Morphological and proinflammatory expression of the experimental autoimmune prostatitis in the rat model / 中华男科学杂志

<p><b>OBJECTIVE</b>To establish a Wistar rat model of chronic abacterial prostatitis (CAP) by injecting purified prostate protein and Freund's complete adjuvant, and to study the influence on the morphology and proinflammatory expression.</p><p><b>METHODS</b>Male rats were injected with the Pertussis-Diphteria-Tetanus vaccine into the abdominal cavity and purified prostate protein and Freund's complete adjuvant intradermally at 0 and 30 days. At 60 days, the rats were sacrificed, and then the prostate specimens were observed, under the light microscope and electron microscope, and the changes of proinflammatory expression was observed too, using PCR technique.</p><p><b>RESULTS</b>The products of proinflammatory expression, such as eotaxin, iNOS and IL-4 increased markedly. The change of chronic inflammation was shown by light microscope and electron microscope.</p><p><b>CONCLUSION</b>Chronic prostatitis is associated with autoimmunity.</p>

Relación entre la helmintiasis intestinal y el estado nutricional-hematológico en niños de una escuela rural en el estado Sucre Venezuela / Relantionship between intestinal helminthiasis and Nutritional-haematologic status on rural schoolchildren at Sucre state Venezuela

Se realizó una evaluación parasitológica, nutricional y hematológica en 103 niños de ambos sexos, entre 4-12 años de una escuela rural en Santa Fe, estado Sucre, Venezuela, durante el período enero-marzo 2003. Las muestras de heces se analizaron mediante un examen al fresco, Willis-Malloy y Kato-Katz cuantitativo. El estado nutricional se determinó utilizando la combinación de los índices antropométricos. Los parámetros hematológicos fueron evaluados por los métodos clásicos, y el grado de eosinofilia se expresó en valores absolutos de eosinófilos. 93,2 por ciento de los escolares estaban parasitados, presentando elevado poliparasitismo (83,3 por ciento). La prevalencia de helmintos intestinales fue de 82, por ciento, destacando la asociación de Trichuris trichiura y Ascaris lumbricoides (69,4 por ciento) y predominando una intensidad de infestación leve. De los individuos con desnutrición, el 91,2 por ciento (31/34) tenían helmintiasis. En 97,6 por ciento de los escolares infestados por helmintos se encontró eosinofilia (p<0,001). Del 23,3 por ciento de los niños con anemia, 83,3 por ciento (20/24) presentaron helmintiasis. El 88,8 por ciento de los niños con helmintiasis intestinal pertenecían al estrato socioeconómico V. Estos hallazgos sugieren que la población escolar evaluada habita en una zona hiperendémica de helmintos, consistente con el estrato socioeconómico encontrado. Adicionalmente, se estableció que la eosinofilia en estos escolares es un factor asociado a la helmintiasis intestinal

Selective suppression of leukocyte recruitment in allergic inflammation

Allergic diseases result in a considerable socioeconomic burden. The incidence of allergic diseases, notably allergic asthma, has risen to high levels for reasons that are not entirely understood. With an increasing knowledge of underlying mechanisms, there is now more potential to target the inflammatory process rather than the overt symptoms. This focuses attention on the role of leukocytes especially Th2 lymphocytes that regulate allergic inflammation and effector cells where eosinophils have received much attention. Eosinophils are thought to be important based on the high numbers that are recruited to sites of allergic inflammation and the potential of these cells to effect both tissue injury and remodelling. It is hoped that future therapy will be directed towards specific leukocyte types, without overtly compromising essential host defence responses. One obvious target is leukocyte recruitment. This necessitates a detailed understanding of underlying mechanisms, particularly those involving soluble che-moattractants signals and cell-cell adhesion molecules.

Expression of eosinophil chemotactic factors in stomach cancer

We have occasionally experienced eosinophilic abscess of the liver in patients with gastric carcinoma, suggesting that some eosinophil mobilizing (chemotactic and proliferative) factors might be produced by carcinoma cells. The aim of this study was to determine whether or not gastric carcinoma expresses the well-known eosinophil chemotactic factors (ECFs) and whether or not the expression is related to the histologic subtypes. Seventeen consecutive surgically removed tumor-bearing stomachs were collected: 7 signet ring cell type, 7 poorly differentiated tubular adenocarcinoma, and 3 moderately differentiated tubular adenocarcinoma. Hematoxylin-eosin stained sections were re-evaluated for eosinophil and mast cell infiltration. The expression of IL-2, IL-5 and granulocyte-macrophage colony stimulating factor (GM-CSF) were examined by immunocytochemical stain. There was no available frozen tissue for IL-2 and IL-5 in one case. Gastric carcinoma expressed IL-2 in all 16 cases, IL-5 in 12 of 16 cases and GM-CSF in 10 of 17 cases. Of particular interest, 7 of 10 GM-CSF-expressing carcinomas were signet ring cell type. Even in the remaining 3 cases, most GM-CSF-positive cells were signet ring cells scattered within tubular adenocarcinoma. No correlation of ECF expression between either eosinophil/mast cell infiltration or peripheral blood eosinophilia was identified. In conclusion, most gastric carcinomas express the well-known ECFs and the expression of GM-CSF is specific for signet ring carcinoma cells.

Effect of selective phosphodiesterase inhibitors on the rat eosinophil chemotactic response in vitro

In the present study, we have performed a comparative analysis of the effect of selective inhibitors of phosphodiesterase (PDE) type III, IV and V on eosinophil chemotaxis triggered by platelet activating factor (PAF) and leukotriene B4 (LTB4) in vitro. The effect of the analogues N6-2'-O-dibutyryladenosine 3':5' cyclic monophosphate (Bt2 cyclic AMP) and N2-2'-O-dibutyrylguanosine 3':5' cyclic monophosphate (Bt2 cyclic GMP) has also been determined. The eosinophils were obtained from the peritoneal cavity of naive Wistar rats and purified in discontinuous Percoll gradients to 85-95 per cent purity. We observed that pre-incubation of eosinophils with the PDE type IV inhibitor rolipram suppressed the chemotactic response triggered by PAF and LTB4 in association with an increase in the intracellular levels of cyclic AMP. In contrast, neither zaprinast (type V inhibitor) nor type III inhibitors milrinone and SK&F 94836 affected the eosinophil migration. Only at the highest concentration tested did the analogue Bt2 cyclic AMP suppress the eosinophil chemotaxis, under conditions where Bt2 cyclic GMP was ineffective. We have concluded that inhibition of PDE IV, but not PDE III or V, was able to block the eosinophil chemotaxis in vitro, suggesting that the suppresive activity of selective PDE IV inhibitors on tissue eosinophil accumulation may, at least, be partially dependent on their ability to directly inhibit the eosinophil migration.

Participation of interleukin-5, interleukin-8 and leukotriene B4 in eosinophil accumulation in two different experimental models

There are several experimental models descibing in vivo eosinophil (EO) migration, including injection of a large volume of saline (SAL) or Sephadex beads (SEP). The aim of this study was to investigate the mechanisms involved in the EO migration in these two models. Two consecutive injections of SAL given 48 hr apart, induced a selective recruitment of EO into peritoneal cavity of rats, which peaked 48 hr after the last injection. SEP, when injected, promoted EO accumulation in rats. The phenomenom was dose-related and peaked 48 hr after injection. To investigate the mediators involved in this process we showed that BW A4C, MK 886 and dexamethasone (DXA) inhibited the EO migration induced by SAL and SEP. To investigate the source of the EO chemotactic factor we showed that mast cells, macrophages (MO), but not lymphocytes, incubated in vitro in presence of SAL released a factor which induced EO migration. With SEP, only mast cells release a factor that induced EO migration, which was inhibited by BW A4C, MK 886 and DXA. Furthermore, the chemotactic activity of SAL-stimulated mast cells was inhibited by antisera against IL-5 and IL-8 (interleukin). SAL-stimulated MO were only inhibited by anti-IL-8 antibodies as well as SEP-stimulated mast cells. These results suggest that the EO migration induced by SAL may be dependent on resident mast cells and MO mediated by LTB4, IL-5 and IL-8. SEP-induced EO migration was dependent on mast cells and may be mediated by LTB4 and IL-8. Furthermore, IL-5 and IL-8 induced EO migration, which was also dependent on resident cells and mediated by LTB4. In conclusion, EO migration induced by SAL is dependent on mast cells and MO, whereas that induced by SEP is dependent on mast cells alone. Stimulated mast cells release LTB4, IL-5 and IL-8 while MO release LTB4 and IL-8. The IL-5 and and IL-8 release by the SAL or SEP-stimulated resident cells may act in an autocrine fashion, thus potentiating LTB4 release.

Description of an in vivo model for assessment of eosinophil chemoattractants in the mouse

Chemokines (chemoattractant cytokines) induce potent and selective chemotaxis of leukocyte subsets in vitro. Here, we review briefly the chemokines shown to induce eosinophil chemotaxis in vitro and describe a novel model for the study of the ability of chemokines to stimulate eosinophil migration in vivo. Eosinophils were purified from the blood of mice over-expressing the IL-5 gene and labelled with 111In. Only the C-C chemokines, eotaxin and MIP-1 alpha, but not RANTES, MCP-1, MCP-3, MIP-1ß. KC and MIP-2, effectively induced the recruitment of 111In-eosinophils in mouse skin. We suggest that this mouse model will be useful in assessing the role of endogenously-generated chemokines in mediating eosinophil migration to sites of allergic inflammation in vivo.

The eosinophils in parasitic infections

Local and peripheal eosinophilia is a common feature of many helminth infections that present large, non-phagocytable surfaces to the inmune system. The effect of the eosinophils on these organisms has been studied in the last 18 years using schistosoma mansoni, trichinella spiralis, and other helminths as models. The early infection causes a nonspecific inflammation rich in macrophages, lymphocytes and neutrophils that sets the stage for a subsequent inmune response. The predominant effector elements of the inmune response are anaphylactic antibodies, mast cells, and eosinophils. Mast cell products attract eosinophils and concentrate antibodies and complement-covered parasites by their Fc and/or C3c receptors and release oxygen radicals and/or preformed proteins on the helmith surface. The radicals alter molecules of the parasite and the proteins disrupt its tegument or cuticle. Occasionally, they may harm host cells. Eosinophils also phagocytize and harm extracellular trypanosoma cruzi and may play a role in the damage to the host heart tissue. The eosinophil response is regulated by eosinophilopoietic factors (interleukines [IL] 3 and 5, and granulocyte macrophage colony-stimulating factor) eosinophilotactic factors (C5a from complement, eosinophil chemotactic factor of anaphylaxis [ECF-A], histamine, platelet stimulating factor, and other ECFs from mast cells and basophils, and ECF from parasites), and eosinophiloactivating factors (IL-5 from Th2 lymphocytes, tumor necrosis factor from macrophages, antibodies, and complement components). Other phagocytic cells (macrophages and neutrophils) also exhibit important anti-helminthic activities

Chemotactic effect of PAF-acether on peritoneal eosinophils from normal rats

The chemotactic activity of PAF-acether was compared with that of tetrapeptide eosinophil chemotactic factors of anaphylaxis (ECF-A, Ala-Gly-Ser Glu and Val-Gly-Ser-Glu) using eosinophils obtained from the peritoneal cavity of normal rats. Cells were isolated by separation over discontinuous metrizamide gradients which resulted in eosinophil suspensions of 80 to 90% purity. PAF-acether produced 7-fold greater than the maximal activity obtained with the ECF-A-tetrapeptides. BN 52021 and WEB 2086 inhibited PAF-acether-induced eosinophil chemotaxis in a dose-dependent manner, suggesting that this phenomenon is mediated by specific PAF-acether receptors