Altered lysophospholipase B responsiveness in lactating mice infected with intestinal nematode parasites

Parasitology ◽  
1980 ◽  
Vol 81 (1) ◽  
pp. 17-26 ◽  
Author(s):  
B. Z. Ngwenya
Keyword(s):  
Trichinella Spiralis ◽  
Temporal Relation ◽  
Intestinal Lumen ◽  
Nippostrongylus Brasiliensis ◽  
Intestinal Tissue ◽  
Faecal Pellets ◽  
Intestinal Nematode ◽  
Nematode Parasites ◽  
Worm Expulsion ◽  
Small Intestines

SUMMARYLactating and nulliparous outbred Swiss (CF-1 strain) mice were infected at 12–16 weeks of age with Nippostrongylus brasiliensis or Trichinella spiralis. Lysophospholipase B levels in the intestinal tissue and faecal pellets were greatly depressed in infected lactating mice in contrast to infected nulliparous mice. Correlated with these depressions in lysophospholipase levels were markedly reduced numbers of bonemarrow eosinophils in infected lactating mice. Although the peak levels of lysophospholipase in the intestinal tissues occurred in both nulliparous and lactating mice by days 9 and 14 after infection with N. brasiliensis and T. spiralis, respectively, lactating mice had significantly lower lysophospholipase peak levels than nulliparous mice. The peak of luminal levels of the enzyme coincided with peak levels of the enzyme in the intestinal tissues and with theexpulsion of the majority of the worms from the small intestines of nulliparous mice. However, lactation delayed the temporal relation between the peak of lysophospholipase levels in the intestinal lumen and worm expulsion. These results suggest that lactation depressed the levels of the enzyme and interfered with its release into the intestinal lumen.

scholarly journals Intestinal epithelial cell secretion of RELM-β protects against gastrointestinal worm infection

2009 ◽  
Vol 206 (13) ◽  
pp. 2947-2957 ◽  
Author(s):  
De'Broski R. Herbert ◽  
Jun-Qi Yang ◽  
Simon P. Hogan ◽  
Kathryn Groschwitz ◽  
Marat Khodoun ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Trichinella Spiralis ◽  
Intestinal Lumen ◽  
Th2 Cells ◽  
Nippostrongylus Brasiliensis ◽  
Intestinal Epithelial ◽  
Cell Secretion ◽  
Heligmosomoides Polygyrus ◽  
Parasitic Helminths

Th2 cells drive protective immunity against most parasitic helminths, but few mechanisms have been demonstrated that facilitate pathogen clearance. We show that IL-4 and IL-13 protect against intestinal lumen-dwelling worms primarily by inducing intestinal epithelial cells (IECs) to differentiate into goblet cells that secrete resistin-like molecule (RELM) β. RELM-β is essential for normal spontaneous expulsion and IL-4–induced expulsion of Nippostrongylus brasiliensis and Heligmosomoides polygyrus, which both live in the intestinal lumen, but it does not contribute to immunity against Trichinella spiralis, which lives within IEC. RELM-β is nontoxic for H. polygyrus in vitro but directly inhibits the ability of worms to feed on host tissues during infection. This decreases H. polygyrus adenosine triphosphate content and fecundity. Importantly, RELM-β–driven immunity does not require T or B cells, alternative macrophage activation, or increased gut permeability. Thus, we demonstrate a novel mechanism for host protection at the mucosal interface that explains how stimulation of epithelial cells by IL-4 and IL-13 contributes to protection against parasitic helminthes that dwell in the intestinal lumen.

Nutritional control of gastrointestinal parasitism in lactating rats

2005 ◽  
Vol 2005 ◽  
pp. 11-11 ◽  
Author(s):  
J.G.M. Houdijk ◽  
N.S. Jessop ◽  
D.P. Knox ◽  
I. Kyriazakis
Keyword(s):  
Immune Responses ◽  
Indirect Evidence ◽  
Host Protein ◽  
Nippostrongylus Brasiliensis ◽  
Host Immune Responses ◽  
Protein Nutrition ◽  
Intestinal Nematode ◽  
Nematode Parasites ◽  
Periparturient Period ◽  
Protein Supply

Small ruminant studies have shown that a reduction in protein scarcity, through either an increase in protein supply or reduction in protein demand, results in reduced nematode egg excretion and worm burdens during the periparturient period (Houdijk and Athanasiadou, 2003). Whilst this reduced degree of parasitism indirectly suggests that such nutritional effects are mediated through changes in host immune responses, there is only limited direct evidence for this. A rodent model may be used for directly assessing immune responses that underlie nutritional control of nematode parasites. There is indirect evidence that lactating rats undergo a breakdown of immunity to the intestinal nematode Nippostrongylus brasiliensis (Houdijk et al., 2003). Provided that this breakdown is sensitive to protein nutrition, this model may be used for elucidating interactions between nutrition and immunity to parasites. Therefore, we assessed whether breakdown of immunity to N. brasiliensis in the lactating rat is sensitive to host protein nutrition.

Host–parasite interactions in rodent nematode infections

2003 ◽  
Vol 77 (2) ◽  
pp. 125-131 ◽  
Author(s):  
Y.R. Mahida
Keyword(s):  
Neutralizing Antibodies ◽  
Host Response ◽  
Trichinella Spiralis ◽  
Host Responses ◽  
Nippostrongylus Brasiliensis ◽  
Trichuris Muris ◽  
Epithelial Phenotype ◽  
Worm Expulsion ◽  
Genetically Manipulated ◽  
Host Parasite

AbstractIn rodents,Trichinella spiralisandNippostrongylus brasiliensisinfect the small intestine andTrichuris murisresides in the colon. The intestinal host response in these animals is characterized by changes in mucosal architecture and inflammation and is associated with worm expulsion. The requirement of T cell-mediated host response in worm expulsion has been demonstrated over many years. Subsequent studies have shown that Th2-type, but not Th1-type, responses mediate resistance to the nematodes. Investigations using neutralizing antibodies and genetically manipulated mice have characterized the contribution of individual Th2-type cytokines in not only worm expulsion, but also specific cellular changes that occur in the mucosa, such as alterations in epithelial phenotype and smooth muscle. There is also increasing appreciation of the contribution of non-bone marrow-derived cells in innate and adaptive host responses in these models.

Increased intestinal muscle contractility and worm expulsion in nematode-infected mice

1997 ◽  
Vol 272 (2) ◽  
pp. G321-G327 ◽  
Author(s):  
B. A. Vallance ◽  
P. A. Blennerhassett ◽  
S. M. Collins
Keyword(s):  
Trichinella Spiralis ◽  
Isometric Tension ◽  
Mucosal Inflammation ◽  
Myeloperoxidase Activity ◽  
Muscle Contractility ◽  
Tension Development ◽  
Intestinal Nematode ◽  
Worm Expulsion ◽  
Nih Swiss ◽  
Genetically Determined

Intestinal nematode infections are accompanied by mucosal inflammation and an increase in propulsive motor activity that may contribute to parasite eviction from the gut. To examine whether differences in worm expulsion correspond to the increased intestinal muscle contractility that accompanies nematode infection, we studied mice with genetically determined differences in their ability to expel the nematode parasite Trichinella spiralis. Specifically, we examined isometric contraction of longitudinal muscle, worm counts, and inflammation, as measured by myeloperoxidase activity, in two strains of mice infected with T. spiralis. The strong responder strain, NIH Swiss, expelled the parasites by day 16 postinfection, whereas the poorer responding B10.BR strain was still heavily infected by day 21 postinfection. However, both strains developed similar increases in jejunal myeloperoxidase activity. Both strains demonstrated increased isometric tension development after infection, but peak tension occurred earlier in NIH Swiss mice (day 8 vs. day 12 postinfection) and was of significantly greater magnitude than in B10.BR mice. We conclude that the ability to expel T. spiralis from the small bowel is not related to the degree of granulocyte-dependent mucosal inflammation but is reflected in the magnitude of the accompanying increase in force generation by intestinal smooth muscle.

Effect of dietary condensed tannins on gastrointestinal nematodes

2001 ◽  
Vol 137 (4) ◽  
pp. 461-469 ◽  
Author(s):  
N. L. BUTTER ◽  
J. M. DAWSON ◽  
D. WAKELIN ◽  
P. J. BUTTERY
Keyword(s):  
Condensed Tannins ◽  
Trichinella Spiralis ◽  
Condensed Tannin ◽  
Intestinal Lumen ◽  
Parasitic Nematodes ◽  
Nippostrongylus Brasiliensis ◽  
Small Intestinal Mucosa ◽  
Quebracho Tannin ◽  
Small Intestinal

It has been previously shown in this laboratory that feeding a model condensed tannin, quebracho tannin, reduces the small intestinal nematode burden in sheep and rats. The aim of the current programme was to determine whether this occurs through direct toxicity against the parasites. Both in vivo and in vitro studies were conducted. The first study compared the effect of dietary quebracho tannin (40 g/kg) on the establishment of the parasitic nematodes Nippostrongylus brasiliensis and Trichinella spiralis in the rat small intestine. The burden of N. brasiliensis, which, although closely associated with the mucosa, actually dwells within the small intestinal lumen, was significantly reduced (P<0·001) by dietary quebracho tannin. In contrast, T. spiralis, which penetrates into the small intestinal mucosa, was unaffected (>0·05) by the dietary inclusion of quebracho tannin. The second study involved monitoring the survival of adult N. brasiliensis and T. spiralis when incubated in vitro in varying concentrations of quebracho tannin in Hanks’ balanced salt solution. The survival of N. brasiliensis was compromised at concentrations as low as 0·01% (w/v) quebracho tannin but improved with the addition of 0·1% (w/v) polyethylene glycol, which binds to, and inactivates, tannin. T. spiralis was similarly affected, but much more rapidly. These results suggest that dietary quebracho tannin may reduce nematode worm burdens through a toxic effect that requires direct contact between parasite and tannin. This raises the possibility that feeding locally available plant material containing condensed tannins may be an alternative method for controlling parasite infections, especially in areas such as the tropics and subtropics.

Use of cortisone derivatives to inhibit resistance to Nippostrongylus brasiliensis and to study the fate of parasites in resistant hosts

Parasitology ◽  
1965 ◽  
Vol 55 (4) ◽  
pp. 723-730 ◽  
Author(s):  
Bridget M. Ogilvie
Keyword(s):  
Cellular Response ◽  
Marked Effect ◽  
Trichinella Spiralis ◽  
Early Stage ◽  
Acquired Resistance ◽  
Challenge Infection ◽  
Cortisone Acetate ◽  
Nippostrongylus Brasiliensis ◽  
Initial Infection ◽  
Nematode Parasites

Acquired resistance to some nematode parasites can be suppressed by daily administration of cortisone acetate to the host. Cortisone treatment completely suppressed previously acquired resistance of mice to Trichinella spiralis (Coker, 1956) and suppressed, at least partially, the acquisition of resistance to T. spiralis by rats during initial infection (Markell & Lewis, 1957).A previous report (Weinstein, 1955) suggested cortisone acetate treatment was less effective in the suppression of acquired resistance of rats to Nippostrongylus brasiliensis. Weinstein showed that daily treatment with 2 mg cortisone acetate throughout five immunizing infections and continued during the challenge infection increased the number of worms in the intestine and had a marked effect on the cellular response in the skin and lungs. However, there was no significant effect when daily cortisone treatment commenced only on the fifth day before the challenge infection. This result suggested that acquisition of immunity to N. brasiliensis was partially overcome by cortisone treatment, but the same level of drug treatment had no effect on immunity already acquired.In the experiments reported here, previously acquired resistance to N. brasiliensis was suppressed completely and the initiation of immunity stopped, either completely or at a very early stage, by treatment with the cortisone derivatives prednisolone or betamethasone. The complete suspension of all manifestations of acquired resistance obtained by treatment with these drugs was used to investigate the fate of larvae migrating in an immune host.The rats and strain of parasite, and the methods of handling them, have been described previously (Ogilvie, 1965).

scholarly journals Nippostrongylus brasiliensisin the rat: Failure to relate intestinal histamine and mast cell levels with worm expulsion

Parasitology ◽  
1971 ◽  
Vol 63 (3) ◽  
pp. 473-481 ◽  
Author(s):  
R. Keller
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Technical Assistance ◽  
Second Step ◽  
Nippostrongylus Brasiliensis ◽  
Essential Factor ◽  
Intestinal Tissue ◽  
Adult Age ◽  
Adult Rat ◽  
Worm Expulsion

This paper describes experiments to determine whether intestinal tissue mast cells and/or intestinal histamine are involved in the second, expulsive step of worm elimination. In neonatal rats, intestinal tissue contains only very little histamine and mature mast cells are encountered only sporadically. From birth to the adult age, there was a gradual rise in both intestinal mast cells and histamine.DuringNippostrongylus brasiliensisinfection in the adult rat, the concentration of histamine in the small intestine was clearly lower than in uninfected controls.Especially low histamine values were found to occur on days 6–12 of a primary infection in the region where the main worm burden was located. Similarly, the number of tissue mast cells present in the epithelium of the jejunum was decreased in the same region and during the same period of time. From the observation that the bulk of the parasites are expelled at a time when histamme and mast cell levels are low, it was concluded that mast cells and their constituents were not an essential factor in the second step of worm eliminationThis work was supported by the Schweizerische Nationalfonds zur Förderung der wissenschaftlichen Forschung (Grant 5200.3). The skilful technical assistance of Miss I. Beeger, Miss R. Keist and Miss M. Iseli is gratefully acknowledged. I thank Mr H. Berchtold, Biostatistisches Zentrum der Universität Zürich, for the statistical evaluation of the data.

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 Muc5ac: a critical component mediating the rejection of enteric nematodes

2011 ◽  
Vol 208 (5) ◽  
pp. 893-900 ◽  
Author(s):  
Sumaira Z. Hasnain ◽  
Christopher M. Evans ◽  
Michelle Roy ◽  
Amanda L. Gallagher ◽  
Kristen N. Kindrachuk ◽  
...  
Keyword(s):  
De Novo ◽  
Trichinella Spiralis ◽  
Nematode Infection ◽  
Nippostrongylus Brasiliensis ◽  
Chronic Infections ◽  
Trichuris Muris ◽  
Intestinal Nematode ◽  
Ifn Γ ◽  
Deficient Mice

De novo expression of Muc5ac, a mucin not normally expressed in the intestinal tract, is induced in the cecum of mice resistant to Trichuris muris infection. In this study, we investigated the role of Muc5ac, which is detected shortly before worm expulsion and is associated with the production of interleukin-13 (IL-13), in resistance to this nematode. Muc5ac-deficient mice were incapable of expelling T. muris from the intestine and harbored long-term chronic infections, despite developing strong TH2 responses. Muc5ac-deficient mice had elevated levels of IL-13 and, surprisingly, an increase in the TH1 cytokine IFN-γ. Because TH1 inflammation is thought to favor chronic nematode infection, IFN-γ was neutralized in vivo, resulting in an even stronger TH2-type immune response. Nevertheless, despite a more robust TH2 effector response, the Muc5ac-deficient mice remained highly susceptible to chronic T. muris infection. Importantly, human MUC5AC had a direct detrimental effect on nematode vitality. Moreover, the absence of Muc5ac caused a significant delay in the expulsion of two other gut-dwelling nematodes (Trichinella spiralis and Nippostrongylus brasiliensis). Thus, for the first time, we identify a single mucin, Muc5ac, as a direct and critical mediator of resistance during intestinal nematode infection.

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