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Skeletal muscle healing after injury can be divided into three distinct but overlapping phases. The destruction phase is characterized by rupture followed by necrosis of muscle fibers, formation of hematoma and inflammatory reaction. During the repair phase a necrotic tissue is phagocyted by macrophages, muscle fibers are regenerating and connective tissue scars are formed. The remodeling phase concerns the period when regenerating muscle fibers mature, scar contraction and reorganization occurs and the muscle recovers its functional efficiency. Proinflammatory cytokines (IL-1β, IL-6, IL-8, TNF-α) and growth factors (FGF, IGF, TGF-β, HGF) play a critical role in all phases of muscle repair. Moreover, chemokines expressed at early stages of myogenesis can regulate the survival and proliferation of myoblasts. Chemokines expressed in vivo in muscle cells can directly influence myogenesis, but can also act in a paracrine manner by recruiting the immune cells (macrophages) to injured skeletal muscles, which is crucial for the regeneration process. Identification of molecules regulating myogenesis, like cytokines, chemokines and growth factors, contributes to the exploration of molecular mechanisms that can improve muscle regeneration after injury, diseases, surgery and increase the effectiveness of cell transplantation.
The paper reviews literature on the immunological response to influenza virus (IV) infection. The first part of the paper focuses on humoral response involving antibodies against IV and proinflamatory cytokines. The response involves mainly antibodies of IgA, IgG and IgM classes, produced against antigenic proteins of IV - hemagglutinin and neuraminidase. The antibodies are presented in blood and in BALB from 7 DPI and remain at a high level for 8-10 weeks post infection. Moreover, cytotoxic T lymphocytes are more specific to NP and M proteins. Virus titres in the lungs are tightly correlated with the level of IFN-α, TNF-α, IL-4, IL-6, IL-10 and IL-12 in BALF. There is no correlation between virus replication and cytokines in serum. The biological effects of immunosuppressive activity caused by IV are discussed in the second part of this review. Some of IV strains posses NS protein in the form known as IFN-inducing particles (IFP), some others in the form of INF-suppressing particles (ISP). IL-10 activity of the host was also described as an immunosuppressive factor. The third part of the paper summarizes the relationship between the pathogenesis of influenza and the acute phase proteins induced by cytokines. To recapitulate, immunological response to infection caused by influenza virus is a multistage and multifactor process, including specific and unspecific humoral and cell response. The response involves mainly proinflammatory cytokines and acute phase proteins. Undoubtedly, biological properties of IV, especially its suppressive effect on the secretion of INF along with IL-10 activity, reduce cell response, influencing the defense of the organism against infection. This model of influenza virus infection may be valuable for assessing the therapeutic potential of cytokine antagonists.
Cytokines are a group of peptides or small proteins that are involved in intercellular communication. Most of them are involved in local processes but some have endocrine activity. Cytokines are produced mainly by lymphocytes, monocytes, granulocytes, but also by fibroblasts, endothelial and epithelial cells. Disturbances of the integrity of tissues are the main inducers of cytokine synthesis connected with local immune response. On the other hand there is the group of constitutively produced cytokines that regulates the processes of hematopoesis, tissue remodeling, and lymphocytes migration. At present over one hundred biologically active substances described as cytokines have been identified. High levels of TNF-α, IL-1β i IL-6 are demonstrated both in severe cardiac insufficiency with cachexia and in the left sided cardiac failure. It has been established in several studies that proinflamatory cytokines contribute to dilated cardiomiopathy involvement, decreased blood perfusion in skeletal muscles, and exert endothelial injury of vessels, develop cachexia and inappetance and stimulate cardiac myocytes apoptosis. It was confirmed that cardiac myocytes are able to synthetize TNF-α in response to different types of overload, e.g. volume overload, pressure or ischemic (post infarct). TNF-α and IL-2 impart a negative inotropic effect on the heart proportional to their concentration. TNF-α, IL-1 and IL-6 regulate cardiac functioning indirectly due to the activity of the following: nitric oxide, reactive oxygen species, sphingolipid mediators, arachidonic acid and the modulation of β-adrenergic response.
Due to a similar chemical structure to 17β-estradiol (E₂), phytoestrogens may inhibit or modulate endogenous estrogen action. Although the authors demonstrated that phytoestrogens did not influence basal progesterone (P4) secretion, nonetheless it simultaneously inhibited the stimulation of luteinizing hormone (LH) and prostaglandin (PG) E₂ on P4 release in bovine corpus luteum (CL) in vitro. Since phytoestrogens are luteolytic factors in the late luteal stage (enhanced PGF₂α secretion in vitro and the level in plasma), these factors possibly also play some role in cytokine action (mediators of PGF₂α during luteolysis) in cattle. The aim of this study was to determine the influence of phytoestogen metabolites on the sensitivity of bovine corpus luteum cells on tumor necrosis factor α, interferon γ and interleukin 1β action, by measuring the level of PGF₂α and stable metabolites of nitric oxide and by determining the viability of CL cells on day 15 of the estrous cycle. Phytoestrogens can increase functional luteolysis by enhancing PGF₂α and NO synthesis stimulated by cytokines. Moreover, phytoestrogens can modulate structural luteolysis by increasing the sensitivity of steroidogenic cells on the cytotoxic action of cytokines in bovine CL.
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