Search

Copyright of Advances in Biochemistry / Postepy Biochemii is the property of Polish Biochemical Society / Acta Biochimica Polonica and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Prostaglandins are hormones found in almost all mammalian tissues. As signaling molecules, they play a key role in the regulation of many physiological processes, including hair growth cycle. The article describes the history of the discovery of prostaglandins, including the work of Professor Ryszard Gryglewski – the discoverer of prostacyclin. Particular attention was paid to the synthetic analogue of prostaglandin F2α - latanoprost. Indicated for the treatment of glaucoma, the drug is known for inducing eyelash growth as a side effect. A prodrug, latanoprost is converted to its active metabolite, latanoprost acid. Recent research demonstrated that latanoprost acid has a chance to become an effective alternative to minoxidil and finasteride - the only drugs currently registered for the treatment of androgenetic alopecia. The development of anti-alopecia drugs containing prostaglandin derivatives, including latanoprost acid, will be a much faster process compared to the traditional path of product development based on a new chemical compound.

Taking into account the role of mast cells in different physiological and pathological processes, as well as in host defense it seems very important to recognize mast cell receptors and their role in activation of these cells. In the last few years it has been indicated that mast cells can express Toll-like receptors (TLRs), molecules that play an essential role in the activation of innate immune response to microbial pathogens and take part in the development of adaptive immunity, as well. It has been defined that mast cells express TLR2, TLR4, TLR1 and TLR6. There is also some data proving that mast cells possess TLR5, TLR3 and TLR9 molecules. The presence of TLR7, TLR9, and TLR10 on mast cells is still unclear. Some data indicate that TLR expression by mast cells can be modulated by various cytokines, such as granulocyte-macrophage colony stimulating factor (GM-CSF) and interferon (IFN)-g, cathelicidin LL-37 as well as by some bacterial components. It is now established that TLRs are involved in mast cell response to bacterial stimulation; some data also indicate that TLRs take part in virus-induced mast cell activation. What is more, it is now suggested that TLRs might regulate IgE-FceRI-dependent mast cell stimulation. Further research is needed to fully understand and describe the role of TLRs in mast cell biology.

Unlabelled: Transforming growth factor-beta1 (TGF-beta1) is known to play a key role in processes of cell proliferation and differentiation. It also plays an important role in modulation of the immune response. Various diseases may arise both from excessive and insufficient activity of this cytokine. THE AIM OF THE STUDY was to evaluate the role of TGF-beta1 in the pathogenesis of chronic hepatitis (Ch.h.) and to assess whether TGF-beta1 level in plasma or its tissue expression can be useful in diagnosing and monitoring of clinical course of this disease., Patients and Methods: Twenty-one children with chronic hepatitis were included in the study and 42 healthy children constituted the control group. Liver function tests and TGF-beta1 plasma levels measured by ELISA method were evaluated in both groups of patients. In liver tissue obtained by needle biopsy, the histopathological grading and staging of hepatitis was evaluated, TGF-beta1 protein was assessed by immunohistochemical methods and TGF-beta1 gene expression was measured by reverse transcription and real-time polymerase chain reaction., Results: In chronic hepatitis group of patients the plasma TGF-beta1 level did not differ from the control group and did not correlate with grading and staging of the liver tissue while positive correlation was observed with gamma-glutamyl transpeptidase activity in the serum. There was no correlation between tissue TGF-beta1 expression and TGF-beta1 plasma level and staging or grading in liver tissue. TGF-beta1 gene expression correlated positively with ESR and ALAT activity but no correlation with TGF-beta1 plasma level, TGF-beta1 gene or protein expression, grading or staging in liver tissue were observed., Conclusion: 1. In children with chronic hepatitis, TGF-beta1 plasma level is not related to grading or staging in the liver tissue. This finding may be due to low level of fibrosis observed in the studied children. 2. It appears that local expression of TGF-beta1 in liver tissue should not be used as a sole marker in differentiating and monitoring the course of chronic hepatitis. 3. In children with chronic hepatitis assessment of liver TGF-beta1 gene expression is not helpful in the evaluation of pathological changes in liver tissue. 4. Due to the relatively low number of patients in the analysed groups it seems advisable to perform similar complex studies in larger groups of children with chronic hepatitis.

The pathomechanism of inflammatory bowel disease (IBD), i.e. Crohn's disease and ulcerative colitis, is not well understood. There is growing evidence that mast cells take part in the course of these diseases. It is well known that mast cells are numerous in the gastrointestinal tract. What is more, the number of mast cells increases in intestinal tissues in IBD. Mast cells release several mediators, cytokines, and chemokines that can influence the inflammatory process in the gastrointestinal tract in various ways. One mediator that plays a very important role in the development of IBD is tumor necrosis factor (TNF). Other mast cell-derived cytokines and chemokines also seem to be involved in the development of intestinal inflammation. Moreover, some unique mast cell mediators, such as histamine, tryptase, and chymase, play crucial roles in the course of IBD. Finally, there is some data showing that mast cell-derived metalloproteinases (especially MMP-9), leukotrienes (LTs), platelet activating factor (PAF), and heparin take part in inflammation during IBD. It seems that current data about the role of mast cell-derived mediators and cytokines in IBD should be taken into consideration when new approaches to treating these diseases are being introduced.