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Most of morbidity and mortality rates in both human and animals are caused by Gastrointestinal Nematodes. For any disease mechanism to take place as a result of parasitic infection, parasite should come up with ways of invading the host cell and strategies of reaching final destination so that it can cause the infection. During invasion, Nematodes rely on specific protainase which are either excretory or secretory products to help in invasion to the host. Once the parasite has invaded the host, it must come up with various modes of feeding to help it to survive within the host cell.

Zinc metalloproteinase which are found in lumen of nematode intestine helps them in feeding (Dzik 2005). After the establishment, parasite the induce type II (TH2) antibody dependent responses. Gastro intestinal nematode produces antigens which they usually use in defence. These antigens are usually processed by the lymphoid tissue through their initiation of cascade immune responses. TH2 attracts the B cells, eosinophils and mucosal mast cells by chemotaxis to the gut where proliferation takes place (Sheerer, 2005).

Worm expulsion is enabled by contribution of TH2 cytokines and effectors G1 nematode have different mechanisms which they use in order to evade, the defence mechanism of the host. They have exterior cuticle which enable them to resist digestion. Nematode have cleaving protease which is immunologic in nature and protease inhibitors, it produces antioxidant, it has prostaglandin and they also have immuno suppressive factors which help in defence against the host cell. Therefore due to these defence mechanisms, parasite can survive in host cell for a long time without being eliminated from host. Classification of Nematodes

Retrieved from article on nature genetics published on 2004, Nature Publishing Group. The phylum nematode is classified using the SSU, vRNA Phylogeny. It shows morphological and development evidence of the nematodes. Tropic biology in each of the species which is targeted is shown by small icon. Each species is grouped into cluster and a consensus sequence for each cluster is usually predicted. Evolution Origin of genes and family and unique genes in phylum nematode the upper number refers to the number of genes which are unique to each clade while the lower indicates gene families as shown below.

Retrieved from article on nature genetics published on 2004, Nature Publishing Group GI nematodes play quite a vital role in TH2 responses in protection of the host. They usually evolve to modulate TH2 responses locally (Balic, et-el, 2005). This shows that, helmith whereby nematodes lies can provide anti allergic therapeutic and also those of bacteria against various auto immune diseases. In some of the Cameroonians TH2 responses which are usually originate from stimulated peripheral blood mononuclear cells can be used in predicting susceptibility of G1 nematodes.

Nematodes also offer protection against a topic, allergic and various auto immune infections protection is usually associated with IL-10 increased levels and immediate from blocking of IL-10 activities. In some cases infection with G1 nematodes can provide protection from Colitis which is usually induced by various drugs used to treat the infection (Maizel, et al, 2005). These G1 nematodes are of great importance since they play quite vital roles in preventing various infections by their ability to produce IL2. Therefore they are of quite great importance in human since they usually provide defence mechanisms.

There are quite a number of GI nematode species which usually cause infection to both human beings and animals. These includes, Spiruvida, Trichocephhalida, Ascandida and strongylida and Rhabditida their envision are quite different and they usually manifest their symptoms differently. In the key features of the lifecycle of G1 nematodes it’s important to note that G1 nematodes are usually released to the environment inform of eggs and they usually find their way out of the host through urine or faeces (Lochnit, et al, 2005).

The host usually get infected through oral ingestion or through penetration through the skin by the eggs which are voided to the environment or the resulting larva transmission stage. They usually have the ability to re-infect host and they can persist for host cell involves crossing through host tissue, basement membrane extra cellular matrixes, blood and lymph vessels. In invading the host G1 nematodes depend entirely on specific proteases which are usually released as excretory or secretory products. The protease releases usually hydrolyze fibrinogen, collagen and haemoglobin.

After the parasite has invaded the host cell, free radical generation of leucocytes usually occur which is usually accompanied by intestinal pathology and this lot of changes in physical appearance of the host. Tissue destructions of intestinal absorptive area which is usually enabled by swamping of antioxidant defences results to low absorption of macronutrients in the host cells and they can also be impaired. After the parasite has invaded the intestines, immediately immunity is caused. In G1 nematodes, they usually cause type II (TH2) which is an antibody-dependent response (Khan, Collins, 2004).

In G1 nematode’s defence against the host, lymphoid tissue which is the extra rhythmic site of lymphocyte, processes antigens which are usually released by G1 nematodes which eventually initiate cascade of immune response. TH2 cytokines initially occurs in mesenteric lymph node and payer patches which are then followed in spleen, they attracts the progenitor B cell, eosinophils by chemotaxis and at the mucosal mast cells and they hence proliferate at the gut and they finally mature in response due to stimulatory signals of TH2 cytokines and parasite antigen (Mulcahy , et al, 2003).

Warm expulsion usually occurs through combined effort of TH2 cytokines and effectors. G1 nematode have different ways of evading the host, there are through exterior cuticles, immunoglobulin cleaving proteases and protease inhibitors which are usually found at the surface of the parasite, through secreted and surface antioxidants such as super peroxide mutase and also Glutathione s-transfers, through prostaglandin and also adult warms can be evaded by various immuno suppression factors. Parasites can also gain their entry to the host cell through the mucosal surface i.

e. oral entry of G1 nematodes (McKay, 2005). This enables them to adopt and live at the mucosal surface of G1T or go beyond the barrier to other sites. Mouse is usually the most suitable animal species which cab is used by scientist to help in studying about the intestinal parasite. There are the best models for studying about helmenth infections. Mouse is quite important since it delineate the functioning of macrophages (Suchitra, Joshi, 2005). Anti-proliferation usually occurs in all the mouse strains which are tested and they are dependent on type II cytokines.

Mouse are human are quite similar since when infected by the common parasites as man they initiate the same immune responses and the manifestation of disease in mouse is usually quite similar to that of human. In both cases the mononuclear cells of both mouse and those of human are quite the same. Mouse and human have the same antigenic sites whereby the disease usually manifests itself (Joseph, et al, 2005). Therefore when mouse is used to test various responses of the G1 nematodes they are quite effective because they will manifest the disease condition in the same way.

The genes also that are expressed in mouse are quite similar to those of man which are quite substantial for carrying out the experience. Adaptation of profiling gene adaptation and analysis of the way intestinal warms are expelled which was meant to make an effort to identify novel type two dependent cytokines immune effectors mechanism which was involved in immunity (Parkinson, 2004). Dependent type II cytokines can take place in absence of effectors mechanisms which are usually associated by the type 2 responses such as activation of B cells, antibody production, mastocytosis and eosinophilia.

Expulsion of type 2 cytokine in worms is well established and therefore the immune cell effectors and their molecular mechanisms produced by these responses have been elusive. Therefore it’s quite clear that most cells can be important in expulsion of intestinal nematodes since when it depend (Koski, Scott, 2003) entirely on type 2 cytokines, expulsion can take place in absence of effectors mechanism. Therefore effectors play quite a substantial role in G1 nematodes to ensure that they are fully expulsed from the host cell. This merely happens with the help of type 2 cytokines but it can otherwise take place without them.

There are quite a number of mechanisms which are involved in evasion of Gastro Intestinal nematodes which usually they apply in defence against the host defence mechanism. They have exterior cuticle which is quite hard and it usually resist digestion of the parasite by the host’s digestive juices which are secreted within the body of the host (Falcon, Pritchard, 2005). Apart from this external hard cuticle, G1 nematodes have immunoglobulin cleaving protease inhibitors which are usually located on the surface of the parasite; it also has antioxidants which help it to resist oxidation.

Immuno suppressive serine, cystine are used to expel adult worms and prostaglandin and various metalloproteinase can cleave on FC receptor of 1gm, 1gG and 1gA but they cannot cleave on 1gD and 1gE. Antioxidants usually help in scavenging and eradicating free radicals which are usually released by the host cells which enable them to escape from the lethal effect. Parasitic immune defence would cause molecular balance if components are neutralised in chronic infection which usually favours the host in G1 tract has non-specific barrier function in the case of specific immune responses.

Host cells usually secrete mucus and form tight cells which resist entrance of pathogens to the host (Weinstocks, et al 2005). Infection starts when ingestion of egg or larvae takes place or the parasite larvae penetrates to the body through the skin or vectors (percutaneous routes). After larvae have gained access to various gastro intestinal tissues, some of the parasites can choose to remain within the gastro intestinal tract throughout. Most nematodes larvae that usually penetrates intestinal tissues and they are carried through venous blood to the final deposition in the live (Tawill, Sarah 2004).

These nematodes can undergo moulting in the liver. After they moult in the liver, they are then carried to the heart through pulmonary artery and are then deposited to the lungs. While in lungs, most of these larvae find their way to capillaries and alveoli. From this point, they go up through the respiratory tract and they finally enter the pharynx where the individual coughs them out and then re-swallow. The life cycle finally ends in the intestine and it’s at this point where they mature to adult stage.

Most of nematodes can either gain their access to host either orally or through percutaneous infection route in order to arrive to the lungs (Maizel, et-el, 2005). In most nematodes since they moult, secretion of enzymes process is controlled by hormones and enzymes such as proteolytic enzymes digests those proteins which are found in cuticles and in other cases they are involved in re-absorption of old cuticles. Routes of infection. Helminths gain their access to human body through various routes, where they either spend their life, on the mucosa surface or before crossing the mucosa to predilection site.

The oral route is the most common route, whereby, Trichiuris trichiura, trichinella spiralis, ascaris lumbricoides, enterobius vermiculaliss chlonorchis sinensis, fasciolopsis buski, paragonimus species, as well as the taenia species use the oral route (Else, 2005). The other route used by helminths is through the skin, and the species associated with this route include, Necator americanus and Ancylostoma duodenale, the strongyloides species, brugia malayi and wuchereria bancrofti and schistosoma species, among others.

Both the soil and water borne helminths can use either of the route depending on the vector of infection and where the vector is found. Mechanism for immunodulation is mediated by cytokines. When an individual is infected with helminths, an allergic induction occurs, where by interleukin 3; IL-15 and Il-4 are produced. Some species do not respond strongly to the helminths infection, for example in cases where H contortus infects sheep, while when a primary infection of helminths to mouse, a strong cytokines response is evidenced.

When an immunised sheep is given a challenge infection, a high regulation of IFNY and cytokines is induced, with the individual cytokine kinetic expression varying with IL-13,Il-5 and IFNY becoming higher within the first three days after the induction while the IL-4 levels taking longer to peak. The IL-4 peaks on the fifth day. When an immune sheep rejected challenge, a markable increase in the expression of cytokines, equivalently to the response previously observed. IL-4 is necessary in expulsion process, and on the other hand eosinophils and Il-5 and IL-5 are necessary in delayed rejection.

Most of helmiths exhibits direct immune response which is usually away from those modes which can cause damage to them (Artis, 2006). They hence regulate various immune responses which make them to have a place to feed properly and to reproduce. Helmiths has strong TH2 responses and has various factors which help in restraining. TH2 Immunity from removing the parasite from the host’s body. T. cells also play quite a vital role in restraining various responses of the host cell. TH2 usually accompanies active infection.

Immunomodulation can also occur in molecular level. Therefore helmiths usually have direct immune responses which keep them away from those things which damage them (Elliot, et al, 2004). Proteins which are usually produced by can be indirectly being implicated in the process of tissue repair. Infection of host by most of the G1 nematodes results to production of various immune responses in the host cells which are elicited to fight the infection. This can cause mast cells to build up which are meant to exclude the parasite from host body (Casbarre, 1997).

Mast cells are then triggered to produce mediators by consequently binding to the surface of 1GE receptors which initiates rapid expulsion of parasite. In most cases inflammatory responses are not usually initiated in host anima (Sheerer, 2005). In times of increased infection rate, leukocyte numbers decreases so that larvae can be expelled and therefore in this case the L3 will reach tissue riche which will enable it to produce inflammatory response by production of a lot of T2 cytokines and eosincephils.

Eosinophils can therefore kill the larvae in tissue and in GIT by antibody mediated release of granules and proteins and other cytotoxic molecules .

Reference:

Dzik M. , 2005, Molecules related with Helmith parasites involved in host colonization, Warzawa: Poland Balic A. , et-el, 2005, Cell Cytokines and Other Molecules associated with rejection of Gastrointestinal Nematodes, Melboume, Australia. Artis D. , 2006, new weapon in the war of worms: Mechanism of immune expulsion of GI Nematodes, Philladelphia, United State. Koski G. K. , Scott E. M.2003, GI Nematodes, Trace elements and Immunity, Journal of Trace Elements in experimental medicine, Quebec Canada. Else, 2005, Have GI Nematodes outwitted Immune System?

Manchester University, United Kingdom. Maizel. M R. et-el, 2005, Evasion by Helmith Parasite, Nottingham, United Kingdom Casbarre C. L. , 1997, effect of G1 nematodes on ruminant immune system, Betts Ville USA. Weinstocks V. J et al 2005. Role of helmith in regulating mucosal inflation, Springers, Verlag. Falcon H. F. , Pritchard D. , 2005, Parasite’s role reversal Nottingham, UK. Vol 21(4) Elliot D.E et al, 2004, helmiths and modulation in mucosal inflammation, Lippincott Williams and Wilkins, UK Joseph A. J et al, 2005, G1 nematodes variation is associated with variation in innate immune responsiveness, Nottingham, United Kingdom.

Mulcahy G. , et al, 2003, Helmith at mucosal barrier Sydney Australia, 56 p. 853-868 Khan W. I. , Collins M. S. , 2004, parasite immunology, Ontario Canada 26 319-326. Lochnit G. et al, 2005, Searching new target for helmith strategies, Journal for parasitology, Glessen, Germany 35 p. 911-923. Maizel R. M. , et al, 2005, Regulation master, Edinburgh United Kingdom.

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