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Infected Rats (infected + rat)
Selected AbstractsExacerbation of experimental autoimmune encephalomyelitis in rodents infected with murine gammaherpesvirus-68EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 7 2003James Abstract Viral infections have long been suspected to play a role in the pathogenesis of multiple sclerosis. In the present study, two different rodent models of experimental autoimmune encephalomyelitis (EAE) were used to demonstrate the ability of murine gammaherpesvirus-68 (,HV-68) to exacerbate development of neurological symptoms. SJL mice received UV-inactivated ,HV-68 or intranasal,HV-68, followed by immunization against proteolipid-protein peptide 139,151. Infected mice became moribund within 10,days post-immunization, whereas mice exposed to UV-inactivated ,HV-68 recovered. In the second model, Lewis rats were exposed to UV-inactivated ,HV-68 or to ,HV-68, followed by passive transfer of encephalitogenic T lymphocytes specific for myelin basic protein. Consistently, infected rats had higher clinical scores, and this result was observed during acute or latent ,HV-68 infection. It is unlikely that this ,HV-68-induced exacerbation was due to significant viral replication within the central nervous system since nested PCR, viral plaque assays, and infectious-centers assays demonstrated no detectable virus in spinal cords or brains of infected rodents undergoing EAE. Taken together, these studies demonstrate increased clinical symptoms of EAE in rodents infected by a gammaherpesvirus that has a limited ability to invade the central nervous system. [source] In vivo morphological and antifungal study of the activity of a bergamot essential oil by-productFLAVOUR AND FRAGRANCE JOURNAL, Issue 4 2006Francesco Carmelo Pizzimenti Abstract The in vivo antifungal activity of a bergamot processing by-product, named ,Peratoner', was evaluated through applications to male Wistar rats' back skin, previously infected with Candida albicans. Following the treatment, samples were taken to evaluate the fungal load and punch biopsies were carried out for morphological studies. In infected rats without Peratoner treatment, skin detachment with infiltrating cells was observed. The presence of C. albicans cells was evident on the surface strata of the epidermis, which was detached from the basal cells. After 24 h, in the case of Peratoner treatment, the epidermic strata were still few in number, while the infiltrating elements in the dermis were fewer in quantity and a small cluster of C. albicans cells, above the stratum corneous, was also visible. After 48 h of treatment, the skin revealed proliferation of the strata, while in the dermis infiltrating cells were still evident. Following this period and up to a week after treatment, a full recovery of the cutaneous structure was observed. Copyright © 2006 John Wiley & Sons, Ltd. [source] Effect of experimentally induced Escherichia coli epididymo-orchitis and ciprofloxacin treatment on rat spermatogenesisINTERNATIONAL JOURNAL OF UROLOGY, Issue 3 2007Aslan Demir Abstract: We investigated the effects of epididymo-orchitis and ciprofloxacin on rat testicular histology and spermatogenesis. The control group underwent left orchiectomy. The second group received oral ciprofloxacin (150 mg/kg/day) for 10 days. Escherichia coli (106 cfu/mL, 0.1 mL) was injected into the proximal right ductus deferens in the third group. The fourth group received ciprofloxacin treatment 48 h after E. coli inoculation. In groups 3 and 4, bilateral orchiectomy was performed 14 days after the challenge. In healthy rats, ciprofloxacin caused recognizable histological damage associated with a mild decrease in testicular volume and sperm concentration. Infected testicles in groups 3 and 4 revealed severe histological damage associated with severe testicular atrophy and impaired spermatogenesis that were more significant in infected rats which received ciprofloxacin treatment. Contralateral testicles in these animals showed similar histopathological changes to a lesser extent. The results of our study suggest a gonadotoxic potential for ciprofloxacin and this potential in humans should be addressed with further studies. [source] Survival of Escherichia coli O157 in faeces of experimentally infected rats and domestic pigeonsLETTERS IN APPLIED MICROBIOLOGY, Issue 5 2000In order to evaluate the role of some synanthropic animals in the spreading of Escherichia coli O157, laboratory rats and domestic pigeons were experimentally infected per os with E. coli O157. Rats infected with 105 colony forming units (cfu) (n = 5) and 109 cfu (n = 5) shed E. coli O157 for 2 ± 1·7 d and 9·8 ± 1·3 d, respectively. In the faeces of infected rats stored at 4 °C in a moist environment, at 4 °C in a dry environment or at 20 °C in a moist environment, E. coli O157 survived for 34 weeks. When stored at 20 °C or ,,20 °C in a dry environment, E. coli O157 survived for , 36 weeks. Pigeons infected with 105 cfu (n = 5) and 109 cfu (n = 5) shed the pathogen for 14·8 ± 3·4 d and 20·2 ± 5·2 d, respectively. Both species, rats and pigeons can be important in spreading of the E. coli O157 infection in cattle. [source] Omega-3 fatty acid regulates inflammatory cytokine/mediator messenger RNA expression in Porphyromonas gingivalis -induced experimental periodontal diseaseMOLECULAR ORAL MICROBIOLOGY, Issue 4 2007L. Kesavalu Introduction:,Porphyromonas gingivalis is strongly implicated in the etiology of adult periodontitis by inducing inflammatory cytokines, resulting in gingival and periodontal tissue inflammation and alveolar bone resorption. This study tested the hypothesis that supplementing the diet with omega-3 fatty acid (,-3 FA; i.e. fish oil) would exert anti-inflammatory effects in the gingival tissues of P. gingivalis -infected rats. Methods:, Rats were fed either fish oil or corn oil diets ad libitum for 22 weeks and infected with P. gingivalis strain 381 or strain A7A1-28. After sacrifice, rat gingival tissues were excised and the RNA was isolated and analyzed for proinflammatory mediators [interleukin-1, (IL-1,), tumor necrosis factor-, (TNF-,), IL-6], T helper type 1 and type 2 cytokines [interferon-, (IFN-,), IL-4, IL-10), antioxidant enzymes [catalase (CAT), superoxide dismutase (SOD)], and genes critical for eicosanoid mediator production [cyclo-oxygenase-2 (COX-2), 5-lipoxygenase (5-LO)] by reverse transcription-polymerase chain reaction using rat-specific primers. Results:, Rats on the ,-3 FA diet exhibited decreased proinflammatory cytokine gene expression (IL-1,, TNF-,) and enhanced IFN-,, CAT and SOD messenger RNA expression compared to rats fed a corn oil diet, supporting a diet-induced modulation of host inflammatory reactions. Analyses of alveolar bone resorption in the rats related to gene expression profiles demonstrated significant positive correlations with IL-1,, IL-6 and COX-2 and negative correlations with CAT and SOD. Conclusion:, These findings suggest that diets enriched for ,-3 FA modulate the local gingival inflammatory milieu of the host following oral P. gingivalis infection, which impacts on alveolar bone resorption in rats. [source] Alterations of intestinal motor responses to various stimuli after Nippostrongylus brasiliensis infection in rats: role of mast cellsNEUROGASTROENTEROLOGY & MOTILITY, Issue 3 2000J. Gay Nippostrongylus brasiliensis infection induces jejunal mastocytosis associated with enteric nerve remodelling in rats. The aim of this study was to evaluate the intestinal motility responses to meals and to neurotransmitters involved in the control of gut motility (acetylcholine (carbachol), substance P and neurokinin A) in both control and N. brasiliensis -infected rats 30 days post-infection. All rats were equipped with NiCr electrodes in the jejunum to record myoelectrical activity. The duration of disruption of the jejunal migrating myoelectrical complexes (MMC) induced by the different stimuli was determined. Meal ingestion and substance P administration disrupted the MMC pattern for similar durations in the two groups. Carbachol and neurokinin A induced a significantly longer MMC disruption in post-infected rats than in controls (125 ± 8.3 vs. 70 ± 6 min for carbachol 100 ,g kg,1 and 51 ± 4 vs. 40 ± 2 for neurokinin A 50 ,g kg,1). The enhanced motor response in postinfected rats was reduced by previous mast cell stabilization with ketotifen or mast cell degranulation with compound BrX 537 A. In conclusion, the increased intestinal motor reactivity to carbachol and neurokinin A in post- N. brasiliensis -infected rats depends upon intestinal mast cell hyperplasia and degranulation. [source] In vivo inhibition of inducible nitric oxide synthase decreases lung injury induced by Toxocara canis in experimentally infected ratsPARASITE IMMUNOLOGY, Issue 11-12 2002Elsa Y. Espinoza SUMMARY The direct effect of nitric oxide (NO) on the viability of Toxocara canis larvae was studied. We observed that the nitric oxide donors, SIN-1 and SNOG, exert no cytotoxic effect on the in vitro viability of T. canis larvae. In addition, we developed a model in rats to elucidate the role of NO during T. canis infection. We evaluated different indicators in four experimental groups: morphological parameters, the total number cells and cell types recovered, nitrite and protein concentration, lactate dehydrogenase and alkaline phosphatase enzymatic activity in the bronchoalveolar lavage fluid, lung index and detection of anti- T. canis specific antibodies. We observed significant differences between non-infected and infected groups. The infected animals treated with the inducible nitric oxide synthase (iNOS) inhibitor aminoguanidine were less damaged than infected, non-treated animals. Our results suggest that the in vivo inhibition of the synthesis of NO triggered by iNOS diminishes the deleterious effects of the parasite upon the host, especially the vascular alterations in the lungs. We could show that in vivo production of NO induced by infection with T. canis results in direct host damage. Thus, this induction may constitute an evasion/adaptation mechanism of the parasite. [source] Nerve growth factor mediates steroid-resistant inflammation in respiratory syncytial virus infection,,PEDIATRIC PULMONOLOGY, Issue 6 2007Lida Mohtasham MD Abstract Neurotrophic factors and receptors are upregulated in the respiratory tract of humans and rodents infected by the respiratory syncytial virus, leading to airway inflammation and hyperreactivity. The contribution of neurotrophic pathways to the recruitment of immuno-inflammatory cells and their response to anti-inflammatory therapy remains unclear. We sought to determine whether selective nerve growth factor inhibition prevents the immuno-inflammatory response against infection, and explored the effect of inhaled corticosteroids on virus-induced neurotrophic upregulation and the consequent recruitment of immuno-inflammatory cells into the airways. We tried to inhibit the recruitment of lymphocytes and monocytes into the airways of infected weanling rats using immunologic inhibition of nerve growth factor with a specific blocking antibody, or chemical inhibition of receptor tyrosine kinase with K252a. The anti-inflammatory activity of inhaled corticosteroids was studied in infected rats treated with budesonide, fluticasone, or vehicle. Immunological or chemical inhibition of nerve growth factor or its high-affinity receptor tyrosine kinase pathway inhibited the recruitment of inflammatory cells triggered by nociceptive irritation of infected rat airways, thereby reducing local and systemic immuno-inflammatory responses against the virus. Neurotrophic upregulation in infected airways was not affected by inhaled corticosteroids. As a logical consequence, these commonly used drugs were also unable to stop the recruitment of immune and inflammatory effector cells into infected airways. Overexpression of neurotrophic factors and receptors in airways infected by respiratory syncytial virus is critical for the development of airway inflammation and hyperreactivity, which is resistant to the anti-inflammatory effect of inhaled corticosteroids. Pediatr Pulmonol. 2007; 42:496,504. © 2007 Wiley-Liss, Inc. [source] Effects of Ureaplasma urealyticum infection on the male reproductive system in experimental ratsANDROLOGIA, Issue 5 2010Y. Wang Summary To study the effects of Ureaplasma urealyticum (Uu) infection on the male reproductive system, the mechanism of infertility induced by Uu infection was investigated in experimental rats. Male Sprague,Dowley rats were infected with Uu4 (serotype 4) through repeated natural sexual intercourse for 8 weeks to establish infection. After 8 weeks, the blood samples of the animals were collected and analysed for cytokine production, and the animals were microdissected for the analysis of the reproductive system. Morphological study showed that spermatozoa exhibited curling and breaks in the rats infected at different dosages. Of the infected rats, 27.5% had both soft and hard calculi in the urinary tract, compared with 12% in the control groups. Uu infection resulted in a decline of sperm quality, eventually leading to the death of the spermatozoa. In the infected animals, the serum interleukin 6 and interleukin 8 levels increased significantly (P < 0.05), while tumour necrosis factor-alpha and interferon-gamma showed only modest changes. Our observations showed that Uu infection has an impact on sperm morphology, leading to the death of the spermatozoa. It is plausible that the morphological alterations of spermatozoa induced by Uu infection are one of the possible factors that contribute to male infertility. [source] | ||||||||||