scholarly journals The dynamics of genetically markedAscaris suuminfections in pigs

Parasitology ◽  
2008 ◽  
Vol 136 (2) ◽  
pp. 193-201 ◽  
Author(s):  
P. NEJSUM ◽  
A. ROEPSTORFF ◽  
T. J. C. ANDERSON ◽  
C. JØRGENSEN ◽  
M. FREDHOLM ◽  
...  

SUMMARYThe genotypes of both host and parasite may influence the outcome of parasitic infections, but few attempts have been made to quantify the effect of parasite genotype on macroparasite infections of socio-economic importance. We examined variation in particular traits during the infection in pigs with the parasitic nematodeAscaris suum. We infected 26 pigs with mixtures of equal proportions of embryonated eggs from 4 single female worms each with a unique mtDNA haplotype – the eggs from each female worm were a mixture of siblings and half-siblings. Pigs were necropsied on days 14, 17 and 28 following inoculation, which corresponded to time-points before, during and after the main immune responses against the nematode. A total of approximately 11 000 worms were recovered at necropsy. The location in the small intestine was recorded for all worms and the length and mtDNA haplotype were determined for about 4200 individual worms. There were significant differences in the distribution and abundance of the 4 individual haplotypes among individual pigs demonstrating strong interactions between parasite and host. We found significant differences in the abundance and position in the small intestine as well as the size of worms among haplotypes. We conclude that both parasite and host effects as well as the interplay between them play important roles in determining the characteristics and outcome of infection.

2015 ◽  
Vol 129 (7) ◽  
pp. 515-527 ◽  
Author(s):  
Angela L. Man ◽  
Eugenio Bertelli ◽  
Silvia Rentini ◽  
Mari Regoli ◽  
Graham Briars ◽  
...  

This work described how important features of the intestinal barrier change across life. In aging individuals the integrity of the epithelial barrier appear to be partially compromised and immune responses to certain microbial antigen show signs of decline.


Parasitology ◽  
1981 ◽  
Vol 83 (3) ◽  
pp. 489-496 ◽  
Author(s):  
Erling Bindseil ◽  
Jørn Andreassen

SUMMARYMice inoculated with 2000 Ascaris suum eggs 7 days before an infection with 2 cysticercoids of Hymenolepis diminuta harboured significantly fewer and/or smaller tapeworms than control mice by day 7 post-infection. When the interval between the infections was increased, the effect on H. diminuta decreased and no effect was found 21 days after the A. suum infection or if the infections were given simultaneously in ńaive or in mice immune to A. suum. Two possible explanations for the rejection and/or stunting of H. diminuta in mice infected 7 days earlier with A. suum are suggested; either a host reaction in the small intestine stimulated by the returning larvae of A. suum after their hepato–pulmonary migration or an indirect effect of decreased food intake of the host caused by this migration. It is concluded that experiments on possible immunodepressive or immunostimulating effects of parasites ought to include studies on living agents and that they should not rely on measurements of immune responses only.


2020 ◽  
Author(s):  
Wan-Chung Hu

Human host immune responses to parasitic infections are complex. They can be categorized into four immunological pathways against four types of parasitic infections. For intracellular protozoa, the eradicable host immunological pathway is TH1 immunity involving macrophages, interferon gamma (IFNg) CD4 T cells, innate lymphoid cells 1 (ILC1), CD8 T cells, invariant natural killer T cells 1 (iNKT1) cells, and immunoglobulin G3 (IgG3) B cells. For free-living extracellular protozoa, the eradicable host immunological pathway is TH22 immunity involving neutrophils, interleukin (IL)-22/IL-17 CD4 T cells, innate lymphoid cells 3 (ILC3), iNKT17 cells, and IgG2 B cells. For endoparasites (helminths), the eradicable host immunological pathway is TH2a immunity with inflammatory eosinophils (iEOS), IL-5/IL-4 CD4 T cells, IL-25 inducing inflammatory innate lymphoid cells 2 (iILC2), mast cells-tryptase (MCt), iNKT2 cells, and IgG4 B cells. For ectoparasites (parasitic insects and arachnids), the eradicable host immunological pathway is TH2b immunity with inflammatory basophils, mast cells-tryptase/chymase (MCtc), IL-3/IL-4 CD4 T cells, IL-33 inducing nature innate lymphoid cells 2 (nILC2), iNKT2 cells, and immunoglobulin E (IgE) B cells. The tolerable host immunity against ectoparasites and endoparasites is TH9 immunity with regulatory eosinophils, regulatory basophils, IL-9 mast cells (MMC9), thymic stromal lymphopoietin inducing innate lymphoid cells 2, IL-9 CD4 T cells, iNKT2 cells, and IgA2 B cells. This categorization provides a complete framework of immunological pathways against four types of parasitic infections.


2019 ◽  
Vol 18 (4) ◽  
pp. 67-75
Author(s):  
V. H. Hryn ◽  
Yu. P. Kostylenko

Over the past two decades, there have been many publications dealing with the further development of an urgent issue on the immune system of the mucous membranes of the digestive tract, called mucoseassociated lymphoid tissue (MALT), which includes spheres of innate (non-specific) and adaptive (specific) immunity. Most structured formations and indicators of adaptive immunity in the intestinal mucosa are lymphoepithelial formation (Peyer's patches). The data on the formation of the peripheral part of the immune system are carried through the epithelium, mechanisms of interaction between pathogenic intestinal microflora and immunocompetent cells, thereby initiating the development of immune responses in the mucous membranes. A concept has long been established in the literature, according to which a leading role in mediating these reactions belongs to a special type of enterocytes, called M-cells. Before the concept of the initial role of these cells in the development of immune responses in the mucous membranes of the intestinal tract they were known as caveolated cells. The purpose of this study was to determine the shape and topological relations of M-cells with other types of enterocytes, and also with lymphoid elements Peyer's patches of the small intestine. 30 mature albino male rats weighted 200,0±20,0 g were involved into the study. After vivisection, which was carried out by an overdose of thiopental anesthesia (75 mg / kg of animal body weight intramuscularly in the upper third of the thigh of the hind paw) [1] in compliance with the requirements for dissection of the abdominal cavity, the entire complex of the gastrointestinal tract was removed, which was preserved in 10 % formalin solution. Subsequently, short sections of the small intestine, containing Peyer’s patches, were selectively excised. Finding the latter was not difficult due to their clear visualization on the external (nonmesenteric) surface of the small intestine in the form of whitish spots. The specimens, after washing from formalin and dehydration in alcohol of increasing concentration, were embedded into paraffin blocks, from which serial sections of 4 µm thick (Microm HM 325) were obtained with subsequent staining with hematoxylin-eosin and Van Gieson. Their study and documentation was carried out using the “Konus” light microscope equipped with the Sigeta DCM-900 9.0MP digital microphoto attachment and the Biorex 3 program (serial number 5604) adapted for these studies. In the study of many series of paraffin sections stained with hematoxylin-eosin, it was found that while maintaining the general shape of the structure, lymphoid nodules are susceptible to plastic variability, which depends on situationally changing factors of antigenic effect, i.e., functional polymorphism is characteristic of them. This is especially true of their lymphoidassociated epithelium, which appears in a rather diverse form, which depends not only on the section angle, but also, probably, on its reactive state. Thus, in some cases it is a relatively even monolayer of intestinal epithelium, consisting mainly of absorbing enterocytes, among which the most distinct are goblet cells. At the same time, it draws attention to itself that in the apical sections of some of them there are clear signs of rupture of the plasmolemma and the presence in the cytoplasm of basophilic granular fibrous material of an unknown nature. Along with this picture, other histological sections of large lymphoid nodules of Peyer's patches of the small intestine demonstrate a different configurational character of lymphoid-associated epithelium, in which the cluster principle of cell distribution in the form of limited portioned sets is clearly noted. While maintaining the general structural shape, Peyer's patches were found to be subjected to plastic variability, which depends on situationally changing factors of antigenic exposure, i.e., functional polymorphism is characteristic of them. This is especially true of their lymphoid-associated epithelium. Identification of M-cells using only traditional histological methods in practice is complicated. And yet, in the process of a focused study of serial paraffin sections, it was possible to detect some morphological signs indicating their location.


mSphere ◽  
2019 ◽  
Vol 4 (6) ◽  
Author(s):  
Ana A. Weil ◽  
Rachel L. Becker ◽  
Jason B. Harris

ABSTRACT Vibrio cholerae is a noninvasive pathogen that colonizes the small intestine and produces cholera toxin, causing severe secretory diarrhea. Cholera results in long lasting immunity, and recent studies have improved our understanding of the antigenic repertoire of V. cholerae. Interactions between the host, V. cholerae, and the intestinal microbiome are now recognized as factors which impact susceptibility to cholera and the ability to mount a successful immune response to vaccination. Here, we review recent data and corresponding models to describe immune responses to V. cholerae infection and explain how the host microbiome may impact the pathogenesis of V. cholerae. In the ongoing battle against cholera, the intestinal microbiome represents a frontier for new approaches to intervention and prevention.


2007 ◽  
Vol 82 (4) ◽  
pp. 1777-1786 ◽  
Author(s):  
M. Souza ◽  
M. S. P. Azevedo ◽  
K. Jung ◽  
S. Cheetham ◽  
L. J. Saif

ABSTRACT We previously characterized the pathogenesis of two host-specific bovine enteric caliciviruses (BEC), the GIII.2 norovirus (NoV) strain CV186-OH and the phylogenetically unassigned NB strain, in gnotobiotic (Gn) calves. In this study we evaluated the Gn calf as an alternative animal model to study the pathogenesis and host immune responses to the human norovirus (HuNoV) strain GII.4-HS66. The HuNoV HS66 strain caused diarrhea (five/five calves) and intestinal lesions (one/two calves tested) in the proximal small intestine (duodenum and jejunum) of Gn calves, with lesions similar to, but less severe than, those described for the Newbury agent 2 (NA-2) and NB BEC. Viral capsid antigen was also detected in the jejunum of the proximal small intestine of one of two calves tested by immunohistochemistry. All inoculated calves shed virus in feces (five/five calves), and one/five had viremia. Antibodies and cytokine (proinflammatory, tumor necrosis factor alpha [TNF-α]; Th1, interleukin-12 [IL-12] and gamma interferon [IFN-γ]; Th2, IL-4; Th2/T-regulatory, IL-10) profiles were determined in serum, feces, and intestinal contents (IC) of the HuNoV-HS66-inoculated calves (n = 5) and controls (n = 4) by enzyme-linked immunosorbent assay in the acute (postinoculation day 3 [PID 3]) and convalescent (PID 28) stages of infection. The HuNoV-HS66-specific antibody and cytokine-secreting cells (CSCs) were quantitated by ELISPOT in mononuclear cells of local and systemic tissues at PID 28. Sixty-seven percent of the HuNoV-HS66-inoculated calves seroconverted, and 100% coproconverted with immunoglobulin A (IgA) and/or IgG antibodies to HuNoV-HS66, at low titers. The highest numbers of antibody-secreting cells (ASC), both IgA and IgG, were detected locally in intestine, but systemic IgA and IgG ASC responses also occurred in the HuNoV-HS66-inoculated calves. In serum, HuNoV-HS66 induced higher peaks of TNF-α and IFN-γ at PIDs 2, 7, and 10; of IL-4 and IL-10 at PID 4; and of IL-12 at PIDs 7 and 10, compared to controls. In feces, cytokines increased earlier (PID 1) than in serum and TNF-α and IL-10 were elevated acutely in the IC of the HS66-inoculated calves. Compared to controls, at PID 28 higher numbers of IFN-γ and TNF-α CSCs were detected in mesenteric lymph nodes (MLN) or spleen and Th2 (IL-4) CSCs were elevated in intestine; IL-10 CSCs were highest in spleen. Our study provides new data confirming HuNoV-HS66 replication and enteropathogenicity in Gn calves and reveals important and comprehensive aspects of the host's local (intestine and MLN) and systemic (spleen and blood) immune responses to HuNoV-HS66.


2002 ◽  
Vol 48 (3) ◽  
pp. 282-287 ◽  
Author(s):  
Norie Arai ◽  
Chiyo Yoshizane ◽  
Chikako Arai ◽  
Toshiharu Hanaya ◽  
Shigeyuki Arai ◽  
...  

2006 ◽  
Vol 80 (4) ◽  
pp. 397-407 ◽  
Author(s):  
L.M.M. Alkazmi ◽  
M.S. Dehlawi ◽  
J.M. Behnke

AbstractHookworms are known to cause marked changes to the intestinal mucosa, especially in relation to erosion of the villi. However, since the development of enteropathy has not been examined thoroughly through quantitative experiments on infected animals, the results of experiments conducted in hamsters infected with Ancylostoma ceylanicum are reported. Changes to intestinal architecture were first apparent between 12 and 14 days after infection, and then increased in intensity for 3–4 weeks, persisting for as long as worms were present (>63 days). Following infection, the height of villi declined from a mean of 1002 μm in naïve controls to less than 200 μm and as low as 18 μm in one case. The depth of the crypts of Lieberkuhn increased from a baseline value of 166 μm in naïve controls to in excess of 600 μm within 6 weeks of infection. Mitotic figures had a baseline value of 5.5 per villus-crypt unit, and this rose to in excess of 25 in some experiments. Changes were dependent on the intensity of the parasite burden on day 20, but by 30 days after infection changes in all three values were maximal and density-dependent relationships were no longer clearly apparent. Villus height and crypt depth returned to near normal values within a week of the removal of worms, although group means for both remained different from naïve controls for at least 3 weeks after treatment. Cellular division, as reflected in numbers of mitotic figures, stayed elevated for over 5 weeks after removal of worms. The results suggest that enteropathy in hookworm infections stems from a combination of intestinal immune responses and from the grazing activities of the adult worms on the mucosal surface, but is not sufficient per se for expulsion of this parasite.


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