993 ◽

Vol 264 (1) ◽

pp. L36-L42 ◽

Cited By ~ 2

Author(s):

E. M. Denholm ◽

S. M. Rollins

Keyword(s):

Growth Factor ◽

Alveolar Macrophages ◽

Transforming Growth Factor Beta ◽

Transforming Growth Factor ◽

Chemotactic Activity ◽

Beta Activity ◽

Dependent Manner ◽

Tgf Beta ◽

Growth Factor Beta

Bleomycin-induced fibrosis in rodents has been used extensively as a model of human pulmonary fibrosis. The influx of monocytes observed during the early stages of fibrosis is at least partially regulated by the elaboration of chemotactic factors in the lung. Exposure of alveolar macrophages (AM phi) to bleomycin either in vivo or in vitro stimulated secretion of monocyte chemotactic activity (MCA). This MCA has been previously characterized as being primarily due to fibronectin fragments. The present experiments revealed that bleomycin also induced AM phi to secrete a second chemotactic factor, transforming growth factor-beta (TGF-beta). However, the TGF-beta secreted by macrophages was in latent form, since no TGF-beta activity was detected unless AM phi conditioned medium (CM) was acid-activated. After acidification, chemotactic activity in CM from AM phi stimulated with bleomycin in vitro was increased by 3.6, whereas activity in AM phi CM from fibrotic rats increased by 2 and that of a bleomycin-stimulated AM phi cell line increased by 1.6. This acid-activatable chemotactic activity was inhibited by antibody to TGF-beta. Bleomycin-stimulated AM phi s secreted significantly more TGF-beta than did unstimulated controls. Further, in vitro exposure of AM phi to bleomycin induced TGF-beta mRNA expression in a time- and concentration-dependent manner, with maximal mRNA being detected following a 16-h incubation with 1 microgram/ml bleomycin.

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