Trichinella spiralis: Nonspecific resistance and immunity to newborn larvae in inbred mice

1985 ◽  
Vol 60 (1) ◽  
pp. 101-110 ◽  
Author(s):  
R.G. Bell ◽  
Ching Hua Wang ◽  
R.W. Ogden
1988 ◽  
Vol 74 (2) ◽  
pp. 283 ◽  
Author(s):  
Donald L. Wassom ◽  
Debra A. Dougherty ◽  
Terry A. Dick

Parasitology ◽  
1994 ◽  
Vol 108 (1) ◽  
pp. 69-75 ◽  
Author(s):  
M. E. Roses ◽  
D. Wakelin ◽  
P. Hesketh

SUMMARYParasitological and immunological interactions between Eimeria vermiformis or E. pragensis and Trichinella spiralis were investigated during concurrent infections in NIH, BALB/c and B10.G inbred mice. The establishment of T. spiralis was unaffected by the presence of either coccidium, but expulsion of adult worms was delayed significantly in mice infected with E. vermiformis; E. pragensis did not have this effect. Replication of E. vermiformis was enhanced in concurrent infections with T. spiralis, but that of E. pragensis was reduced. Specific immune responses to each parasite were unaffected in mice infected with T. spiralis and E. pragensis, but levels of some responses were reduced when T. spiralis and E. vermiformis were combined. Thus both in vitro antigen-induced proliferation of mesenteric lymph node cells (MLNC) and intestinal mastocytosis were lower than in singly infected mice. Mitogen (Con A) responsiveness of MLNC was not affected in mice infected with T. spiralis and E. vermiformis, and cells from these mice were capable of transferring protective immunity to the nematode in naive recipients. Injection of monoclonal antibody to interferon gamma, a major component of the cytokine response to E. vermiformis, did not prevent delay of worm expulsion in concurrent infections. The results are discussed in terms of possible interactions between the T helper cell subsets or the inflammatory components of the responses induced by each parasite.


Parasitology ◽  
1990 ◽  
Vol 100 (3) ◽  
pp. 491-497 ◽  
Author(s):  
F. Bolas-Fernandez ◽  
D. Wakelin

SUMMARYComparisons were made of the infectivity and antigenicity of 4 Trichinella spiralis isolates (S, D, Y, W), of quite different geographical origins, and T. pseudospiralis (P) in rapid- and slow-responder inbred mice. Infectivity was measured by the Index of Reproductive Capacity (ICR) expressed as the ratio between the number of muscle larvae recovered on day 30 post-infection (p.i.) and the numbers of larvae given at infection. Antigen recognition was measured by the degree of proliferation of mesenteric lymph node cells (MLNC) to in vitro stimulation with crude muscle larvae antigen (CMLA) and by the total antibody responses to CMLA at day 25 p.i. as measured by ELISA. Regarding infectivity the isolates fell into two groups, high infectivity (S, D and Y) and low infectivity (W and P). Analysis of CMLA, detergent-stripped (CTAB) and I-labelled surface larval proteins was made by SDS—PAGE under reducing conditions. Differences in antigen profiles were seen in all antigen preparations, being most noticeable in CTAB and 125I-labelled proteins from W and P isolates. Antigen recognition by polyclonal infection-derived antisera and by monoclonal antibodies raised against the T. spiralis London strain (L) was studied in the W (Arctic) and S (Spanish) isolates. Polyclonal antisera recognized different antigens in the S and W isolates, as did the monoclonal antibody, although recognition was more restricted. Neither antibody recognized a 64 kDa band in the W isolate which was clearly visible in the others tested.


Parasitology ◽  
1989 ◽  
Vol 99 (1) ◽  
pp. 83-88 ◽  
Author(s):  
F. Bolas-Fernandez ◽  
D. Wakelin

SUMMARYA comparison was made of the development, survival and reproduction of 5 isolates of Trichinella spiralis in inbred mice. Low responder C57BL/10 mice allowed worms of all isolates to survive longer and reproduce more successfully than did high responder NIH mice, suggesting that host immunity exerted a dominant influence upon infectivity. One isolate (Is-5 (W) — an arctic isolate) had a markedly lower infectivity than all other isolates, and was selected for more detailed study, together with isolate Is-1 (S) (a temperate isolate) which showed high infectivity. The lower infectivity of Is-5 (W) reflected a more rapid onset of immunity in mice infected with this parasite, immunity reducing the reproductive potential of female worms and causing an early expulsion from the intestine. No evidence of a dose-dependent suppression of immunity was found to explain the higher infectivity of Is-1 (S). Is-5 (W) provided a very rapid mucosal mastocytosis in infected mice, whereas Is-1 (S) caused no measurable response. In contrast, Is-1 (S) elicited higher levels of circulating parasite-specific antibodies than did Is-5 (W). These results are discussed in relation to the interplay of parasite immunogenicity and host immune responsiveness in determining infectivity, and point to the importance of identifying those immunodominant parasite molecules which control the balance of the host—parasite relationship.


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