Structural changes in the jejunal mucosa of mice infected with Schistosoma mansoni, fed low or high protein diets

Couto, Janira Lúcia Assumpção; Ferreira, Haroldo da Silva; Rocha, Dinalva Bezerra da; Duarte, Maria Eugênia Leite; Assunção, Monica Lopes de; Coutinho, Eridan de Medeiros

doi:10.1590/s0037-86822002000600010

Cited by 9 publications

(6 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Concurrent infection with S. mansoni significantly altered the aforementioned anatomical sites mainly during chronic infection, irrespective of diet and the intestinal segment. Our results suggest that morphological alterations begin by week 9 and are aggravated by week 17, consistent with other studies of intestinal pathology (Borgers et al 2000;Couto et al 2002;Siqueira et al 2010). In this study, the damage to the intestinal tissue could be the result of inflammation (Trobojević-Stanković et al 2010) due to the higher number of eggs trapped in the intestine in mice fed a high-fat diet (Neves et al 2007, Alencar et al 2009.…”

Section: Discussionsupporting

confidence: 91%

Changes in the small intestine ofSchistosoma mansoni-infected mice fed a high-fat diet

et al. 2012

View full text Add to dashboard Cite

The consumption of a high-fat diet modifies both the morphology of the small intestine and experimentally tested effects of schistosomiasis mansoni. However, whether a schistosomiasis infection associated with a high-fat diet causes injury to the small intestine has never been investigated. Mice were fed either a high-fat or a standard-fat diet for 6 months and were then infected with Schistosoma mansoni cercariae. Physical characteristics of the intestinal tissue (mucosal thickness, small intestinal villi length and height, and abundance of goblet cells and enterocytes on the villous surface) and the distribution of granulomas along the intestinal segments and their developmental stage were measured at the time of sacrifice (9 or 17 weeks post-infection). The group fed a high-fat diet exhibited different granuloma stages, whereas the control group possessed only exudative granulomas. The chronically infected mice fed a high-fat diet exhibited higher granuloma and egg numbers than the acutely infected group. Exudative, exudative/exudative-productive and exudative-productive granulomas were present irrespective of diet. Computer-aided morphometric analysis confirmed that villus length, villus width, muscular height and submucosal height of the duodenal and jejunal segments were affected by diet and infection. In conclusion, a high-fat diet and infection had a significant impact on the small intestine morphology and morphometry among the animals tested.

show abstract

Section: Discussionsupporting

confidence: 91%

Changes in the small intestine ofSchistosoma mansoni-infected mice fed a high-fat diet

et al. 2012

View full text Add to dashboard Cite

show abstract

“…Differentiated Paneth cells migrate to the crypt base and they occupy this position for about three weeks before they are replaced. Allocation of cells into these four lineages is known to change in response to disease states, environmental or surgical insult, or position along the small intestine (Dvorak & Dickersin 1980, Ehrmann et al 1990, Kamal et al 2001, Couto et al 2002, Porter et al 2002, Wasserberg et al 2003, Wong, et al 2004). However, the complex set of cues that control this process are unknown.…”

Section: Introductionmentioning

confidence: 99%

Epithelial lineages of the small intestine have unique patterns of GATA expression

Dusing

Wiginton

2005

J Mol Hist

View full text Add to dashboard Cite

The ability of the GATA family of factors to interact with numerous other factors, co-factors, and repressors suggests that they may play key roles in tissues and cells where they are expressed. Adult mouse small intestine has been shown to express GATA-4, GATA-5, and GATA-6, where they have been implicated in the activation of a number of intestinal genes. Determination of which GATA factor(s) are involved in a specific function in tissues expressing multiple family members has proven difficult. The immunohistochemical analysis presented here demonstrate that within the mouse small intestine GATA-4/-5/-6 are found to be uniquely distributed among the various differentiated lineages of the intestinal epithelium. Among differentiated cells GATA-4 is found only in the villous enterocytes. GATA-5 is absent from enterocytes, but was found in the remaining lineages: goblet, Paneth and enteroendocrine. Additionally, high levels of GATA-6 are found in only one of these differentiated cell types, the enteroendocrine lineage. The observed distribution suggests that the GATA factors may have distinct roles in lineage allocation, lineage maintenance, and/or terminal differentiation events in small intestine.

show abstract

“…Schistosoma-infected mice exhibit morphological changes in the jejunal villi. [32] Leaf-shaped and flattened villi are abundant in The transitional zone between different types of epithelium is well-known as the site of precancerous conditions, such as the cornea-conjunctiva, [2] esophagogastric, [1] anorectal, [33] and endoectocervix junctions. [3] Among them, the tissue area from the esophageal squamous epithelium to simple columnar cells in the stomach is called Barrett's esophagus, [34] which is the the primary site esophageal adenocarcinoma.…”

Section: Discussionmentioning

confidence: 99%

Tumor formation at ileocecal junction associated with interleukin‐1β upregulation in aryl hydrocarbon receptor‐deficient mouse

Ikuta,

Kanda

2024

J Biochem & Molecular Tox

View full text Add to dashboard Cite

Aryl hydrocarbon receptor (AhR) is a ligand‐dependent transcription factor. We previously reported spontaneous ileocecal tumorigenesis in AhR‐deficient mice after the age of 10 weeks, which originated in the confined area between ileum and cecum. This study aimed to investigate the underlying mechanism that causes tumor development at this particular location. To observe mucosal architecture in detail, tissues of ileocecal region were stained with methylene blue. Gene expression profile in the ileocecal tissue was compared with cecum. Immunohistochemical analysis was performed with ileocecal tissues using antibodies against ileum‐specific Reg3β or cecum‐specific Pitx2. In AhR+/+ mice and AhR+/− mice, that do not develop lesions, methylene blue staining revealed the gradually changing shape and arrangement of villi from ileum to cecum. It was also observed in AhR‐deficient mice before developing lesions. Microarray‐based analysis revealed abundant antimicrobial genes, such as Reg3, in the ileocecal tissue while FGFR2 and Pitx2 were specific to cecum. Immunohistochemical analysis of AhR‐deficient mice indicated that lesions originated from the ileocecal junction, a boundary area between different epithelial types. Site‐specific gene expression analysis revealed higher expression of IL‐1β at the ileocecal junction compared with the ileum or cecum of 9–11‐week‐old AhR‐deficient mice. These findings indicate that AhR plays a vital function in the ileocecal junction. Regulating AhR activity can potentially manage the stability of ileocecal tissue possessing cancer‐prone characteristics. This investigation contributes to understanding homeostasis in different epithelial transitional tissues, frequently associated with pathological states.

show abstract

Structural changes in the jejunal mucosa of mice infected with Schistosoma mansoni, fed low or high protein diets

Cited by 9 publications

References 16 publications

Changes in the small intestine ofSchistosoma mansoni-infected mice fed a high-fat diet

Changes in the small intestine ofSchistosoma mansoni-infected mice fed a high-fat diet

Epithelial lineages of the small intestine have unique patterns of GATA expression

Tumor formation at ileocecal junction associated with interleukin‐1β upregulation in aryl hydrocarbon receptor‐deficient mouse

Contact Info

Product

Resources

About