Immune suppression infectious disease

While profound immunosuppression can lead to an increased incidence of infectious or neoplastic diseases, interpreting data from experimental immunotoxicology studies or epidemiological studies for quantitative risk assessment purposes can be problematic. This is because inadvertent exposures to immunotoxic agents may often be expressed as a mild-to-moderate change, reflected, for example, by a 15 to 25% decrement in an immune parameter compared to control values. To help address the clinical consequences of mild-to-moderate immunosuppression, we examined available experimental, clinical and epidemiological studies that examined the association between suppression of immune function and infectious disease, independent of the etiology of suppression. 

Suppression of local (at the site of UV exposure) and systemic (at a distant, unexposed site) immune responses to a variety of antigens has been demonstrated in both humans and animals exposed to UV-B. There is reasonably good evidence that such immunosuppression plays a role in human carcinogenesis however, the implications of such immunosuppression for human infectious diseases are still unknown. 

Experimental studies in laboratory rodents have demonstrated that a diverse array of chemical exposures suppress immune function (Table 19.2). In addition a limited number of clinical and epidemiologic studies have reported suppression of immune function and/or increased frequency of infectious and/or neoplastic disease following exposure of humans to some of these agents. From the description above it is clear there are a number of cellular and molecular targets for chemicals that act as immunosuppressants. Clearly, a chemical that disrupts cell proliferation would affect clonal expansion. Disruption of T cell maturation in the thymus is another potential mechanism for immune suppression. Chemicals may also interfere with receptor ligand binding at the cell... 

Patients exposed to higher levels of radiation will experience more severe radiation sickness that will appear more rapidly. A patient receiving a dose of about 400 rad has a 50% chance of death without medical intervention, primarily from radiation-induced immune system suppression and subsequent infectious disease. 

During periods of immune system response, for example, at times of infectious disease, cytochrome P450-dependent metabolism of xenobiotics is reduced. This effect is attributed to the production of interferon by the immune system as it responds to a challenge. Human interferon has been shown to suppress the metabolism of benzo [a] pyrene in laboratory animalsJ19 ... 

Chemicals that attack the immune system render the body less capable of responding in times of need. Such chemicals are defined as immunotoxins, and immunotoxicology is the study of adverse health effects that result from the interactions of xenobiotics and the immune systemNumerous individual chemicals, including benzene, PCBs, and dioxins, suppress immune system function in humans and lead to increased incidences and intensities of infectious diseases and cancer. 

There are practical reasons to focus on those things you can control. Sources of chronic distress can lead to chronically elevated levels of stress hormones such as cortisol that suppress your immune system. In turn, you become more vulnerable to getting sick with infectious diseases or even with certain kinds of cancer. Ongoing fear and anxiety can contribute to a learned-helplessness mindset. That by itself can induce depression. And depression can further impair cognition. 

A study in 6 healthy subjects found that a single dose of ecstasy produced a time-dependent immune dysfunction. Ecstasy impaired CD4 T-cell function, which is responsible for cellular immunity. Alcohol alone may produce a decrease in T-helper cells and in B lymphocytes, which are responsible for humoral immunity. Concurrent ecstasy and alcohol increased the suppressive effect of ecstasy on CD4 T-cells and increased natural killer cells. It was suggested that the transient defect in immunological homoeostasis could have clinical consequences such as increased susceptibility to infectious diseases. More study is needed. 

As many scientists have indicated, NIV stimulates or suppresses the immune system depending on the dose as well as the presence of DON. Oral administration of 10 and 15 mg of NIV induced apoptosis in CD4(+) and CDS (+) cells in thymus, Peyer s patch, and spleen in a dose-dependent manner [93, 94]. The effect of NIV on susceptibility against infectious diseases was shown by an in vivo infection experiment using BALB/c mice in which NIV at 6 mg/kg had no effect on survival rate against Salmonella infection [95]. However, in an in vitro experiment using RAW 264.7 cells, NIV inhibited the transcription activity and expression of inducible NO synthase (iNOS) by lipopolysaccharide (LPS) [96] (Sugiyama 2010). 

Recent advanced technologies are clarifying the important roles of immune functions in disease progression. Immune dysfunction may result in infectious diseases and cancer, and hyper immune reactions may cause auto-immune diseases including allergy and rheumatoid arthritis. Thus, the development of an immune modifier, which stimulates necessary functions and suppress unnecessary functions, is truly desired. 

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