Analysis of intestinal intraepithelial lymphocyte populations in experimental Trichinella spiralis infection of mice

Božić, Frane; Tran, Albert; E, Duraković

doi:10.14411/fp.2000.010

Cited by 15 publications

(9 citation statements)

References 18 publications

(13 reference statements)

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“…Previous studies on nematode infection in mammals showed that T cells are attracted locally to the site of infection (Almeria et al, 1997;Bozic et al, 2000;Balic et al, 2002;Perez et al, 2008). It was suggested that T lymphocytes, especially CD4 ' cells, may play a significant role in resistance to worm infection (Betts et al, 2000;Khan & Collins, 2004;Little et al, 2005;Rausch et al, 2008;Patel et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

Pathobiology ofHeterakis gallinarummono-infection and co-infection withHistomonas meleagridisin layer chickens

et al. 2011

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Little is known about the induction and modulation of gut-associated immune reactions after nematode infection in the chicken. The objective of the present study was to compare the pathogenesis, induction of immune reactions and electrophysiological changes of the gut after mono-infection with Heterakis gallinarum and after dual infection with H. gallinarum and Histomonas meleagridis in layer chickens. In two experiments 3-week-old chickens were inoculated with embryonated H. gallinarum eggs, which were positive for H. meleagridis. While birds of the first experiment were left untreated, those of the second experiment were treated with dimetridazol to prevent H. meleagridis co-infection. Mild to moderate histological lesions and local immune reactions with a significant increase in CD4(+), CD8α(+), TCRαβ(+) and TCRδγ(+) cells in the lamina propria and induction of the T-helper type 2 (Th2) cytokine interleukin-13 dominated the H. gallinarum immune response at 2 weeks post infection. Co-infection with H. gallinarum and H. meleagridis induced an increase in mRNA expression of the T-helper type 1 (Th1) cytokine interferon-γ, a decrease in splenic CD4(+) cells and severe destruction of the caecal mucosa in association with strong T-cell infiltration in the caecal lamina propria. There was no obvious effect on the chloride secretion of the caecal epithelium, which was investigated once the mucosa had almost recovered from the infection, in either experiment. These results suggest that the local T-cell reactions to nematode infections in chickens may be comparable with mammals and may be shifted from a Th2-dominated to a Th1-dominated response when accompanied by a protozoan infection.

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Section: Discussionmentioning

confidence: 99%

Pathobiology ofHeterakis gallinarummono-infection and co-infection withHistomonas meleagridisin layer chickens

et al. 2011

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“…Work with T. gondii (13,14), L. major (21) and T. cruzi (22) all demonstrate that CD8 + T cells are a significant source of the type 1 cytokine IFN‐γ, vital for resolution of these diseases. Other studies with T. spiralis (17), E. tenella (18) and C. parvum (19) have shown a correlation between expansion of the CD8 + T cell pool within the gut and resistance to infection. Together these studies and our data signify a role for these cells in Th1 polarized immune responses, especially at this mucosal site, and this function is independent of whether the response is protective or leads to chronic infection.…”

Section: Discussionmentioning

confidence: 94%

“…Experiments with a diverse range of disease models, such as Toxoplasma gondii (13,14), Encephalitozoon cuniculi (15) and lymphocytic choriomeningitis virus (16), have demonstrated a critical role for gut CD8 + IEL T cells, acting as a barrier against pathogen replication and producing the key cytokines that orchestrate disease resolution. Further data from experiments with Trichinella spiralis (17), Eimeria tenella (18) and Cryptosporidium parvum (19) have established a strong correlation between onset of disease resolution and a large expansion of CD8 + IEL T cells. Thus IELs and especially CD8 + IELs sitting at the luminal/epithelial interface are in a unique position to influence and regulate immune responses to gut‐dwelling pathogens.…”

Section: Introductionmentioning

confidence: 99%

The role of CD8⁺ cells in the establishment and maintenance of a Trichuris muris infection

Humphreys

Worthington

Little

et al. 2004

Parasite Immunology

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Chronic infection by the caecal-dwelling intestinal murine nematode Trichuris muris occurs if given as a high-dose infection to 'susceptible' AKR mice or as a low-dose infection to the normally 'resistant' C57BL/6 mouse strain. Both regimes result in a type 1 cytokine response, i.e. high levels of IFN-gamma and IL-12. Here we show this susceptible response is associated with a large population of CD8(+) IFN-gamma(+) cells within the mesenteric lymph nodes and numerous CD8(+) cells infiltrating the caecal mucosa. Despite this, the in vivo abolition of CD8(+) cells within AKR and C57BL/6 mice, either prior to infection or once infection has become established, failed to affect chronicity, implying that CD8(+) T cells are not essential for the initiation or maintenance of the susceptible response to T. muris. Interestingly, the percentage of IFN-gamma(+) CD4(+) cells increased in treated groups, perhaps in a compensatory role. The majority of antigen-specific cytokine responses were comparable in both treated and control groups, although IL-5 was fivefold higher in animals receiving anti-CD8 mAbs and IFN-gamma was also raised in treated mice. Mastocytosis was unaltered by CD8 depletion, however, paradoxically, eosinophilia within the caecum was reduced in treated mice. Together these data clearly demonstrate that CD8(+) T cells are associated with chronic T. muris infection; however, these cells are dispensable for both the early and late phases of this response, but do appear to play a role in the regulation of certain cytokines and caecal eosinophilia.

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“…In helminth infections, TCRγδ + cells are associated, through the secretion of IL-4, IL-5 and IL-13, with the development of a Th2 response [38]. In trichinellosis, TCRγδ + cells would be involved in the stimulation of goblet cells at the intestinal level, since they increase from 4 dpi in the gut epithelia [39]. Considering that TCRγδ + cells also promote epithelial repair [38], it can be postulated that in our model, the role of these cells would be to act as a source of cytokines at the beginning of the infection (coincident with the increase in IL-4 levels, Fig.…”

Section: Discussionmentioning

confidence: 99%

Cellular and molecular changes and immune response in the intestinal mucosa during Trichinella spiralis early infection in rats

et al. 2020

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Background: The main targets of the host’s immune system in Trichinella spiralis infection are the adult worms (AW), at the gut level, and the migrant or newborn larvae (NBL), at systemic and pulmonary levels. Most of the studies carried out in the gut mucosa have been performed on the Payer’s patches and/or the mesenteric lymph nodes but not on the lamina propria, therefore, knowledge on the gut immune response against T. spiralis remains incomplete. Methods This study aimed at characterizing the early mucosal immune response against T. spiralis, particularly, the events taking place between 1 and 13 dpi. For this purpose, Wistar rats were orally infected with muscle larvae of T. spiralis and the humoral and cellular parameters of the gut immunity were analysed, including the evaluation of the ADCC mechanism exerted by lamina propria cells. Results A marked inflammation and structural alteration of the mucosa was found. The changes involved an increase in goblet cells, eosinophils and mast cells, and B and T lymphocytes, initially displaying a Th1 profile, characterised by the secretion of IFN-γ and IL-12, followed by a polarization towards a Th2 profile, with a marked increase in IgE, IgG1, IL-4, IL-5 and IL-13 levels, which occurred once the infection was established. In addition, the helminthotoxic activity of lamina propria cells demonstrated the role of the intestine as a place of migrant larvae destruction, indicating that not all the NBLs released in the gut will be able to reach the muscles. Conclusions The characterization of the immune response triggered in the gut mucosa during T. spiralis infection showed that not only an effector mechanism is directed toward the AW but also towards the NBL as a cytotoxic activity was observed against NBL exerted by lamina propria cells.

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Analysis of intestinal intraepithelial lymphocyte populations in experimental Trichinella spiralis infection of mice

Cited by 15 publications

References 18 publications

Pathobiology ofHeterakis gallinarummono-infection and co-infection withHistomonas meleagridisin layer chickens

Pathobiology ofHeterakis gallinarummono-infection and co-infection withHistomonas meleagridisin layer chickens

The role of CD8⁺ cells in the establishment and maintenance of a Trichuris muris infection

Cellular and molecular changes and immune response in the intestinal mucosa during Trichinella spiralis early infection in rats

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Analysis of intestinal intraepithelial lymphocyte populations in experimental Trichinella spiralis infection of mice

Cited by 15 publications

References 18 publications

Pathobiology ofHeterakis gallinarummono-infection and co-infection withHistomonas meleagridisin layer chickens

Pathobiology ofHeterakis gallinarummono-infection and co-infection withHistomonas meleagridisin layer chickens

The role of CD8+ cells in the establishment and maintenance of a Trichuris muris infection

Cellular and molecular changes and immune response in the intestinal mucosa during Trichinella spiralis early infection in rats

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The role of CD8⁺ cells in the establishment and maintenance of a Trichuris muris infection