Infections caused by M. avium are common in AIDS patients and patients with chronic lung diseases. The bacterium can be acquired both by the intestinal route and respiratory route. M. avium is capable of invading mucosal epithelial cells and translocate across the mucosa. The bacterium can infect macrophages interfering with several functions of the host cell. The host defense against M. avium is primarily dependent on CD4+ T lymphocytes and NK cells. Activated macrophages can inhibit or kill intracellular bacteria by mechanisms that are currently unknown but M. avium can invade resting macrophages and suppress key aspects of its function by triggering the release of TGF-beta and IL-10. Co-infection with HIV-1 appears to be mutually beneficial with both organisms growing faster.
Up to day pathogenesis of immune deficiency in chronic renal failure have not been clearly elucidated.There is no agreement where is situated the primary disturbance that makes that category of patients more susceptible to infections and neoplasms.Possible influence of many biochemical abnormalities and effect of renal replacement therapies on main elements of immune system are discussed.
The simplest plant growth and development hormone, ethylene, belongs (together with S.A. and JA) to key molecules governing the plant defense response. Production of ethylene is stimulated by wounding, flooding, metal ions, senescense and abscission processes, pathogene attack and ethylene itself. High level of ethylene induces the expression of many classes of pathogenesis-related proteins (PR). In order to properly function, ethylene must be precisely regulated, especially at the biosynthesis and signalling pathways. Two main enzymes involved in ethylene biosynthesis are ACC synthase and ACC oxidase. The ethylene signal transduction pathway is very complicated and needs to be further investigated. Ethylene binds to its receptors ETRs, then the signal is transduced to CTR1 and through phosforylating kinases cascades to EINs and EREBPs, directly binding to DNA GCC boxes. As a consequence, many PR proteins are activated.
Fever is a part of the acute phase response to infection and inflammation. We now understand that fever is a complex physiological response that is aimed at facilitating survival of the host. The fever is induced by endogenous inflammatory mediators, such as prostaglandins and pyrogenic cytokines, that are released by immune cells activated by exogenous pyrogens. Although the pathways (humoral and/or neuronal) responsible for transfer of the pyretic signals from the blood to the brain are still under discussion, it is generally accepted that they act on the level of the anterior hypothalamus to raise the thermoregulatory set-point. Results of studies of the adaptive value of fever demonstrate an association between a rise in body temperature and a decrease in mortality and morbidity during infection. These data along with data from evolutionary studies provide a strong support for the concept that fever is a beneficial during infection in endotherms and ectotherms, vertebrates as well as in invertebrates. There are also evidence showing that fever may be used as a therapeutic tool, especially in cancer therapy. Based on the data reviewed in this article, it can be concluded that fever has evolved as a host defense mechanism which was preserved within the animal kingdom through hundreds of millions of years of evolution.
Chronic hepatitis C virus infection is a leading cause of progressive liver fibrosis, liver cirrhosis and hepatocellular carcinoma. Iron overload is frequently observed in cases of chronic hepatitis C and has been suggested as a negative prognostic factor for this disease. Although the mechanisms leading to iron accumulation are not fully explained yet, both host and viral factors seem to contribute towards the development of this pathology. Better understanding of the interplay between hepatitis C virus replication and expression of iron regulatory molecules may elucidate new and interesting targets for the effective treatment of chronic hepatitis C.
Systemic lupus erythematosus is a prototypic autoimmune disease that predominantly afflicts women during child-bearing age. The disease is characterized by the production of autoantibodies and immune complexes in association with a diverse array of clinical manifestations. Investigation into the etiopathogenesis has been directed at identifying the genes that provide susceptibility to the disease, the complex cellular and cytokine aberrations and the biochemical abnormalities that are responsible for them. Understanding the immune cell signaling and gene transcription abnormalities will help us tailor new strategies for efficient biotherapy of the disease.
The objective was to study the pathogenesis of contact lens-associated giant papillary conjunctivitis (CL-GPC). Materials and Methods: Twenty-one biopsies of conjunctival giant papillae were obtained from soft contact lens wearers. The tissues were fixed in 4% paraformaldehyde and embedded in paraffin. Sections of 5 mum thickness were used for studies of histology and immunohistochemistry of pan-B and pan-T cell distributions. Results: Conjunctival epitheliums on the top of conjunctiva-associated lymphoid tissue typically lacked goblet cells. Lymphocytes from underlying lymphoid follicle were pressed into intra-epithelial 'pockets' formed through epithelial invagination. Under the follicle-associated epithelium, pan-B cells were mostly gathered in the central folliclar area and intraepithelial pockets, while CD3-positive T cells were predominantly distributed in parafolliclar region, but only a few in the intraepithelial pockets. Conclusions: Membranous epithelial cells (M cells) play a key role in the pathogenesis of CL-GPC for the binding and translocation of antigen and pathogen.
There are many evidences that nonimmunologic factors contribute to pathogenesis of primary glomerulonephritides. Proteolytic enzymes plays important role in glomerular protein turn-over and their altered activities may have influence on glomerular function. The purpose of this paper was to review the role of proteolytic enzymes in initiation and progression of idiopathic glomerular diseases.
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