Muscle cells, infected

Due to lack of specific reagents, products of 8- and y-stichocytes were not evaluated in irradiated larval experiments and cannot be excluded from a role in the muscle infection. Interestingly, NA were detected in nuclei of muscle cells infected by irradiated larvae, which suggested that these products may influence the infected cell phenotype but are not derived Irom a- and P-stichocytes. 

Figure 7 - Effect of glycosphingolipid on the infectivity of the Dm 28c clone of T. cruzi with heart muscle cells. Control (open column), heart muscle cells infected with T. cruzi. Dm 28c clone. Experiment 1 (slippled column), metacyclic forms, preincubated with glycolipid for 30 min, following addition to the cell culture. Experiment 2 (solid column), heart muscle cells incubated with glycolipid for 30 min, before metacyclic addition. Experiment 3 (cross-hatched column), heart muscle cells incubated simultaneously with metacyclic forms and glycolipid.

Jasmer, D.P., Yao, S., Vassilatis, D., Despommier, D. and Neary, S.M. (1994) Failure to detect Trichinella spiralis p43 in isolated host nuclei and in irradiated larvae of infected muscle cells which express the infected cell phenotype. Molecular and Biochemical Parasitology 67, 225-234. 

Trichinellosis is caused by the parasitic nematode Trichinella spiralis. This parasite has a complex life cycle that alternates between intestinal and muscle cell compartments of the host. This nematode infection is unusual because 7. spiralis is an intracellular parasite of mammalian cells. In addition, the broad host range of this parasite includes most mammals. The disease in humans has intrigued parasitologists, other biologists and public health workers for over a century (Cambell, 1983). The attraction to trichinellosis pardy stems from the debilitating and sometimes fatal effects that characterize this disease. 

The muscle phase of the infection is initiated by newborn larvae (immature LI larvae). These larvae originate from female worms located in the small intestine of the host. On recognition of skeletal muscle cells, larvae invade and initiate the processes that culminate in long-term intracellular infection of these cells. Following infection, both the parasite and host muscle cell undergo significant changes, over the course of the first 15 days (referred to here as the initiation phase), which is followed by... 

Infection-induced cell cycle re-entry and suspension in G2/M occur early in infection and are likely to influence regulation of some of the other host cell effects (Jasmer, 1993). The earliest indication that 7. spiralis induces terminally differentiated skeletal muscle cells to re-enter the cell cycle came... 

Therefore, it is anticipated that chronic repression of muscle gene expression does not require chronic regulation by the parasite. Rather, this effect is expected to result from chronic suspension of infected cells in a non-Go/Gi gene regulatory environment. A simple hypothesis derived from known characteristics of skeletal muscle cells is that induction of cell cycle re-entry is sufficient to cause both chronic suspension in G2/M and repression of muscle gene expression. This possibility has implications for the number of regulatory points at which the parasite might influence the host cell and possible methods to screen for those products. 

Finally, several experiments indicate that excretory/secretory products (ESP), derived from newborn larvae or pepsin-HCl isolated mature muscle larvae, induce muscle cell basophilia (Blotna-Filipiak et al, 1998 Wranicz et al., 1998) or nuclear hypertrophy (Leung and Ko, 1997), respectively. Effects were observed in vivo and in vitro. Although correspondence of these general changes to biochemical or genomic characteristics of the infected cell and nuclei were not established, these observations may facilitate dissection of the parasite products that are responsible. 

Information on which parasite products might regulate infected muscle cell characteristics is unresolved. Parasite proteins will be the focus of this discussion. This focus results in part from general lack of information on other secreted products/metabolic wastes and their potential influences on the host cell. In addition, arguments for cell-permeable parasite products are less compelling, and no clear evidence exists for a bystander effect in which bona fide infected cell characteristics become established in neighbouring, uninfected host muscle cells. 

Two additional parasite proteins with apparent HLH binding properties were identified, based on the idea that direct antagonism of host HLH transcription factors might be responsible for muscle cell subversion. One is a MyoDdike protein (Connolly el al., 1996) and another (110 kDa) is located in the vicinity of the hypodermis or somatic musculature of muscle larvae (Lindh el al., 1998). Secretion of these proteins into the infected cell has not been reported. 

Gustowska, L., Gabryel, P., Blotna-Filipiak, M. and Rauhut, W. (1989) The role of the muscle cell nucleus in the mechanism of its transformation after infection by Trichinella spiralis larvae. II. Histochemical features of the functional transformation of the muscle cell nucleus in the course of infection. Wiadomosci Parazytologiczne 35, 1401-1411. 

Jasmer, D.P. (1993) Trichinella spiralis infected skeletal muscle cells arrest in G2/M is associated with the loss of muscle gene expression. Journal of Cell Biology 121, 785-793. 

Jasmer, D.P., Bohnet, S. and Prieur, D.J. (1991) Trichinella spp. differential expression of acid phosphatase and myofibrillar proteins in infected muscle cells. Experimental Parasitology 72, 321-331. 

Yao, C. and Jasmer, D.P. (1998) Nuclear antigens in Trichinella spiralis infected muscle cells nuclear extraction, compartmentalization and complex formation. Molecular and Biochemical Parasitology 92, 207—218. 

Fibrosis resulting in the loss of normal organ structures is the hallmark of chronic rejection. The fibrosis may be due to wound healing, which is then followed by the cellular necrosis of acute rejection. However, it must be pointed out that chronic rejection develops many times in the absence of acute rejection. Fibrosis may be a result of several diverse factors such as equation of chronic rejection with chronic delayed-type hypersensitivity reaction, injury to blood vessels and resulting response to chronic ischemia, the proliferation of smooth muscle cells in the intima of arterial walls producing vascular occlusion, or persistent viral infections that will induce cellular immune response. 

Ivermectin binds to chloride ion channels in parasitic nerve and muscle cells, thereby increasing membrane permeability to chloride. Increased intracellular chloride results in hyperpolarization of nerve and muscle tissues, which results in paralysis and death of the parasite. Ivermectin is well tolerated during shortterm use in mild-to-moderate infections. Administration in more severe infections may cause swollen or tender lymph glands, fever, skin rash, itching, and joint and muscle pain, but these reactions may be... 

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