STRONA G£”WNA » Lecture - 7 (1st DDS program)

Wydzia≥ Lekarski
MD (6-year)
DDS (5-year)
Pharmacy (6-year M.Sc.)


Lecture - 7 (1st DDS program)

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Defensive mechanisms in parasite-host system can be categorize into:
•†defensive mechanisms on the part of the host in response to infection;
•†defensive mechanisms on the part of the parasite in response to the host.

The first type of these mechanisms allows the differentiation between the substance and self-cells from foreign cells. They can be divided into: innate and acquired.
Innate (natural) defense is:
• non-specific;
• activated on contact with the pathogen;
• immunity cells are activated when the receptors located on their surface are stimulated;
• it includes natural barriers located on the surface of the body and in natural foramens;
• cells which phagocytize macrophages and granulocytes play an important role;
• phagocytes reacting to the pathogenic factor regulate specific immunity;
• interleukins secreted by macrophages (Il –1, Il-6, Il-12, Il-18) stimulate helper lymphocyte T to crake specific immunity;
• another important factor in the non-specific congenital defense is the complement system consisting of about 20 components located in cytoplasm with are reciprocally stimulated;
•†the complement cascade activation causes damage of pathogenic membranes. The complement system can operate by means of an alternative complement pathway when stimulated by the antigen, or by means of a classical pathway when stimulated by antigen with the participation of antibody.Immunological defensive mechanisms which evolved in the host’s organism.
Acquired (specific) defense:
•†develops after some time following the contact with the infection factor;
•†is specific to parasite’s antigens and characterized by the memory and possibility of proliferation between own tissues† and external factors;
•†lymphocytes B and T participate in acquired defense.

Antigens are substances foreign to a given organism. The organism develops immune response against antigen. Parasites, regardless of their size, include a number of different antigens of which the most important ones for the host are those located on the surface of the parasite or its products.
They are three types of parasitic antigens
a)†endoantigens (somatic, structural): •†antigens originate in the parasitic structures; •†activate when the parasite is phagocited;
b)†egzoantigens (secretory, excretory-secretory): •†a number of them have the characteristics of enzymes; •†are produced when the parasite inhabits the host organism including the digestive tract;
c)†soluble: •†circulate in the host liquids and tissues; •†may result from physiological processes of the parasite or its destruction.
Parasites act as antigenic impulse and induce immunity reactions, for example:
•†cellular immunity in the tissue infections;
•†humoral immunity in the digestive tract or blood infections.

Defence mechanisms of the parasite
Parasitic defense against the host can be categorized into:
•†Prophylactic defense is the defense against the recognition of the parasite by the host immunological system;
•†Active defense is the defense against direct host reactions.

There are five types of the defense against the recognition of the parasite by the host immunological system:
•†antigen mimicry;
•†antigenic variation;
•†immune distraction;
•†intracellular inhabitance.

There are 3 hypotheses related to antigen mimicry:
•†Hypothesis I is† natural selection;
•†Hypothesis II is antigen induction;
•†Hypothesis III is antigen masking.
According to these hypotheses, parasite’s antigens transform into antigens similar: •†to those of the host; •†to the antigens of the host.

The African trypanosome undergoes antigenic variation: the molecule that forms its surface coat, the variable surface glycoprotein (VSG) changes to protect the underlying surface membrane from the host’s defence mechanisms. New populations of parasites are antigenically distinct from previous ones. Several antigens of Plasmodium also undergo antigenic variation.

Most parasites interfere with the immune response. Immunosuppresion is a universal feature of parasite infection and has been demonstrated for both antibody and cell-mediated responses. Whereas some parasites can cause disruption of lymphoid cells or tissue directly, much of the suppression may be due to interference with macrophage function. Their cells may become overloaded with free antigens as many worms secrete quantities of† polysaccharides and glycoconjugates which interfere with antigen processing.

Immune distraction. Soluble parasite antigens released in huge quantities may impair the host’s response by a process termed immune distraction. Thus the soluble antigens of Plasmodium falciparum are thought to mop up circulating antibody, providing a “smokescreen” and diverting the antibody from the body of parasite.

Some extracellular parasites hide from immune attack: •†Some species of protozoa (e.g. Entamoeba histolytica) and of helminthes (e.g. Trichinella) for protective cysts, while adult worms of Onchocerca in the skin induce the host to surround them with collagenous nodules; •†intestinal nematodes and tapeworms are preserved from many host responses simply because they are†in the intestine.

There are two pathogenic mechanisms evolved by the parasites: •†the presence of parasites in the host organism induces changes in organs and systems and result in clinical symptoms;† •†pathological changes can be categorized into direct-local or indirect-general.

Direct – local pathological changes:†•†mechanical action (pressure, occlusion);
•†bleedings; •†malabsorption;†•†digestive enzymes of parasite.
Idirect - general pathological changes are the sign of the defense factor activation on the part of the host and of biochemical factors excreted by the parasite.

The characteristic of the defense factor activation on the part of the host are:
•†The more immunogenic the parasite is the stronger the immunological reactions to it are and the clearer the clinical symptoms;
•†Clinical symptoms of the parasitic invasion are often independent of the intensity of infection, and depend on the host individual immunological reaction.

Four basic types of host defense immunological reactions which lead to tissue damage and, therefore, to clinical symptoms.

Hypersensitivity Type 1
•†mast cells bind IgE with Fc receptor;
•†on contact with the alergen the following mediators are secreted: histamine, heparin, proteases and chemotactic factor for eosinophiles and neutrophiles;
•†trombocyte activating factor, prostaglandins and leukotriens are synthesized and secreted;
•†neutrophils, eosinophils, lymphocytes and macrophages are accumulated.
Effects of Type I hypersensitivity - in intestinal nematode infection the following can be observed in the intestine:
•†muscular layer contraction;
•†dilation of† blood vessels,
•†epithelium damage, which causes malabsorption, diarrhea, vomits.

Hypersensitivity Type II is cytotoxic hypersensitivity:
•†antibodies participate in it;
•†and tissue damage caused by parasites may result in the accessibility of the immunity system of intracellular components and in the production of antibodies against self-tissue.

Hypersensitivity Type III initiates immunological complexes:
•†excess of circulating parasitic soluble antigens creates immunological complexes with circulating antibodies;
•†complement is activated;
•†and chemotactic factors are released for hypersensitivity eosinophils, neutrophils and mast cells.

Hypersensitivity Type IV is delayed-type hypersensitivity:
•†participation of lymphocytes T which contact with antigen release cytokines which recruit and activate other cell;
•†macrophages are accumulated;
•†this type of hypersensitivity is observed in intracellular parasitism;
•†high eozynophilia occurs;
•†parasites may be destroyed together with the cell which they inhabit.

As far as immunological factors on the part of the host are concerned, immuno-pathological processes observed in the organism inhabited by parasites result from immune response developed by the organism rather than being a direct outcome of parasitic infection.

 Author: Piotr Nowosad date: 2020-04-22  print    back  
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