Invasion of chicken caecal and intestinal lamina propria by crypt epithelial cells infected with coccidia

Ma, Fernando; Am, Lawn; Rose, Marie E.; Ma, Al-Attar

doi:10.1017/s0031182000050587

Cited by 20 publications

(20 citation statements)

References 19 publications

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“…This ®nding demonstrated an epithelial origin for the infected cells, since keratin IF have been shown to characterize epithelial cells (Steinert and Roop 1988). In addition, it further reinforces previous reports, which state that after ®rst-generation merozoites reenter the crypt epithelial cells, the parasitized cells move from the crypt epithelium into the connective tissue between the crypts (Fernando et al 1983). …”

Section: Discussionsupporting

confidence: 88%

“…Therefore, the ®nding of cells harboring trophozoites and immature schizonts devoid of immunostaining for keratin may re¯ect a reorganization of the cytoskeleton, indicating that these cells are migrating cells, which consequently lack desmosomes. Thereafter, desmosomes reappear as described by Bergmann (1970) and Fernando et al (1983), who found desmosomes connecting cells together in the lamina propria harboring mature schizonts. It seems reasonable to assume that the appearance of desmosomes indicates that the migration of parasitized cells is over.…”

Section: Discussionmentioning

confidence: 58%

“…This makes it dicult to identify clearly the cell type in which the development of this stage takes place. Previous reports have proposed results indicative of either an epithelial (Fernando et al 1983) or a mesenchymal (Bergmann 1970;Lee and Long 1972) origin for these cells. In the current research the identity of the cells was con®rmed by the immunodetection of keratin in the host cells within the lamina propria infected with mature schizonts.…”

Section: Discussionmentioning

confidence: 90%

“…More recently, on the basis of electron microscope studies, Fernando et al (1983) have reported the epithelial origin of the cells harboring schizonts in the lamina propria as evidenced by the observation of interconnection by desmosomes and tight junctions between these parasitized cells.…”

Section: Introductionmentioning

confidence: 99%

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Immunohistochemical identification of the cells parasitized by second-generation schizonts of Eimeria tenella

López-Bernad

Cacho²,

Gallego³

et al. 1997

Parasitology Research

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Conflicting reports exist in the literature concerning the type of cells within the lamina propria of the ceca that harbor second-generation schizonts of Eimeria tenella. Most of the previous studies concerning these cells have been performed using routine light or electron microscopy. Consequently, difficulties are evident in precise definition of the type of these cells using normal morphological criteria, since growth of the schizonts of E. tenella alters the morphology of the parasitized cell, making it difficult to recognize the cell type. This has led us to investigate the possibility of precisely identifying the subepithelial cells that are parasitized by mature schizonts. For this purpose we used cytoskeletal markers, namely, keratin and vimentin intermediate filaments, which allow the discrimination between epithelial and mesenchymal cells. Localization of keratin and vimentin on frozen cecal sections was studied immunohistochemically using specific monoclonal antibodies. Sites of antigenicity were detected by the avidin-biotin complex (ABC) immunoperoxidase technique and visualized by the deposition of diaminobenzidine. The identity of the cells was confirmed by the immunodetection of keratin intermediate filaments in the cytoplasm of the cells. Immunoreactivity for vimentin was absent in the parasitized cells. Therefore, we conclude that the development of second-generation schizonts of E. tenella takes place in epithelial cells within the lamina propria, which are presumably crypt epithelial cells that leave the crypts and enter the lamina propria after infection by first-generation merozoites.

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 58%

Section: Discussionmentioning

confidence: 90%

Section: Introductionmentioning

confidence: 99%

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Immunohistochemical identification of the cells parasitized by second-generation schizonts of Eimeria tenella

López-Bernad

Cacho²,

Gallego³

et al. 1997

Parasitology Research

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“…This situation occurs in the chick caecum after infection with Salmonella species, where passage of bacteria from the epithelium to the lamina propria occurs within macrophages (Popiel and Turnbull, 1985). Enterocytes infected with coccidia are also known to penetrate the basement membrane into the lamina propria (Fernando et al, 1983). However, almost nothing is known about the method by which enteroviruses initiate infection in vivo (Heinz and Cliver, 1988).…”

Section: Figs í6 á I 7 F/ew Case From Flock F Showing Enterocytes (mentioning

confidence: 99%

Infectious stunting syndrome of chickens in Great Britain: Intestinal ultrastructural pathology

Frazier

Reece²

1990

Avian Pathology

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SUMMARYThe ultrastructural pathology of the intestine of field and experimental cases of 4-to 6-day-old chickens showing early signs of stunting syndrome was studied. Changes were most frequently observed in the lamina propria, with infiltrations of lymphoid cells, mesenchymal cells and macrophages. Cysts were observed in the crypts. Early, small cysts were lined with both epithelial cells and myofibroblasts, with no underlying basment membrane. Larger cysts were composed of cuboidal epithelial cells surrounded by a basement membrane with underlying fibroblasts and collagen fibrils.Membrane-bound cytoplasmic inclusions containing picornavirus-like particles about 20 nm in diameter were present in mesenchymal cells and macrophages in the lamina propria, both at the base of the villi and in the corium of the villus. Cells containing particles were associated with early cysts, but not with large, mature cysts. Particles were occasionally observed in enterocytes, particularly in field cases.A brief description of the normal chick intestinal lamina propria is also included.

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From celiac disease to coccidia infection and vice‐versa: The polyQ peptide CXCR3‐interaction axis

et al. 2021

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Zonulin is a physiological modulator of intercellular tight junctions, which upregulation is involved in several diseases like celiac disease (CeD). The polyQ gliadin fragment binds to the CXCR3 chemokine receptor that activates zonulin upregulation, leading to increased intestinal permeability in humans. Here, we report a general hypothesis based on the structural connection between the polyQ sequence of the immunogenic CeD protein, gliadin, and enteric coccidian parasites proteins. Firstly, a novel interaction pathway between the parasites and the host is described based on the structural similarities between polyQ gliadin fragments and the parasite proteins. Secondly, a potential connection between coccidial infections as a novel environmental trigger of CeD is hypothesized. Therefore, this report represents a promising breakthrough for coccidian research and points out the potential role of coccidian parasites as a novel trigger of CeD that might define a preventive strategy for gluten-related disorders in general. Also see the video abstract here: https://youtu.be/oMaQasStcFI

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Invasion of chicken caecal and intestinal lamina propria by crypt epithelial cells infected with coccidia

Cited by 20 publications

References 19 publications

Immunohistochemical identification of the cells parasitized by second-generation schizonts of Eimeria tenella

Immunohistochemical identification of the cells parasitized by second-generation schizonts of Eimeria tenella

Infectious stunting syndrome of chickens in Great Britain: Intestinal ultrastructural pathology

From celiac disease to coccidia infection and vice‐versa: The polyQ peptide CXCR3‐interaction axis

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