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Monterde, Gonzalo; Rodríguez-Fabián, Guillermo; Vara, Elena; López, Laudino; Árias, Jorge L.; Aller, María-Ángeles; Árias, Jaime

doi:10.1023/a:1005588918516

Cited by 35 publications

(5 citation statements)

References 28 publications

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“…It is well known that PRL and GCs are stress hormones, which systemic levels are increased during adverse stimuli [24], [25]. Under these conditions, increased PRL could protect the host from an exacerbated immunosuppressive response mediated by GCs.…”

Section: Discussionmentioning

confidence: 99%

Trypanosoma cruzi Disrupts Thymic Homeostasis by Altering Intrathymic and Systemic Stress-Related Endocrine Circuitries

et al. 2013

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We have previously shown that experimental infection caused by Trypanosoma cruzi is associated with changes in the hypothalamus-pituitary-adrenal axis. Increased glucocorticoid (GC) levels are believed to be protective against the effects of acute stress during infection but result in depletion of CD4+CD8+ thymocytes by apoptosis, driving to thymic atrophy. However, very few data are available concerning prolactin (PRL), another stress-related hormone, which seems to be decreased during T. cruzi infection. Considering the immunomodulatory role of PRL upon the effects caused by GC, we investigated if intrathymic cross-talk between GC and PRL receptors (GR and PRLR, respectively) might influence T. cruzi-induced thymic atrophy. Using an acute experimental model, we observed changes in GR/PRLR cross-activation related with the survival of CD4+CD8+ thymocytes during infection. These alterations were closely related with systemic changes, characterized by a stress hormone imbalance, with progressive GC augmentation simultaneously to PRL reduction. The intrathymic hormone circuitry exhibited an inverse modulation that seemed to counteract the GC-related systemic deleterious effects. During infection, adrenalectomy protected the thymus from the increase in apoptosis ratio without changing PRL levels, whereas an additional inhibition of circulating PRL accelerated the thymic atrophy and led to an increase in corticosterone systemic levels. These results demonstrate that the PRL impairment during infection is not caused by the increase of corticosterone levels, but the opposite seems to occur. Accordingly, metoclopramide (MET)-induced enhancement of PRL secretion protected thymic atrophy in acutely infected animals as well as the abnormal export of immature and potentially autoreactive CD4+CD8+ thymocytes to the periphery. In conclusion, our findings clearly show that Trypanosoma cruzi subverts mouse thymus homeostasis by altering intrathymic and systemic stress-related endocrine circuitries with major consequences upon the normal process of intrathymic T cell development.

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Section: Discussionmentioning

confidence: 99%

Trypanosoma cruzi Disrupts Thymic Homeostasis by Altering Intrathymic and Systemic Stress-Related Endocrine Circuitries

et al. 2013

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“…Therefore, the excess number of mast cells in the duodenal mucosa of rats with portal hypertension could be related with their capacity to release the stored TNF-α rapidly and in abundant quantity when the appropriate stimulus is provided, that is, bacterial translocation. This fact could explain the high plasma concentration of this cytokine in this experimental model of prehepatic portal hypertension [27]. …”

Section: Discussionmentioning

confidence: 99%

Increased Duodenal Mucosa Infiltration by Mast Cells in Rats with Portal Hypertension

Diez-Arias¹,

Aller

Palma

et al. 2001

Dig Surg

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Background: Enteropathy characterized by vascular and inflammatory alterations in the submucosa and mucosa has been described in patients with portal hypertension. Aims: To verify the theory of inflammatory etiopathogenesis in experimental portal hypertensive duodenopathy, a prehepatic portal hypertension model based on the development of a single and triple partial ligation of the portal vein was used in the rat. Methods: Five rats in each group (male Wistar, 230–255 g) were subjected to single (group II) or triple (group III) partial ligation of the portal vein and then compared to 5 control animals (group I, no operation). The animals were sacrificed 6 weeks later to analyze the histological parameters of the duodenal mucosa and submucosa, i.e., number, diameter and area of submucosal vessels, density of mast cells and mitotic cells. Body, liver and spleen weights and collateral circulation type were also assayed. Results: As was demonstrated by the collateral circulation in all of the animals, the partial portal ligation was successful. Compared to the controls, the number of vessels per microscopic field (25 ± 3.16 vs. 18.60 ± 1.52), their diameter (20.09 ± 2.90 vs. 12.61 ± 3.97 µm, p < 0.05) and consequently their total area (12,749.30 ± 2,298.26 vs. 3,455.82 ± 1,702.33 µm²) were increased in the animals with a single partial ligation (group II) as well as in animals receiving triple partial ligation (group III) (33 ± 12.88, p < 0.05; 22.92 ± 6.72 µm, p < 0.05 and 51,376.95 ± 43,732.24 µm², p < 0.05, respectively). In addition, the density of mast cells increased from 3.26 ± 1.18 in controls to 10.74 ± 1.47, p < 0.01 and 22.50 ± 6.42, p < 0.01 in single and triple partial portal ligated animals, respectively. Mitosis was significantly induced in crypts of the duodenal mucosa of the single portal ligated animals (25.20 ± 1.78 vs. 17.40 ± 1.14, p < 0.01) but was inhibited in triple partial ligated animals (12.40 ± 5.12, p < 0.05). Compared to controls, both groups of rats developed liver atrophy with a greater decrease in the liver/body weight ratio in the single (2.71 ± 0.50%, p < 0.01) compared to the triple partial ligated animals (3.33 ± 0.09%, p < 0.01). Conclusions: The correlation of the degree of portal hypertension with the vascular changes and mast cell density suggests that both the hypertensive state and inflammation may play a role in the development of portal hypertensive intestinal vasculopathy. The inverse relation of portal hypertension with liver atrophy and mitosis rate in the crypts of the duodenal mucosa has not been clarified and should be investigated in future studies.

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“…We performed three equidistant portal ligatures of the portal vein (TPVL) [10] in order to increase the length of the stenosed portal tract and thus increase the initial resistance to the blood flow since, according to the Poiseuille equation (R = 8Ll/Pr 4 ) [13], resistance (R) to the flow of a vessel depends on the length (L), on the radium (r) and on the viscosity coefficient of the blood (P).…”

Section: Discussionmentioning

confidence: 99%

“…The surgical intervention used to produce prehepatic portal hypertension by TPVL has been described previously [10]. In brief, the portal vein was isolated and three partial ligations were performed in its superior, middle and inferior portions.…”

Section: Sham Operation (So) and Triple Partial Portal Vein Ligation mentioning

confidence: 99%

“…If so, those factors that act by increasing the initial resistance to the blood portal flow could aggravate the evolution of this prehepatic portal hypertension experimental model and, consequently, the incidence of BT to the MLN at later stages. To verify this hypothesis, the initial resistance to blood portal flow was increased by increasing the length of the stenosed portal tract with three equidistant partial ligatures [10].…”

Section: Introductionmentioning

confidence: 99%

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Bacterial Translocation to Mesenteric Lymph Nodes Increases in Chronic Portal Hypertensive Rats

et al. 2009

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Untitled

Cited by 35 publications

References 28 publications

Trypanosoma cruzi Disrupts Thymic Homeostasis by Altering Intrathymic and Systemic Stress-Related Endocrine Circuitries

Trypanosoma cruzi Disrupts Thymic Homeostasis by Altering Intrathymic and Systemic Stress-Related Endocrine Circuitries

Increased Duodenal Mucosa Infiltration by Mast Cells in Rats with Portal Hypertension

Bacterial Translocation to Mesenteric Lymph Nodes Increases in Chronic Portal Hypertensive Rats

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