Serum transforming growth factor‐β1 levels increase in response to successful anti‐inflammatory therapy in ulcerative colitis

Abstract

Objective: To investigate serum levels of transforming growth factor‐β1 and interferon‐γ in active ulcerative colitis and to assess changes during treatment. Methods: We prospectively evaluated serum from 25 patients with untreated active ulcerative colitis and 19 healthy controls. Disease activity score (DAI), serum transforming growth factor‐β1 and interferon‐γ levels were measured at baseline and after 7 days of conventional treatment. Disease activity score and transforming growth factor‐β1 were also assessed at 42 days. Results: Baseline transforming growth factor‐β1 levels were significantly higher in patients than in controls (P < 0.02). On the 7th day, transforming growth factor‐β1 levels increased only in patients who responded (P < 0.01); variations in transforming growth factor‐β1 levels and disease activity score were inversely correlated (r=– 0.72, P < 0.001). At day 42, serum transforming growth factor‐β1 decreased significantly compared with the 7th day (P < 0.05). While in controls, interferon‐γ was undetectable; untreated patients had higher, widely variable, levels. At day 7, responders had higher interferon‐γ values than unresponsive cases. Variations in interferon‐γ correlated moderately with changes in transforming growth factor‐β1 (r=0.53, P < 0.05). Cytokine response did not depend upon the type of treatment. Conclusions: Both transforming growth factor‐β1 and interferon‐γ may play a role in the injury–repair process in active ulcerative colitis. Variations in circulating transforming growth factor‐β1 levels in the first week of treatment seem to be related to the therapeutic response.

Transforming growth factor beta1 (TGFbeta1) in physiology and pathology

“…These values were increased slightly during treatment; after successful treatment confirmed by clinical and endoscopic activity, index returned to the normal range [59]. Although the quoted results suggest TGFb1 participation in the processes of repair intestinal tissues that were previously destroyed in autoimmune mechanism, it cannot be excluded that TGFb1 is involved in the initiation of the disease process [84].…”

“…TGFb1 in a concentration of 1-2 fg/cell inhibits the growth of smooth muscle cells, fibroblasts, and chondrocytes; in higher concentrations, it has the opposite effect -it stimulates the growth of these cell types [53]. TGFb1 plays a role in tissue regeneration, on the one hand by promoting cell differentiation [57], and on the other by inhibiting excessive cell proliferation [58,59]. TGFb1 is an important factor inducing apoptosis of liver cells in vitro and in vivo [42,60].…”

“…The intestinal mucosa revealed the presence of TGFb1-3 and their receptors I-III [64]. In vitro TGFb1 inhibits the proliferation of intestinal epithelial cells and promotes their differentiation [57,59]. TGFb1 synthesised by enterocytes and cells of the lamina propria colonic mucosa [64] plays here a role in regulation of proliferation, differentiation and apoptosis [2].…”

“…In mice, lack of TGFb1 gene causes multiple organ inflammatory response, and lethal cachexia develops within two weeks [76]. In transgenic mice lacking the TGFb1 gene (knock out), inflammation of the small intestine and colon develops [59]. In transgenic mice with Smad7 overexpression glomerulonephritis develops caused by antibodies against the basement membrane [77] and inflammation of the respiratory tract [38].…”

Relevant aspects of the influence of chosen growth factors on the activity of the female reproductive system

“…Jej efektem jest śmiertelne wyniszczenie organizmu rozwijające się w ciągu dwóch tygodni (8). Genetycznie modyfikowane zwierzęta z usuniętym genem TGF-β1 wykazują zwiększoną podatność na rozwój stanu zapalnego jelita cienkiego oraz grubego (55).…”