Infections, autoimmune diseases

Heavy metals, like lead and mercury, have been recognized as toxic poisons for centuries. Further, toxic concentrations of mercury, for example, can trigger several effects like autoimmune diseases, infections, unexplained chronic fatigue, depression, nerve impairment, memory problems, decreased mental clarity, and bowel disorders. For several decades, mercury vapor exposure has caused severe health problems among chloralkali workers. This is only an example. It may be repeated that education can effectively minimize exposure to hazardous metals. Basic information and training for proper handling of toxic chemicals will reduce potential adverse health effects. 

Vasculitis affecting the central nervous system (CNS) represents a heterogeneous group of inflammatory diseases that may be idiopathic or associated with autoimmune diseases, infections, drug exposure, radiation, or cancer. Inflammatory cells invade vessel walls, and neuropeptide release increases vasomotor reactivity. These properties lead to vessel narrowing. There is also loss of normal endothelial anticoagulant properties and vessels have increased susceptibility to thrombosis. Consequently, patients with vasculitis develop ischemic and thrombotic infarctions. There is also altered wall competence, which can result in dissection or vessel wall disruption with intracranial hemorrhage. MRA is clinically used to screen for vasculitis, but is less sensitive than DSA (Fig. 6.20). One study of 14 patients with suspected vasculitis reported that MRA can detect distal stenoses in vasculitis with a... 

In a broad sense, the medical applications of activated carbons are based on their powerful non-specific adsorption capacity luirivalled by any other material. They are used to remove undesirable and harmful substances - toxins - from the human body. These substances either enter the human body fiom the external environment via skin, eyes, breathing airways or with food and drinks, or they can be produced internally by the body itself due to organ malfunction, autoimmune diseases, infection or trauma. Considering ourselves as an inseparable part of the environment, both externally and internally generated toxins cause nothing else but pollution of our body, similar to the environmental pollution, which therefore has to be... 

Inflammatory and immune diseases Autoimmune disease (A,I), asthma (A), osteoarthritis (I), rheumatoid arthritis (I), septic shock (A,I), infections (A,I), familial cold auto-inflammatory syndrome (I), Muckle Wells syndrome (I), chronic infantile neurological cutaneous and articular syndrome/neonatal onset multisystemic inflammatory disease (CINCA/NOMID) (I), Crohn s disease (I), gout (I), acute renal failure (A,l)... 

A number of chimerized, humanized, and one human mAb have now been approved for therapeutic use in humans in the treatment of autoimmunity, malignancy, infection and cardiovascular disease (Table 1). Some of the currently licensed mAb will be discussed here. A much larger number of mAb are currently being evaluated in Phase I, II and III trials. In general, chimeric, humanized and human mAb are very well tolerated with few side effects. Chimeric or humanized mAb still have the potential to evoke host immune response to the variable domains or CDRs of the antibody so-called HACA (human anti-chimeric antibody) or HAHA (human anti-human antibody) responses, although these responses are uncommon. Short-lived and occasionally severe infusion-related acute hypersensitivity reactions such as fever, skin itching, shivering, respiratory compromise and low blood pressure sometimes occur-. Such effects may... 

American co net lower, black susans) angustifolia shortens symptoms and duration of upper respiratory Infections (URIs) including colds mild gastrointestinal (Gl) upsets individuals with autoimmune diseases such as tuberculosis, collagenosis, multiple sclerosis, AIDS and HIV infection. 

CCR5 expression likely plays a role in T-cell recruitment and may be involved in the development of autoimmune diseases. There is a negative association between the CCR5A32 mutation and rheumatoid arthritis (Prahalad 2006). Furthermore, additional studies reviewed elsewhere suggest the involvement of CCR5 in multiple sclerosis, diabetes, and transplant rejection (Ribeiro and Horuk 2005). As such, it is likely that CCR5 antagonists developed for the treatment of HIV-1 infection can also be used for other diseases. 

The therapeutic goal in autoimmune diseases such as RA is to control disease, to establish remission, and eventually to cure. In theory, this goal can be achieved using either Ag-specific approaches, for example, elimination of self-reactive T cells (assuming that a finite number of key Ags can be identified as the target of the autoimmune process in RA), or the non-Ag-specific approaches, for example, blockade of cytokines as in the case of TNF-a neutralization. Currently, only the latter types of approaches have yielded clinical benefit, and it is in this category that approaches to block chemokines or receptors may be included. Despite their appeal in terms of effectiveness, non-Ag-specific approaches carry a higher risk of immunosuppression and opportunistic infections (48). 

The overall effect of Li+ on the hematopoietic system is of stimulation of the immune system. Not surprisingly then, Li+ is reported to exacerbate the activity of a number of autoimmune diseases, such as psoriasis [212] and rheumatoid arthritis [213], and to result in the production of autoantibodies in some patients [214]. However, there is no evidence that Li+ s stimulation of the immune system leads to any reduction in the occurrence of viral or bacterial infections in patients on Li+ therapy. 

The activation of specihc immune responses involves the proliferation of lymphocytes. For T-cells, the stimulatory agent can be a combination of anti-CD3 and anti-CD28 or mitogens such PHA or ConA. Dysregulation of cell homeostasis may have severe adverse effects on immune functions, increasing susceptibility to infections and cancer, as well as favoring the development of autoimmune diseases. 

Animal models have established that infections can induce autoimmune disease. For example, coxsackievirus B3 infection of susceptible strains of mice results in inflammation in the heart that resembles the myocarditis and dilated cardiomyopathy that occurs in humans.28 44 The same disease can be induced by injecting mice with cardiac myosin mixed with adjuvant, thereby reproducing the disease in the absence of virus infection, indicating that an active viral infection is not necessary for the development of autoimmune disease.9 29 44 Likewise, a number of autoimmune diseases can be... 

Infections in Humans Associated with Autoimmune Diseases... 

The mechanism most commonly invoked to explain the association of infection with autoimmune disease is molecular mimicry that is, the concept that antigens (or more properly, epitopes) of the microorganism closely resemble self-antigens.50 The induction of an immune response to the microbial antigen thus results in cross-reactivity with selfantigens and the induction of autoimmunity. Although epitope specific cross-reactivity has been shown in some animal models,48,51 53 molecular mimicry is clearly demonstrated to be the causative mechanism in few, if any, human diseases.3 54,55... 

There is considerable interest in the role of infectious agents in the development of autoimmune diseases. Some of this interest is based on the concept of molecular mimicry as a causal mechanism. Molecular mimicry refers to the possible pathologic role of cross-reactive antibodies or T cells to a self-antigen that is structurally similar to, and thus shares epitopes with, a viral or other infectious agent. For most autoimmune diseases, however, evidence of molecular mimicry leading to disease is not conclusive.1819 Viruses and other infections also have a less-specific immune effect, stimulating toll-like receptors and proinflammatory cytokine secretion, which is another mechanism that has been postulated to influence autoimmune disease risk.20... 

Lund, F.E., et al., Regulatory roles for cytokine-producing B cells in infection and autoimmune disease, Curr. Dir. Autoimmun., 8, 25, 2005. 

Kamradt T, Goggel R, Erb KJ Induction, exacerbation and inhibition of allergic and autoimmune diseases by infection. Trends Immunol 2005 26 260-267. 

In general, immunosuppression, expansion of regulatory cells, costimulatory blockade, or promotion of a Th2 cytokine milieu is considered to be supportive of disease control in T-cell regulatory disorders such as autoimmune disease and graft-versus-host disease (GvHD) [2]. In contrast, killer cells, a Thl cytokine milieu, or activated lymphocyte infusions support control of malignancy and infections. Maintaining a balance between the two... 

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