Infections phagocytes cells

Inflammation occurs when a living tissue is injured or infected by microorganisms. It is a beneficial, self-limited response that requires phagocytic cells and elements of circulating plasma to enter the affected area. In principle it may achieve resolution and repair as the ideal outcome of inflammation. The persistent accumulation and activation of leukocytes is a hallmark of chronic inflammation. 

These proteins are called acute phase proteins (or reactants) and include C-reactive protein (CRP, so-named because it reacts with the C polysaccharide of pneumococci), ai-antitrypsin, haptoglobin, aj-acid glycoprotein, and fibrinogen. The elevations of the levels of these proteins vary from as little as 50% to as much as 1000-fold in the case of CRP. Their levels are also usually elevated during chronic inflammatory states and in patients with cancer. These proteins are believed to play a role in the body s response to inflammation. For example, C-reactive protein can stimulate the classic complement pathway, and ai-antitrypsin can neutralize certain proteases released during the acute inflammatory state. CRP is used as a marker of tissue injury, infection, and inflammation, and there is considerable interest in its use as a predictor of certain types of cardiovascular conditions secondary to atherosclerosis. Interleukin-1 (IL-1), a polypeptide released from mononuclear phagocytic cells, is the principal—but not the sole—stimulator of the synthesis of the majority of acute phase reactants by hepatocytes. Additional molecules such as IL-6 are involved, and they as well as IL-1 appear to work at the level of gene transcription. 

In some infections the pathogenic organisms are located intracellularly within phagocytic cells and, therefore, remain relatively protected from drugs which penetrate cells poorly, such as the penicillins and cephalosporins. In contrast, erythromycin, rifampicin and chloramphenicol readily penetrate phagocytic cells. Legionnaires disease is an example of an intracellular infection and is treated with rifampicin and/or erythromycin. 

It has the ability to cross the placenta and therefore provides a major line of defence against infection for the newborn. This can be reinforced by transfer ofcolostral IgG across the gut mucosa of the neonate. It diffuses readily into the extravascular spaces where it can act in the neutralization of bacterial toxins and can bind to microorganisms enhancing the process of phagocytosis (opsonization). This is due to the presence on the phagocytic cell surface of a receptor for Fc. 

The development of sepsis is complex and multifactorial. The normal host response to infection is designed to localize and control bacterial invasion and initiate repair of injured tissue through phagocytic cells and inflammatory mediators.1 Sepsis... 

The most notable medical application of IFN-y relates to the treatment of CGD, a rare genetic condition with a population incidence of between 1 in 250 00 and 1 in 1 000 000. Phagocytic cells of patients suffering from CGD are poorly capable/incapable of ingesting or destroying infectious agents such as bacteria or protozoa. As a result, patients suffer from repeated infections (Table 8.10), many of which can be life threatening. 

A number of cells, including cytotoxic T lymphocytes, NK cells, and mononuclear phagocytic cells, are endowed with cytotoxic abilities and thus mediate important immunosurveillance mechanisms against neoplastic cells and viral infections. In immune-compromised hosts, a correlation has been observed between low NK cell activity and morbidity [22-25] or the incidence and severity of upper respiratory tract infections [24],... 

Invasion of the tissues by an infective agent initiates an inflammatory response in the animal. This is non-specific and is mediated primarily by substances released from tissues that are damaged as a result of either trauma or the toxic effects of the infective agent. The major mediator is the vasoactive amine histamine, which causes an increased local blood flow and capillary permeability, resulting in local oedema. A major aspect of the inflammatory response is the involvement of large numbers of phagocytic cells, particularly the polymorphonuclear leucocytes. These are chemotactically attracted to the inflamed tissues and are mainly responsible for the elimination of particulate material. This often results in the destruction of many of these cells and the formation of pus. 

On the one hand, are the soluble factors such as lysozyme and complement, together with the phagocytic cells that contribute to the innate system, and on the other hand are the lymphocyte-based mechanisms that produce antibody and the T lymphocytes, which represent the main elements of the adaptive immune system. Not only do these lymphocytes provide improved resistance by repeated contact with a given infectious agent, but the memory with which they become endowed shows very considerable specificity to that infection. 

There are also immunodeficiency states that are primary and can be caused by phagocytic cell defects, deficiencies in the complement system, B- and T-cell deficiency, and other causes. Secondary immunodeficiency disorders can result from malnutrition, cytotoxic drugs, infections with pyrogenic bacteria, and infections with an RNA retrovirus, as in the acquired immunodeficiency syndrome (AIDS). 

Leishmaniasis. The causative agents are flagellated protozoa that are transmitted by sand flies to humans. The parasites are taken up into phagocytes, where they remain in phagolysosomes and multiply until the cell dies and the parasites can infect new cells. Symptoms A visceral form, known as kala-azar, and cutaneous or mucocutaneous forms exist (A). An estimated 12 million humans are affected. Therapy is dif cult pen-tavalent antimonial compounds, such as stibogluconate, must be given for extended periods. Adverse effects are pronounced. 

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