Infected Animals (infected + animals)

Distribution by Scientific Domains
Distribution within Medical Sciences


Selected Abstracts


A Profound Effect of Hyperthermia on Survival of Litopenaeus vannamei Juveniles Infected with White Spot Syndrome Virus

JOURNAL OF THE WORLD AQUACULTURE SOCIETY, Issue 4 2001
Oscar M. Vidal
This study was conducted to examine the effect of increasing seawater temperature on White Spot Syndrome Virus (WSSV) infection in juvenile Pacific White shrimp (Litopenaeus vannamei). Infection by WSSV was achieved using two methods, intramuscular injection and per os (oral) administration. Forty injected and 20 per os infected animals were kept in heated tanks at 32.3 ± 0.8 C, and the same number of WSSV infected animals were maintained in tanks at ambient temperature (25.8 ± 0.7 C). Despite the route of exposure, there were no survivors among the animals kept at ambient temperature; whereas, in heated tanks the survival of the WSSV infected juvenile shrimp was always above 80%, suggesting the existence of a beneficial effect from hyperthermia that mitigated the progression of WSSV disease. Moreover, this beneficial effect was not attributable to viral inactivation. Infected animals kept at 32 C had histologically detectable lymphoid organ spheroids suggestive of a chronic viral infection but were PCR negative (hemolymph) for WSSV. These findings might be related to low viral replication in WSSV-infected shrimp held at the higher environmental temperature. When the WSSV-infected shrimp were transferred from 32 C to ambient temperature, the mortality from WSSV ensued and was always 100%. Although the mechanism related to the beneficial effect of heating was not determined, our results indicate that increasing the water temperature modifies dramatically the natural history of the WSSV disease and the survival curves of WSSV-infected juvenile Pacific White shrimp. [source]


Management measures to control a feline leukemia virus outbreak in the endangered Iberian lynx

ANIMAL CONSERVATION, Issue 3 2009
G. López
Abstract The feline leukemia virus (FeLV) is a retrovirus that affects domestic cats all over the world. Its pathogenic effects generally include anemia, immunosuppression or tumors. Dissemination over populations is linked to cat sociality, because the virus is transmitted by direct contact. Although the domestic cat is its common host, FeLV infection has also been described in some wild felids. In the Iberian lynx Lynx pardinus, some sporadic FeLV infection cases have been reported since 1994, but an outbreak with the involvement of several animals has never been described until now. During spring 2007, an FeLV outbreak hit the Doñana (SW Spain) population. The infection rapidly spread throughout the densest subpopulation throughout Doñana. Infected animals showed very acute anemic disease, most of them dying in <6 months. To avoid FeLV dissemination, a control program was carried out that included removal of viremic lynxes, vaccination of negative individuals and reduction of the feral cat population. The program was implemented both in Doñana and in Sierra Morena populations. In Doñana, around 80% of the total lynx population and 90% of the outbreak focus subpopulation were evaluated. Seven out of the 12 infected individuals found died and two reverted to latency; the remaining viremic animals have been kept in captivity. The outbreak appears to have been successfully confined to the subpopulation where the virus appeared and no more cases have been found since August 2007. In the larger Sierra Morena population, 8% of the lynx population was surveyed. Thirty-four uninfected Iberian lynxes were vaccinated at least once. The FeLV prevalence was found to be 27% in the Doñana population and 0% in the Sierra Morena population. [source]


Cooperation between toll-like receptor,2 and,4 in the brain of mice challenged with cell wall components derived from gram-negative and gram-positive bacteria

EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 4 2003
Nathalie Laflamme
Abstract In this study we investigated whether induction of toll-like receptor,2 (TLR2) amplifies the effect of a cell wall component derived from gram-positive bacteria, namely peptidoglycan (PGN). Mice received a first systemic lipopolysaccharide (LPS) injection to pre-induce TLR2 in various regions of the brain, and 6,h later, a second administration of either LPS or PGN. The data show a robust transcriptional activation of TLR2, TNF-, and monocyte chemotactic protein-1 (MCP-1) in microglial cells of mice challenged twice with LPS, whereas PGN essentially abolished this response. TLR4 plays a critical role in this process, because C3H/HeJ mice no longer responded to LPS but exhibited a normal reaction to PGN. Conversely, a robust signal for genes encoding innate immune proteinswas found in the brain of TLR2-deficient mice challenged with LPS. However, the second LPS bolus failed to trigger TNF-, and IL-12 in TLR2-deficient mice, while the same treatment caused a strong induction of these genes in the cerebral tissue of wild-type littermates. The present data provide evidence that cooperation exists between TLR4 and TLR2. While TLR4 is absolutely necessary to engage the innate immune response in the brain, TLR2 participates in the regulation of genes encoding TNF-, and IL-12 during severe endotoxemia. Such collaboration between TLR4 and TLR2 may be determinant for the transfer from the innate to the adaptive immunity within the CNS of infected animals. [source]


Immunoblot Analysis as an Alternative Method to Diagnose Enterohepatic Helicobacter Infections

HELICOBACTER, Issue 3 2009
Torkel Wadström
Abstract Introduction: Enterohepatic Helicobacter species have been associated with chronic infections of the hepatobiliary tract and lower bowel in naturally and experimentally infected mice, Helicobacter -infected animals should thus not be used in studies of diseases associated with chronic inflammation. Helicobacter species induce inflammation and modulate host immune responses, thus emphasizing the need to diagnose these infections in laboratory animals. Materials and Methods: An immunoblot assay was developed to analyze antibodies to enterohepatic Helicobacter species in naturally colonized laboratory mouse colonies. We evaluated the serum antibody responses to cell surface proteins of H. bilis, H. hepaticus, and H. ganmani in 188 mouse sera from four different university animal facilities. Lower bowel tissue specimens from 56 of these animals were available and analyzed by polymerase chain reaction-denaturing gradient gel electrophoresis (PCR-DGGE) and the results compared with matched immunoblot patterns. Results: Specific antibody reactivity to H. bilis was detected in 8 of 186 (4.3%) sera, to H. hepaticus in 45 of 184 (24%) sera, and to H. ganmani in 51 of 188 (27%) of tested sera. These results were compared with PCR-DGGE analyses of tissue samples of corresponding animals, and concordance between the two diagnostic tests was found in 96% for H. bilis, in 91% for H. hepaticus, and in 82% for H. ganmani. The PCR-DGGE also detected DNA of H. typhlonius, H. sp. flexispira, and H. rodentium. Conclusions: Infection with enterohepatic species was common in the laboratory mouse colonies tested, independent of strain and stock. Immunoblot analysis seems to be a promising diagnostic tool to monitor enterohepatic Helicobacter species infections of laboratory rodents. [source]


Lack of response to exogenous interferon-, in the liver of chimpanzees chronically infected with hepatitis C virus,,

HEPATOLOGY, Issue 4 2007
Robert E. Lanford
The mechanism of the interferon-alpha (IFN,),induced antiviral response is not completely understood. We recently examined the transcriptional response to IFN, in uninfected chimpanzees. The transcriptional response to IFN, in the liver and peripheral blood mononuclear cells (PBMCs) was rapidly induced but was also rapidly down-regulated, with most interferon-alpha,stimulated genes (ISGs) returning to the baseline within 24 hours. We have extended these observations to include chimpanzees chronically infected with hepatitis C virus (HCV). Remarkably, using total genome microarray analysis, we observed almost no induction of ISG transcripts in the livers of chronically infected animals following IFN, dosing, whereas the response in PBMCs was similar to that in uninfected animals. In agreement with this finding, no decrease in the viral load occurred with up to 12 weeks of pegylated IFN, therapy. The block in the response to exogenous IFN, appeared to be HCV-specific because the response in a hepatitis B virus,infected animal was similar to that of uninfected animals. The lack of a response to exogenous IFN, may be due to an already maximally induced ISG response because chronically HCV-infected chimpanzees already have a highly up-regulated hepatic ISG response. Alternatively, negative regulation may block the response to exogenous IFN,, yet it does not prevent the continued response to endogenous ISG stimuli. The IFN, response in chronically HCV-infected chimpanzees may be mechanistically similar to the null response in the human population. Conclusion: In chimpanzees infected with HCV, the highly elevated hepatic ISG expression may prevent the further induction of ISGs and antiviral efficacy following an IFN, treatment. (HEPATOLOGY 2007.) [source]


,Flames and fear on the farms': controlling foot and mouth disease in Britain, 1892,2001*

HISTORICAL RESEARCH, Issue 198 2004
Abigail Woods
For over a century, the British government has pursued a policy of national freedom from foot and mouth disease (F.M.D.), a highly contagious disease of cloven-footed animals. One of the cornerstones of this policy was the slaughter of infected animals. However, on several occasions , most notably in 2001 , slaughter struggled to contain F.M.D., and provoked widespread criticism and calls for policy change. Drawing upon a range of previously unexamined sources, this article examines the history of F.M.D. in Britain, in an attempt to explain the twenty-first-century persistence of a Victorian disease control policy. [source]


Modelling the spatial dynamics of parapoxvirus disease in red and grey squirrels: a possible cause of the decline in the red squirrel in the UK?

JOURNAL OF APPLIED ECOLOGY, Issue 6 2000
S.P. Rushton
Summary 1. ,A stochastic individual-based model for simulating the dynamics of an infectious disease in sympatric red and grey squirrel populations is described. The model simulates the spread of parapoxvirus between squirrels in fragmented populations based on the dispersal of infected animals, the probability of encounters between individuals, exposure to the virus and subsequent mortality. 2. ,The disease model was integrated with a spatially explicit population dynamics model that simulated red and grey squirrel populations in real landscapes, using habitat information held in a geographical information system. Latin hypercube sampling was used to create a range of realistic life-history and infection scenarios and the model was used to investigate the dynamics of red and grey squirrels in Norfolk between 1966 and 1980. 3. ,The model predicted that parapoxvirus, like interspecific competition, could have led to the extinction of the red squirrel in Norfolk. The results suggest that the red squirrel,grey squirrel,parapoxvirus interaction represents a system of apparent competition mediated by an infectious agent, as seen in other interactions between resident and exotic species. 4. ,The need for further epidemiological research on the virus is emphasized. We believe that the combined effects on disease transmission of habitat, behaviour and grey squirrels acting as reservoir hosts will lead to a patchy prevalence and sporadic incidence of parapoxvirus disease in red squirrels and a more rapid local replacement by grey squirrels. 5. ,These results have implications for conservation management of the red squirrel in the UK. Schemes in which animals are translocated or given supplementary feeding may enhance disease spread by bringing infected animals into contact with others. [source]


Regulation of Endothelial Cell Adhesion Molecule Expression in an Experimental Model of Cerebral Malaria

MICROCIRCULATION, Issue 6 2002
PHILLIPE R. BAUER
ABSTRACT Objective: Plasmodium falciparum malaria in humans and animal models of this disease have revealed changes in the infected host that are consistent with a systemic inflammatory response. Although it has been proposed that endothelial cell adhesion molecules (CAM) contribute to the adhesive interactions of Plasmodium -infected erythrocytes and immune cells with vascular endothelial cells, ECAM expression has not been systematically studied in Plasmodium -infected animals. Methods: In this study, the dual radiolabeled monoclonal antibody method was used to quantify the expression of different ECAMs (ICAM-1, VCAM-1, P-selectin, E-selectin) in different regional vascular beds of Plasmodium berghei ANKA-inffected mice (PbA), a well-recognized model of human cerebral malaria. The roles of T lymphocytes and certain cytokines (TNF-,, IL-12, IFN-,) in mediating the infection-induced expression of ICAM-1 and P-selectin were assessed by using relevant mutant mice. Results: Wild-type (WT) mice exhibited highly significant increases in the expression of ICAM-1, VCAM-1, and P-selectin (but not E-selectin) in all vascular beds on the 6th day of PbA infection. The PbA -induced upregulation of ICAM-1 was significantly blunted in mice that were either deficient in IFN-,, IL-12 (but not TNF1b) or T lymphocytes (Rag-1 deficiency); however, these responses were tissue specific. Conclusions: These findings indicate that vascular endothelial cells in most regional circulations assume an inflammatory phenotype and that cytokines and immune cells mediate this response in a tissue-specific manner. [source]


Long-lasting changes in small intestinal transport following the recovery from Trichinella spiralis infection

NEUROGASTROENTEROLOGY & MOTILITY, Issue 3 2006
K. Venkova
Abstract, Changes in intestinal motility and visceral sensitivity are found after resolution of acute enteric inflammation. The study investigates whether a transient nematode-induced intestinal inflammation may result in long-lasting remodelling of epithelial transport. Ferrets infected with Trichinella spiralis or sham-infected animals were euthanized on day 10, 30 or 60 postinfection (PI) and the jejunum was isolated. The net transport of electrolytes was measured electrophysiologically as transmucosal short-circuit current (Isc) and responses to electrical field stimulation (EFS: 1,32 Hz) or secretagogues were investigated. Myeloperoxidase (MPO) activity, a marker of mucosal inflammation, was maximal during the enteric stage of T. spiralis infection (day 10 PI) and returned to normal on days 30 and 60 PI. Mucosal inflammation caused a reduction in basal Isc, increased electrical conductance (G) and decreased the maximal responses to EFS, carbachol or histamine. On days 30 and 60 PI the inflammation resolved and basal electrogenic transport appeared normal; however, the secretion induced by EFS, carbachol or histamine remained suppressed. Moreover, EFS-induced responses were shifted from predominantly cholinergic in controls to non-cholinergic in the infected animals. The results suggest that a transient small intestinal inflammation causes a long-term remodelling of epithelial function. [source]


Differences in immune parameters are associated with resistance to Haemonchus contortus in Caribbean hair sheep

PARASITE IMMUNOLOGY, Issue 7 2010
K. M. MacKINNON
Summary Caribbean hair sheep are more resistant to gastrointestinal nematodes than conventional wool breeds, but mechanisms that confer resistance are not fully understood. This study compared immune effector cell populations and antibody concentrations in 12 hair and 12 wool lambs infected with the abomasal parasite Haemonchus contortus and sacrificed at 3 or 27 days post-infection (p.i.) and 14 uninfected animals of each breed. Faecal egg counts were over 2·5-fold higher (P = 0·12) and packed cell volumes approximately 8% lower (P < 0·10) in infected wool lambs. Abomasal lymph nodes were heavier in infected animals (P < 0·05) and infected hair sheep had larger lymph nodes than infected wool sheep (P < 0·05). Tissue eosinophil concentrations were likewise larger (P = 0·07) in hair compared with wool sheep at 3 days p.i. Circulating levels of IgE and IgA in uninfected lambs were higher in hair sheep (P < 0·05) and during infection, hair sheep had higher serum IgA than wool sheep at 3, 5, and 21 days p.i. (P < 0·05). Serum IgE in infected lambs did not differ between breeds, but concentrations of IgE in lymph nodes were higher (P < 0·01) at 27 days p.i. in infected hair sheep. [source]


Changes in lymphocyte populations in suckling piglets during primary infections with Isospora suis

PARASITE IMMUNOLOGY, Issue 4 2010
H. L. WORLICZEK
Summary Isospora suis, a common intestinal parasite of piglets, causes neonatal porcine coccidiosis, which results in reduced and uneven weaning weights and economic losses in pig production. Nevertheless, there are no detailed studies available on the immune response to I. suis. The aim of this study was to carry out phenotypical characterization of lymphocytes during primary infections on day 3 after birth. Infected and noninfected piglets were investigated between days 7 and 16 after birth. Lymphocytes from the blood, spleen and mesenteric lymph nodes (flow cytometry) and of the jejunal mucosa (immunohistochemistry) were analysed. A decrease in T cells, especially with the phenotype of resting T-helper cells, T-cell receptor-,,-T cells, and regulatory T cells in the blood, spleen and mesenteric lymph nodes was noticeable. An increase in cells with the phenotype of natural killer cells in the spleen of infected animals was found, and the subset of TcR-,,-T cells was strongly increased in the gut mucosa. Our findings suggest an accelerated migration of those cells into the gut. This study provides a strong indication for the involvement of adaptive and innate immune response mechanisms in the primary immune response to I. suis, especially of TcR-,,-T cells as a linkage between innate and adaptive immunity. [source]


Enhanced protection by melatonin and meloxicam combination in experimental infection by Trypanosoma cruzi

PARASITE IMMUNOLOGY, Issue 4 2010
L. G. R. OLIVEIRA
Summary The aim of this study was to evaluate a possible synergism between melatonin and meloxicam in up-regulating the immune response in male Wistar rats infected with Trypanosoma cruzi during immunosuppression phenomenon, which characterizes the acute phase of the Chagas' disease. Male Wistar rats were infected with the Y strain of T. cruzi. Experiments were performed on 7, 14 and 21 days post-infection. Several immunological parameters were evaluated including ,-interferon (IFN-,), interleukin-2 (IL-2), nitric oxide (NO) and prostaglandin E2 (PGE2). The combined treatment with melatonin and meloxicam significantly enhanced the release of IL-2 and INF-, into animals' serum, when compared with the infected control groups during the course of infection. Furthermore, the blockade of PGE2 synthesis and the increased release of NO by macrophage cells from T. cruzi -infected animals contributed to regulate the production of Th1 subset cytokines significantly reducing the parasitaemia in animals treated with the combination of both substances. Therefore, our results suggest that the association of melatonin and meloxicam was more effective in protecting animals against the harmful actions of T. cruzi infection as compared with the treatments of meloxicam or melatonin alone. [source]


The immune response during a Strongyloides ratti infection of rats

PARASITE IMMUNOLOGY, Issue 7 2007
C. P WILKES
SUMMARY A range of immune parameters was measured during a primary infection of Strongyloides ratti in its natural rat host. The immune parameters measured were interleukin-4 (IL-4) and interferon-, from both the spleen and mesenteric lymph node (MLN) cells; parasite-specific immunoglobulin G1(IgG1), IgG2a and IgG2b in serum and in intestinal tissue; parasite-specific IgG and total IgE in serum; parasite-specific and total IgA in intestinal tissue and rat mast cell protease II in intestinal tissue. Parasite-specific IgG1, IgG2a and total IgE in serum and parasite-specific IgA and rat mast cell protease II in intestinal tissue all occurred at significantly greater concentrations in infected animals, compared with non-infected animals. Similarly, the production of IL-4 by MLN cells stimulated with parasitic female antigen or concanavalin A occurred at significantly greater concentrations in infected animals, compared with non-infected animals. In all, this suggests that there is a T-helper 2-type immune response during a primary S. ratti infection. These data also show the temporal changes in these components of the host immune response during a primary S. ratti infection. [source]


Antibody-dependent cell-mediated cytotoxicity to newly excysted juvenile Fasciola hepatica in vitro is mediated by reactive nitrogen intermediates

PARASITE IMMUNOLOGY, Issue 9 2001
D. Piedrafita
Passive intraperitoneal transfer of sera from Fasciola hepatica- infected sheep, cattle or rats can protect naive rats from F. hepatica infection, suggesting a parasite killing mechanism within the peritoneal cavity that is dependent on the presence of parasite-specific antibody. We investigated antibody-dependent cell-mediated cytotoxicity by resident peritoneal lavage cell populations, containing large numbers of monocytes/macrophages, as a potential host resistance mechanism by which juvenile flukes could be killed within the peritoneal cavity of naive rats. Comparative studies were conducted using cell populations containing large numbers of monocytes/macrophages from sheep. The results demonstrate that monocyte/macrophage-rich lavage cell populations from rat and sheep differ substantially in their ability to generate nitric oxide . Only resident rat peritoneal lavage cells were able to mediate antibody-dependent cell-mediated cytotoxicity against newly excysted juvenile liver fluke. The mechanism of cytotoxicity was dependent on, and directly proportional to, the production of nitric oxide and required attachment of effector cells to the newly excysted juvenile liver fluke tegument, which occurred following the addition of sera from F. hepatica -infected animals. This is the first report demonstrating a mechanism of cell-mediated cytotoxicity to newly excysted juvenile liver fluke. [source]


Effects of Ureaplasma urealyticum infection on the male reproductive system in experimental rats

ANDROLOGIA, Issue 5 2010
Y. 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]


Fine mapping of the chicken salmonellosis resistance locus (SAL1)

ANIMAL GENETICS, Issue 6 2009
M. S. Fife
Summary Salmonella enterica serovar Typhimurium is a Gram-negative bacterium that has a significant impact on both human and animal health. It is one of the most common food-borne pathogens responsible for a self-limiting gastroenteritis in humans and a similar disease in pigs, cattle and chickens. In contrast, intravenous challenge with S. Typhimurium provides a valuable model for systemic infection, often causing a typhoid-like infection, with bacterial replication resulting in the destruction of the spleen and liver of infected animals. Resistance to systemic salmonellosis in chickens is partly genetically determined, with bacterial numbers at systemic sites in resistant lines being up to 1000-fold fewer than in susceptible lines. Identification of genes contributing to disease resistance will enable genetic selection of resistant lines that will reduce Salmonella levels in poultry flocks. We previously identified a novel resistance locus on Chromosome 5, designated SAL1. Through the availability of high-density SNP panels in the chicken, combined with advanced back-crossing of the resistant and susceptible lines, we sought to refine the SAL1 locus and identify potential positional candidate genes. Using a 6th generation backcross mapping population, we have confirmed and refined the SAL1 locus as lying between 54.0 and 54.8 Mb on the long arm of Chromosome 5 (F = 8.72, P = 0.00475). This region spans 14 genes, including two very striking functional candidates; CD27-binding protein (Siva) and the RAC -alpha serine/threonine protein kinase homolog, AKT1 (protein kinase B, PKB). [source]


Prevalence of Cysticercus bovis in Australian cattle

AUSTRALIAN VETERINARY JOURNAL, Issue 7 2010
BHG Pearse
Objective The first national abattoir survey of Cysticercus bovis (,beef measles') in cattle was conducted in February 2008. Methods During the data collection period, 493,316 cattle were subjected to standard postmortem procedures, including incision of the masseter and heart muscles. On-site veterinarians were asked to record the location of any C. bovis cysts, as well as the National Livestock Identification System ear tag numbers of infected animals. Veterinarians were asked to submit samples for laboratory confirmation by histology and polymerase chain reaction testing. Results Of the 23 samples submitted, none was positive for C. bovis by either diagnostic method. Conclusions Occasional, isolated diagnoses of beef measles are still made in most states of Australia, but since the last regional surveys were conducted 30 years ago, when the estimated prevalence was 50 to 200 per 100,000 cattle slaughtered, the parasite has become extremely rare. [source]


Neospora caninum infections in Australia and New Zealand

AUSTRALIAN VETERINARY JOURNAL, Issue 4 2000
MP REICHEL
Objective To review the current state of knowledge of Neospora caninum infections with particular reference to Australia and New Zealand. Procedure Several databases were searched electronically including Medline, Current Contents, Vet CD using several Key words (Neospora caninum, neosporosis, abortion, cattle, dogs) and authors names. References in original articles were also traced and use made of the author's own original research in the field. ConclusionN caninum is recognised worldwide and is also widespread, in particular in dairy cattle, in Australia and New Zealand. It has been reported in both countries retrospectively (in dogs) from the early 1970s. Abortion storms in dairy herds appear to be the most common feature. Recent reports indicate that the dog is the definitive host, in which the sexual cyle is completed. Further studies are however required to establish important aspects of the epidemiology, such as mode of transmission. In the absence of an effective vaccine, the most effective control strategy is selective culling of infected animals and the prevention of access of dogs to expelled placentas and foetuses and, possibly, to raw beef. [source]


Transient Peripheral Immune Response and Central Nervous System Leaky Compartmentalization in a Viral Model for Multiple Sclerosis

BRAIN PATHOLOGY, Issue 5 2010
María José Navarrete-Talloni
Abstract Theiler's virus-induced demyelination represents an important animal model to study the chronic-progressive form of multiple sclerosis (MS). The aim of the present study was to identify specific genes and pathways in the deep cervical lymph node (cLN) and spleen of experimentally infected SJL-mice, using DNA microarrays. Analyses identified 387 genes in the deep cLN and only 6 genes in the spleen of infected animals. The lymph node presented 27.4% of genes with fold changes ±1.5 at 14 days post infection (dpi) and a reduced transcription at later time points. K- means clustering analyses resulted in five clusters. Accordingly, functional annotation revealed that the B-cell immune response pathway was the most up-regulated cluster at the early phase. Additionally, an increase of CD68- and lysozyme-positive cells in the deep cLN was observed by immunohistochemistry. Polioencephalitis was most intense at 14 dpi, and the spinal cord demyelinating leukomyelitis started at 42 dpi. In summary, early gene expression is indicative of virus-trigged immune responses in the central nervous system (CNS)-draining lymph node. The decreased gene transcription in the deep cLN during the chronic phase and the low number of spleen genes supports the hypothesis of a compartmentalized inflammation within the CNS, as described in progressive MS. [source]


Differential regulation of nitric oxide synthase isoforms in experimental acute Chagasic cardiomyopathy

CLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 1 2000
B. Chandrasekar
We have previously demonstrated induction and high level expression of IL-1,, IL-6 and tumour necrosis factor-alpha in the myocardium during the acute stage of experimental Trypanosoma cruzi infection (Chagas' disease). The myocardial depressive effects of these cytokines are mediated in part by the induction of nitric oxide synthase (NOS), production of nitric oxide (NO) and formation of peroxynitrite. In this study we investigated the expression, activity and localization of NOS isoforms, and the levels of NO, malondialdehyde (a measure of oxidative stress), and peroxynitrite in rats at 1·5, 5, 10 and 15 days after infection with T. cruzi trypomastigotes. The myocardial inflammatory infiltrate and number of amastigote nests increased over the course of infection. A significant increase in tissue nitrate + nitrite levels, NOS2 mRNA, and NOS2 enzyme activity was observed at all time points in the infected compared with uninfected animals. The enzyme activity of constitutive NOS, tissue malondialdehyde levels, and NOS3 mRNA levels was only transiently increased after infection. The protein levels of the NOS isoforms paralleled their mRNA expression. While no positive nitrotyrosine immunoreactivity was detected in control myocardium, its levels increased in infected animals over time. Thus, by 1·5 days post-infection, when no parasite or immune cell infiltration could be detected, the myocardium expressed high levels of NOS and NO metabolites. Nevertheless, the early production of NO in the myocardium was not sufficient to clear the parasites. [source]