Interactions between infections with Eimeria spp. and Trichinella spiralis in inbred mice

Parasitology ◽  
1994 ◽  
Vol 108 (1) ◽  
pp. 69-75 ◽  
Author(s):  
M. E. Roses ◽  
D. Wakelin ◽  
P. Hesketh
Keyword(s):  
Protective Immunity ◽  
Trichinella Spiralis ◽  
Inbred Mice ◽  
T Helper ◽  
Eimeria Spp ◽  
Immunological Interactions ◽  
Concurrent Infections ◽  
Lymph Node Cells ◽  
Worm Expulsion

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.

Infectivity, antigenicity and host responses to isolates of the genus Trichinella

Parasitology ◽  
1990 ◽  
Vol 100 (3) ◽  
pp. 491-497 ◽  
Author(s):  
F. Bolas-Fernandez ◽  
D. Wakelin
Keyword(s):  
Trichinella Spiralis ◽  
Inbred Mice ◽  
Antigen Recognition ◽  
Reproductive Capacity ◽  
Host Responses ◽  
Reducing Conditions ◽  
Sds Page ◽  
Muscle Larvae ◽  
Lymph Node Cells

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.

Immunization of mice against Trichinella spiralis and T. britovi using excretory and secretory antigens

1997 ◽  
Vol 71 (2) ◽  
pp. 109-112 ◽  
Author(s):  
P.K. Goyal ◽  
F. Bolas-Fernandez ◽  
D. Wakelin
Keyword(s):  
Immune Responses ◽  
Protective Immunity ◽  
Trichinella Spiralis ◽  
Antibody Responses ◽  
Current Understanding ◽  
T Helper ◽  
T Helper 2 ◽  
Mesenteric Node ◽  
Specific Igg

AbstractImmune responses to immunization and infection with Trichinella spiralis and T. britovi were studied in NIH high-responder mice. Overall it was shown that T. britovi was the more immunogenic, immunization and challenge with this species giving greater host-protective immunity. This greater immunogenicity was reflected in higher proliferative responses when mesenteric node lymphocytes (MLNC) from immunized mice were restimulated with T. britovi antigens in vitro and in higher levels of T helper 2 (Th2) lymphocyte-dependent specific IgG1 antibody responses against this species. MLNC from mice immunized against T. britovi released more IL-5 when restimulated in vitro, again suggesting a greater T helper 2 subset response, but after infection the highest levels of IL-5 were recorded from MLNC taken from T. spiralis challenged mice. These data are discussed in relation to current understanding of immunological differences between species and isolates of the genus Trichinella.

scholarly journals Resolution of cutaneous leishmaniasis: interleukin 12 initiates a protective T helper type 1 immune response.

1993 ◽  
Vol 177 (6) ◽  
pp. 1797-1802 ◽  
Author(s):  
J P Sypek ◽  
C L Chung ◽  
S E Mayor ◽  
J M Subramanyam ◽  
S J Goldman ◽  
...  
Keyword(s):  
T Cells ◽  
Lymph Node ◽  
Enzyme Linked Immunosorbent Assay ◽  
Th1 Cells ◽  
T Helper ◽  
Ifn Gamma ◽  
Lymph Node Cells ◽  
Helper Type

Resistance to Leishmania major in mice is associated with the appearance of distinct T helper type 1 (Th1) and Th2 subsets. T cells from lymph nodes draining cutaneous lesions of resistant mice are primarily interferon gamma (IFN-gamma)-producing Th1 cells. In contrast, T cells from susceptible mice are principally Th2 cells that generate interleukin 4 (IL-4). Although existing evidence is supportive of a role for IFN-gamma in the generation of Th1 cells, additional factors may be required for a protective response to be maintained. A potential candidate is IL-12, a heterodimeric cytokine produced by monocytes and B cells that has multiple effects on T and natural killer cell function, including inducing IFN-gamma production. Using an experimental leishmanial model we have observed that daily intraperitoneal administration at the time of parasite challenge of either 0.33 micrograms IL-12 (a consecutive 5 d/wk for 5 wk) or 1.0 micrograms IL-12 per mouse (only a consecutive 5 d) caused a > 75% reduction in parasite burden at the site of infection, in highly susceptible BALB/c mice. Delay of treatment by 1 wk had less of a protective effect. Concomitant with these protective effects was an increase in IFN-gamma and a decrease in IL-4 production, as measured by enzyme-linked immunosorbent assay of supernatants generated from popliteal lymph node cells stimulated with leishmanial antigen in vitro. The reduction in parasite numbers induced by IL-12 therapy was still apparent at 10 wk postinfection. In addition, we observed that the administration of a rabbit anti-recombinant murine IL-12 polyclonal antibody (200 micrograms i.p. every other day for 25 d) at the time of infection to resistant C57Bl/6 mice exacerbated disease. These effects were accompanied by a shift in IFN-gamma production in vitro by antigen-stimulated lymph node cells indicative of a Th2-like response. These findings suggest that IL-12 has an important role in initiating a Th1 response and protective immunity.

Accelerated expulsion of adult Trichinella spiralis in mice given lymphoid cells and serum from infected donors

Parasitology ◽  
1976 ◽  
Vol 72 (3) ◽  
pp. 307-315 ◽  
Author(s):  
D. Wakelin ◽  
M. Lloyd
Keyword(s):  
Lymph Node ◽  
Mesenteric Lymph Node ◽  
Adult Stage ◽  
Trichinella Spiralis ◽  
Significant Degree ◽  
Lymphoid Cells ◽  
Mesenteric Lymph ◽  
Lymph Node Cells ◽  
Worm Expulsion

SummaryImmunity to the adult stage of Trichinella spiralis, assessed by an acceleration of worm expulsion, was transferred to recipient mice with mesenteric lymph node cells (MLNC) or serum taken from infected donors. Immunity was transferred most effectively by MLNC taken from donors infected for 8 days, i.e. donors actively responding to infection. Transfer of both MLNC and serum brought about a marked acceleration of worm expulsion in all cases, even where MLNC or serum given separately failed to transfer a significant degree of immunity.

scholarly journals Interleukin-23 Is Required for Development of Arthritis in Mice Vaccinated and Challenged with Borrelia Species

2008 ◽  
Vol 15 (8) ◽  
pp. 1199-1207 ◽  
Author(s):  
Nicholas J. Kotloski ◽  
Dean T. Nardelli ◽  
Sara Heil Peterson ◽  
Jose R. Torrealba ◽  
Thomas F. Warner ◽  
...  
Keyword(s):  
Lymph Node ◽  
Th17 Cells ◽  
Lyme Arthritis ◽  
T Helper ◽  
T Helper 17 ◽  
Survival Factor ◽  
Lymph Node Cells ◽  
Interleukin 23 ◽  
Insight Into

ABSTRACTWe recently hypothesized that T helper 17 (Th17) cells and their associated cytokines are involved in the development of arthritis following infection withBorrelia burgdorferi. Here, we show that interleukin-23 (IL-23), a survival factor for Th17 cells, is required for the induction of arthritis in mice vaccinated withB. burgdorferistrain 297 and challenged with “Borrelia bissettii.” WhenBorrelia-vaccinated and -challenged mice were given antibodies to the p19 subunit of IL-23, they failed to develop the histopathological changes observed in untreated vaccinated and challenged mice. In addition, viableB. bissettiiorganisms stimulated the secretion of IL-17 fromBorrelia-immune lymph node cells during in vitro culture. When anti-IL-23 p19 antibody was included in cultures ofB. bissettiiorganisms andBorrelia-immune lymph node cells, the production of IL-17 was reduced to levels observed in cultures containing immune cells alone. Taken together, these results support the hypothesis that Th17 cell-associated cytokines are involved in the development ofBorrelia-mediated arthritis. These findings provide insight into previously overlooked immune mechanisms responsible for the development of Lyme arthritis.

Immunological interactions between Trichinella spiralis and Trichuris muris in the intestine of the mouse

Parasitology ◽  
1977 ◽  
Vol 74 (2) ◽  
pp. 163-173 ◽  
Author(s):  
R. G. Burce ◽  
D. Wakelin
Keyword(s):  
Small Intestine ◽  
T Cell ◽  
Inflammatory Response ◽  
Large Intestine ◽  
Trichinella Spiralis ◽  
The Other ◽  
Trichuris Muris ◽  
Immunological Interactions ◽  
Concurrent Infections ◽  
Cross Immunity

In outbred (CFLP) and inbred (NIH) mice, the inflammatory response which is thought to be party responsible for the expulsion of Trichinella spiralis from the mid-region of the small intestine, also seemed to be largely responsible fo rthe simulataneous (i.e. early) expulsion of Trichuris muris from the caecum and large intestine during concurrent primary infections. The intractive explusion operated only when the concurrent infections were timed to produce T. Spiralis expulsion before T. muris expulsion would normally occur and the effect persisted for several days after T. Spiralis has been expelled.Interactive expulsion wasss depressed during application of the nonsteroid, anti-inflammatory drug indomethacin and by T-cell expulsion of T. spiralis. These results indicate that a T-cell mediated inflammatory response was probably the basis of the interaction.When the timing of the infections was altered such that the expulsion of T. spiralis there was no reciprocal ecpulsion of the latter. Mice immunized againest one or the other species did not show cross-immunity on heterologus challenge, confirming that the interaction did not involve similar antigens in the two species. The interactive expulsive response is considered as an example of an indirect cross-immunity.

scholarly journals Impaired protective immunity and T helper 2 responses in alymphoplasia (aly) mutant mice infected with Trichinella spiralis

Immunology ◽  
2001 ◽  
Vol 102 (2) ◽  
pp. 218-224 ◽  
Author(s):  
M. Korenaga ◽  
Y. Akimaru ◽  
S. M. Shamsuzzaman ◽  
Y. Hashiguchi
Keyword(s):  
Protective Immunity ◽  
Trichinella Spiralis ◽  
Mutant Mice ◽  
T Helper ◽  
T Helper 2

Transfer of immunity toTrichinella spiralisin the mouse with mesenteric lymph node cells: time of appearance of effective cells in donors and expression of immunity in recipients

Parasitology ◽  
1977 ◽  
Vol 74 (3) ◽  
pp. 215-224 ◽  
Author(s):  
D. Wakelin ◽  
Margaret M. Wilson
Keyword(s):  
Lymph Node ◽  
Mesenteric Lymph Node ◽  
Time Course ◽  
Trichinella Spiralis ◽  
Defence Mechanism ◽  
Spleen Cells ◽  
Mesenteric Lymph Nodes ◽  
Mesenteric Lymph ◽  
Lymph Node Cells ◽  
Worm Expulsion

Cells capable of transferring immunity toTrichinella spiralis, i.e. of accelerating adult worm expulsion, were present in the mesenteric lymph nodes of mice infected for 4, 6 or 8 days, but not in mice infected for only 2 days. The time-course of worm expulsion in mice infected on the day of transfer was similar in recipients of day 8 cells, expulsion becoming marked only when the recipients had been infected for at least 6 days. Transfer of cells 4 or 6 days after infection did not result in an accelerated worm expulsion; transfer 1 or 2 weeks before infection did not enhance the level of immunity in recipient mice. In contrast to the results obtained with mesenteric lymph node cells (MLNC) no immunity was trsnsferred when recipients were given spleen cells taken from donors infected for 8 days. It is suggested that MLNC do not cause worm expulsion directly, but cooperate with another component of the host's defence mechanism. Accelerated expulsion in recipients of cells was accompanied by a premature decline in fecundity of female worms. Evidence is presented to show that worm expulsion and impaired reproduction may represent independent aspects of the immune response toT. spiralis.

scholarly journals Modulation of Intestinal Muscle Contraction by Interleukin-9 (IL-9) or IL-9 Neutralization: Correlation with Worm Expulsion in Murine Nematode Infections

2003 ◽  
Vol 71 (5) ◽  
pp. 2430-2438 ◽  
Author(s):  
W. I. Khan ◽  
M. Richard ◽  
H. Akiho ◽  
P. A. Blennerhasset ◽  
N. E. Humphreys ◽  
...  
Keyword(s):  
Muscle Contraction ◽  
Trichinella Spiralis ◽  
Th2 Cells ◽  
Mucosal Mast Cell ◽  
Cell Hyperplasia ◽  
Trichuris Muris ◽  
Intestinal Nematode ◽  
Worm Expulsion ◽  
Interleukin 9

ABSTRACT Immune responses associated with intestinal nematode infections are characterized by the activation of T-helper 2 (Th2) cells. Previous studies demonstrated that during Trichinella spiralis infection, Th2 cells contribute to the development of intestinal muscle hypercontractility and to worm eviction from the gut, in part through signal transducer and activator of transcription factor 6 (Stat6). Interleukin-9 (IL-9), a Th2-cell-derived cytokine, has pleiotropic activities on various cells that are not mediated through Stat6. In this study, we investigated the role of IL-9 in the generation of enteric muscle hypercontractility in mice infected with the intestinal parasite T. spiralis and the cecal parasite Trichuris muris. Treatment of mice with IL-9 enhanced infection-induced jejunal muscle hypercontractility and accelerated worm expulsion in T. spiralis infection. These effects were associated with an up-regulation of IL-4 and IL-13 production from in vitro-stimulated spleen cells. In addition, increases in the level of intestinal goblet cells and in the level of mouse mucosal mast cell protease 1 (MMCP-1) in serum were observed in infected mice following IL-9 administration. However, the neutralization of IL-9 by anti-IL-9 vaccination or by anti-IL-9 antibody had no significant effect on worm expulsion or muscle contraction in T. spiralis-infected mice. In contrast, the neutralization of IL-9 significantly attenuated T. muris infection-induced colonic muscle hypercontractility and inhibited worm expulsion. The attenuated expulsion of the parasite by IL-9 neutralization was not accompanied by changes in goblet cell hyperplasia or the MMCP-1 level. These findings suggest that IL-9 contributes to intestinal muscle function and to host protective immunity and that its importance and contribution may differ depending on the type of nematode infection.

scholarly journals Critical Role for Signal Transducer and Activator of Transcription Factor 6 in Mediating Intestinal Muscle Hypercontractility and Worm Expulsion in Trichinella spiralis-Infected Mice

2001 ◽  
Vol 69 (2) ◽  
pp. 838-844 ◽  
Author(s):  
W. I. Khan ◽  
B. A. Vallance ◽  
P. A. Blennerhassett ◽  
Y. Deng ◽  
E. F. Verdu ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Muscle Function ◽  
Trichinella Spiralis ◽  
Critical Role ◽  
Interleukin 4 ◽  
Signal Transducer ◽  
T Helper ◽  
Immunological Mechanism ◽  
Worm Expulsion ◽  
Deficient Mice

ABSTRACT Intestinal nematode infections in rats or mice are accompanied by intestinal muscle hyper contractility that may contribute to parasite expulsion from the gut. Previous studies demonstrated that both the expulsion of nematode parasites and the associated muscle hyper contractility are dependent on CD4+ T helper cells. Nevertheless, the precise immunological mechanism underlying changes in intestinal muscle function remains to be determined. In this study, we investigated the role of interleukin 4 (IL-4) and signal transducer and activator of transcription factor 6 (STAT6) in the development of intestinal muscle hypercontractility and worm expulsion by infecting IL-4 and STAT6-deficient mice with Trichinella spiralis. Worm expulsion was almost normal in IL-4-deficient mice but substantially delayed in STAT6-deficient mice. Consistent with delayed worm expulsion, we also observed a marked attenuation of carbachol-induced muscle contraction in STAT6-deficient mice but only a moderate decrease in muscle hypercontractility in IL-4-deficient mice. In addition, we also observed severe impairment of T helper type 2 cytokine responses and intestinal mucosal mastocytosis in STAT6-deficient mice, although some degree of intestinal tissue eosinophilia was evident in these animals. These results are consistent with the hypothesis that STAT6-dependent changes in intestinal muscle function contribute to host protection in nematode infection.

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