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PubMed1970

Antiviral activity of chlorite-oxidized oxyamylose, a polyacetal carboxylic acid.

Intraperitoneal injection of chlorite-oxidized oxyamylose (COAM) protected mice against mengo, vaccinia, Semliki Forest, and influenza APR8 viruses. Topical administration in the eye of rabbits partially inhibited the development of experimental herpetic keratoconjunctivitis. COAM resembled polyacrylic acid in many aspects, but it was markedly less toxic. For systemic administration, the therapeutic index was on the order of magnitude of 1:300 to 1:500. Although the in vivo antiviral effect of COAM wore off faster than that of polyacrylic acid, protection lasted for several weeks. Against mengovirus, such prolonged protection was achieved only when polymer and virus were injected intraperitoneally. Protection against intravenous vaccinia virus was not dependent on the injection route of COAM. Experiments on the mode of action of COAM pointed to macrophages as possible mediators of the antiviral effect. The fact that small amounts of interferon appeared in the serum after administration of high doses of COAM suggests that interferon may play a role in the induction of antiviral resistance by COAM.

Acids↗

PubMed1969

Mouse virulence of K(L) antigen-containing strains of Escherichia coli.

The mouse virulence of two K antigen-containing (L variety) strains of Escherichia coli (serotype O2:K1) isolated from human septicemia, and of their variants which lacked K antigen, was studied. The strains containing envelope antigen (K+) were highly virulent when injected intracerebrally or when suspended in mucin and injected intraperitoneally. After intraperitoneal injection of E-107 K+ (but not K-), there was a marked initial growth in the peritoneal cavity followed by bacteremia and infection of all the organs examined. In the mucin-enhanced lethal infection, this growth continued until death of the animal; in the nonlethal infection, growth ceased and the count dropped quickly after approximately 5 hr. Host defenses were depressed greatly by intraperitoneally, but not intravenously, administered mucin. Bacteria were most virulent when injected intraperitoneally. In vitro phagocytosis of the K+ bacteria required opsonins not needed for phagocytosis of the smooth K- variants. Opsonins were found in immunized rabbit and normal mouse sera. Immune rabbit sera contained antibodies with anti-K specificity which were opsonic in vitro and highly protective in vivo when administered passively. There appears to be a lesser anti-O opsonic and protective activity involving one of the strains (E-107 K+), and colonial morphology, agglutination, and absorption tests indicated a low amount of K antigen on this organism. No anti-O opsonic or protective activity could be shown involving the other strain (E-102 K+). When standard serological typing procedures were used, these two strains appeared to be identical serologically, but they differed greatly in sensitivity to immune rabbit serum in phagocytosis experiments in vitro.

Agglutination Tests↗

PubMed2001

Systemic administration of phenyl-N-tert-butylnitrone protects the retina from light damage.

PURPOSE: This study was conducted to test the hypothesis that phenyl-N-tert-butylnitrone (PBN), a spin-trapping agent known to cross the blood-brain barrier and protect the brain from ischemia-reperfusion injury, is incorporated into the retina after intraperitoneal injection and protects photoreceptor cells from the damaging effects of constant visible light. METHODS: Albino rats were injected intraperitoneally with PBN (aqueous solution) or water, or were not injected, and then were placed in constant light (2700 lux) for 24 hours. The incorporation of PBN into the retina was determined by high-performance liquid chromatography. Electroretinograms (ERGs) were recorded before light treatment and 1 and 15 days after the cessation of exposure to constant light. Eyes were taken for histology at each time point and outer nuclear layer (ONL) thickness determined. RESULTS: PBN was incorporated into the retina after intraperitoneal injection. Both control (water-injected and uninjected) groups exposed to constant light maintained only 28% of ONL thickness and 20% of retinal function, compared with the unexposed control group. In contrast, the PBN-treated animals maintained 80% of ONL thickness and exhibited 87% of retinal function. CONCLUSIONS: PBN protects the albino rat retina from the damaging effects of constant light stress. That light-induced and hereditary retinal degenerations share certain morphologic hallmarks and follow a similar apoptotic mechanism of degeneration raises the possibility of pharmacologic therapy for hereditary and environmentally induced neurodegenerative disorders.

Animals↗

PubMed1984

[Possibility of N-dimethylnitrosamine formation after parenteral administration of amidopyrine and nitrite to rats].

The intravenous or intraperitoneal injection of amidopyrine and sodium nitrite to rats induces liver necrosis caused by endogenic synthesis of carcinogenic N-nitrosodimethylamine (NDMA). Ascorbic acid, which inhibits this synthesis when injected intravenously, phenobarbital, which is an inductor of enzymatic decomposition when injected intraperitoneally, prevented the formation of necrosis.

Aminopyrine↗

PubMed1987

Hypothermia induced by baclofen, a possible index of GABAB receptor function in mice, is enhanced by antidepressant drugs and ECS.

1 Intraperitoneal injection to mice of the gamma-aminobutyric acidB (GABAB) receptor agonist (+/-)-baclofen induces a dose-dependent decrease in rectal temperature. 2 Injection of (-)-baclofen intracerebroventricularly at doses that had no effect when given peripherally induced a marked hypothermia. (+)-Baclofen was without effect. 3 The decrease in rectal temperature induced by (-)-baclofen when injected intraperitoneally was highly correlated with an increase in sedation. 4 Repeated administration of amitriptyline (10 mg kg-1 daily for 14 days) resulted in mice displaying an enhanced temperature and sedation response to injection of (+/-)-baclofen (5 mg kg-1) 24 h after the last dose of antidepressant. 5 An enhanced hypothermic response was also seen following repeated administration of zimeldine, mianserin or desipramine (all 10 mg kg-1 daily for 14 days) or repeated electroconvulsive shock (ECS; 5 ECS over 10 days) 24 h after the last treatment. 6 A single administration of any of the antidepressant drugs or ECS or repeated administration of the anxiolytic drug flurazepam (20 mg kg-1 daily for 14 days) did not alter the baclofen-induced hypothermic response. 7 Administration of (+/-)-baclofen (5 mg kg-1) daily for 5 or 14 days attenuated the baclofen-induced hypothermic response. However, one pretreatment dose did not alter the response. 8 It has previously been reported that repeated baclofen administration decreases GABAB receptor number in the brain while repeated administration of antidepressant drugs and ECS increases the density of this receptor. The current data therefore suggest that baclofen-induced hypothermia may provide a simple index of GABAB receptor function in the brain and strengthens the evidence that GABAB receptor function is enhanced by antidepressant drugs and ECS.

5,7-Dihydroxytryptamine↗

PubMed1998

Intraventricular administration of BDNF increases the number of newly generated neurons in the adult olfactory bulb.

We have previously demonstrated that the most rostral part of the subventricular zone (SVZ) is a source of neuronal progenitor cells whose progeny are destined to become interneurons of the olfactory bulb. To determine whether the number of newly generated neurons in the adult olfactory bulb could be increased by the administration of an exogenous factor, brain-derived neurotrophic factor (BDNF) was infused for 12 days into the right lateral ventricle of adult rat brains. The production of new cells was monitored by either the intraventricular infusion or intraperitoneal injection of the cell proliferation marker BrdU. In both experimental paradigms we observed significantly more BrdU-labeled cells in the olfactory bulbs on the BDNF-infused side than in the olfactory bulb of PBS-infused animals. Analysis of the BDNF-infused brains of animals injected intraperitoneally with BrdU demonstrated a 100% increase in the number of BrdU-labeled cells in the bulb, the preponderance ( approximately 90%) of which were double-labeled with a neuron-specific antibody. These results demonstrate that the generation and/or survival of new neurons in the adult brain can be increased substantially by an exogenous factor. Furthermore, the SVZ, and in particular the rostral part, may constitute a reserve pool of progenitor cells available for neuronal replacement in the diseased or damaged brain.

Animals↗

PubMed2001

The inhibition of nitric oxide synthase suppresses LPS- and psychological-stress-induced fever in rats.

The purpose of this study was to assess the effects of a non-selective nitric oxide synthase (NOS) inhibitor on changes in fever response due to injection of lipopolysaccharide (LPS) or on stress fever caused by exposure to an open field in freely moving biotelemetered rats. N(omega)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of all NOS-isoforms, was injected intraperitoneally (ip) at a dose of 50 mg/kg just before intraperitoneal injection of LPS at a dose of 50 microg/kg or exposure to open field. L-NAME at a dose of 50 mg/kg had no effect on normal day-time body temperature (T(b)) and normal night-time T(b). The same dose of L-NAME administered intraperitoneally caused a significant attenuation of LPS-induced fever. The thermal index calculated for rats pretreated with L-NAME and injected with LPS was reduced by approximately 75% compared to that calculated for saline-pretreated and LPS-injected rats. To examine the effect of NOS inhibition on psychological-stress-induced elevation in T(b), rats were injected intraperitoneally with L-NAME and then immediately exposed to open field for 60 min. After exposure to the open field, rats not treated with NOS inhibitor responded with a rapid rise in T(b), and it was accompanied with an increase of motor activity. L-NAME significantly suppressed the stress fever without any effect on changes in motor activity. Presented data provide clear evidence that NO formation is involved in LPS- and psychological-stress-induced fevers in rats.

Animals↗

PubMed1991

No effect of recombinant human interleukin-1 on numbers of peripheral blood and peritoneal leukocytes during acute inflammation.

Recombinant human interleukin-1 (IL-1) can prolong the survival of mice with severe systemic bacterial or fungal infections. In order to assess whether this is due to an effect of IL-1 on the production of leukocytes or their migration to the site of infection, the influence of IL-1 on the influx of leukocytes to the site of an acute inflammation was studied in normal and in granulocytopenic mice. The numbers of granulocytes, lymphocytes, and monocytes or macrophages in both the circulation and the peritoneal cavity were determined during an acute sterile inflammation elicited by intraperitoneal injection of either newborn calf serum (NBCS) or heat-killed Candida albicans, and during a peritoneal infection with viable C. albicans. After normal mice were injected intraperitoneally with NBCS or 10(7) CFU heat-killed or viable C. albicans, the number of peritoneal granulocytes rose sharply within 6 h. Pretreatment of mice with a single intraperitoneal dose of 80 ng IL-1 24 h before injection of an inflammatory stimulus did not influence the course of the numbers of leukocytes in the circulation or in the peritoneal cavity. When mice were rendered granulocytopenic by cyclophosphamide, both the influx of granulocytes into the peritoneal cavity and the concomitant rise in the number of peripheral blood granulocytes after injection of NBCS, killed or viable C. albicans was virtually absent. Pretreatment of granulocytopenic mice with IL-1 did not influence the course of the numbers of leukocytes in either the circulation or the peritoneal cavity. These findings show that the beneficial effect of a single dose of IL-1 on the course of candidal infections in normal or granulocytopenic mice is not attributable to the influx of granulocytes or monocytes.

Acute Disease↗

PubMed1998

Vagotomy blocks the induction of interleukin-1beta (IL-1beta) mRNA in the brain of rats in response to systemic IL-1beta.

There is considerable interest in the mechanisms by which systemic cytokines signal the CNS to elicit centrally controlled biological actions. This study determined the effects of intraperitoneal injections of interleukin-1beta (IL-1beta) on IL-1beta mRNA and IL-1 receptor accessory protein (IL-1RAP) mRNA production in rat liver and brain using the reverse transcription-PCR. Saline or IL-1beta (0.5 microg/kg) was injected intraperitoneally in subdiaphragmatically vagotomized and sham-operated (SHAM) rats. All injections were performed at dark onset, and rats were killed 2 hr after the injection. In SHAM rats, IL-1beta increased IL-1beta mRNA levels in the liver, hypothalamus, hippocampus, and brainstem. Subdiaphragmatic vagotomy blocked the IL-1beta-induced increase in IL-1beta mRNA in the brainstem and hippocampus and significantly attenuated the increase in the hypothalamus. Vagotomy did not affect IL-1beta-induced IL-1beta mRNA production in the liver. IL-1RAP mRNA was highly expressed in each region examined; however, no significant differences in IL-1RAP mRNA production were found in any region after IL-1beta injection. The current results indicate that the vagus nerve is involved in transmitting cytokine signals to the brain and suggest that the induction of brain cytokines is a critical step in the pathway by which vagal-mediated signals result in centrally controlled symptoms of the acute phase response.

Animals↗

PubMed2002

Inhibition of nitric oxide synthase aggravates cisplatin-induced nephrotoxicity: effect of 2-amino-4-methylpyridine.

BACKGROUND: Nitric oxide (NO) has been shown to play a role in maintaining normal renal function. However, the role of NO in cisplatin (CDDP)-induced nephrotoxicity is still unclear. The aim of the present work was to examine the effect of the NO synthase (NOS) inhibitor, 2-amino-4-methylpyridine, on the severity of CDDP-induced nephrotoxicity. METHODS: Male Wistar rats were divided into six groups. Three control groups received plain drinking water or water containing 1.5% L-arginine. One of the two groups receiving plain water was treated with an intraperitoneal injection of 2-amino-4-methylpyridine (1 mg/kg in normal saline), and the other two control groups were injected intraperitoneally with normal saline. Another three groups were treated in the same manner and injected with CDDP (6 mg/kg, i.p.). CDDP was injected 1 h after 2-amino-4-methylpyridine treatment. Rats were sacrificed 7 days after CDDP treatment, and serum as well as kidneys were isolated and analysed. RESULTS: CDDP-treated rats showed increases in the kidney weight as a percentage of the total body weight and serum creatinine and urea levels and decreases in serum albumin and calcium levels. Also, CDDP treatment induced reductions in the kidney total nitrate/nitrite (NO(x)), reduced glutathione (GSH) and glutathione peroxidase activity (GSH-Px) levels and an increase in the kidney malondialdehyde (MDA) production level. In contrast, 2-amino-4-methylpyridine treatment 1 h prior to CDDP injection induced marked exacerbation of CDDP-induced nephrotoxicity, as manifested by severe aggravation of the indices of nephrotoxicity. Also, 2-amino-4-methylpyridine plus CDDP-treated rats showed exaggeration of the reduction in the kidney total NO(x) content and GSH-Px activity and elevation of the kidney platinum accumulation level with normalization of the kidney MDA production level and rebound in the kidney GSH content. Histopathologically, CDDP-treated rats showed marked interstitial nephritis, tubular atrophy and tubular necrosis. However, treatment with 2-amino-4-methylpyridine 1 h prior to CDDP injection revealed marked exacerbation of CDDP-induced histopathological changes. CONCLUSIONS: The present findings suggest that NO plays a role in CDDP-induced nephrotoxicity. Administration of 2-amino-4-methylpyridine, an NOS inhibitor, exacerbates CDDP-induced nephrotoxicity.

Animals↗

PubMed1988

Changes in leucocyte numbers without diapedesis in rats given platelet-activating factor (PAF-acether).

Changes occurring in the blood and the peritoneal cavity following the intraperitoneal injection of platelet-activating factor (PAF-acether) into rats were compared with those when antigen was injected intraperitoneally into actively sensitised rats. A blood eosinophilia had been produced in the rats by an intravenous injection of Sephadex G200 6 days before either challenge. 5 min after PAF-acether, the total number of cells in the peritoneal washings had decreased and the concentration of extravasated dye-labelled plasma protein had increased with no change in histamine levels. On the other hand, antigen at this time produced nor only a decrease in cells and an increase in dye but also an increase in histamine concentration. Only antigen produced a cellular infiltration into the peritoneal cavity with an increase in numbers of neutrophils in the peritoneal washings at 4 h and of mononuclear cells and eosinophils at 24 h. In the blood at 4 h after either challenge, there was a neutrophilia and an eosinopenia. When PAF-acether and antigen were injected together into actively sensitised rats, leucocyte counts in the peritoneal washings increased by a similar amount, both at 4 and 24 h, as those in rats given antigen alone.

Animals↗

PubMed1993

Role of hypothalamic interleukin-6 and tumor necrosis factor-alpha in LPS fever in rat.

The purpose of this study was to determine, using push-pull perfusion, the levels of interleukin (IL)-1-like, IL-6-like, and tumor necrosis factor-alpha (TNF)-like activity in the anterior hypothalamus during lipopolysaccharide (LPS)-induced fever in rats. Additionally, slow anterior hypothalamic infusions of human recombinant IL-6 (hrIL-6) or TNF (hrTNF) for several hours were performed to determine possible febrile effects of these two cytokines. Artificial cerebrospinal fluid (aCSF) was infused as a control. Samples of cerebrospinal fluid were collected 60 min before and 60, 180, 300, and 420 min after the intraperitoneal injection of LPS. A control group was injected intraperitoneally with saline. The core temperature (measured by biotelemetry) of LPS-injected rats was significantly higher (P < 0.05) than the temperature of the rats injected with saline at 180, 300, and 420 min after the injection. The average postinjection IL-6 levels were significantly higher (P < 0.05) in the LPS-injected group. TNF was significantly higher (P < 0.05) than the baseline only at 180 min. There were no changes in levels of IL-1-like activity. Infusion of hrIL-6 at a level similar to the peak IL-6 level measured during LPS-induced fever resulted in a slowly developing and long-lasting increase in core temperature. Infusion of hrTNF at a level corresponding to the peak TNF level measured during LPS-induced fever did not induce a significant increase in core temperature. These results support the hypothesis that elevated hypothalamic concentrations of IL-6 are involved in the induction of fever elicited by peripheral (intraperitoneal) injection of LPS.

Animals↗

PubMed1988

Enhancement of natural killer cell activity and interferon production by manganese in young mice.

The effect that MnCl2 has on murine splenic natural killer (NK) cell activity was investigated in infant (10 days old), pre-weanling (18 days old) and weanling (24 days old) C57BL/6J mice. A single intraperitoneal injection of 10, 20 or 40 micrograms MnCl2/g body weight caused a significant enhancement in NK activity, as determined by the in vitro 51Cr release assay. Comparable enhancement of NK activity was observed for age-matched mice injected intraperitoneally with polyinosinic polycytidylic acid (Poly I:C). Both MnCl2 and Poly I:C caused elevations in serum interferon levels. Time-course studies revealed that interferon levels returned to normal within 48 hours following injection with either MnCl2 or Poly I:C; however enhanced NK activity persisted for up to 48 hours in Poly I:C-injected mice and 72 hours in MnCl2-injected mice. The administration of rabbit anti-asialo GMl to MnCl2-injected mice completely abrogated the enhanced NK activity. In addition, the injection of rabbit anti-mouse interferon alpha, beta but not gamma completely abrogated the enhanced NK activity. In addition, the injection of rabbit anti-mouse interferon alpha, beta but not gamma completely abrogated the enhancement of NK activity by MnCl2 and to a lesser extent the enhancement of NK activity by Poly I:C. These results indicate that despite low levels of NK activity in pre-weanling mice, MnCl2 is capable of enhancing this activity by 8-9 fold. Furthermore, Mn-enhanced NK activity in these young mice appears to be mediated by the production of interferon alpha, beta.

Animals↗

PubMed2005

Lipopolysaccharide-induced elevation and secretion of interleukin-1beta in the submandibular gland of male mice.

The intraperitoneal injection of lipopolysaccharide (LPS) (400 microg/kg body weight) induced the expression of mRNAs of inflammatory cytokines such as interleukin (IL)-1beta, IL-6 and tumour necrosis factor (TNF)-alpha in the submandibular gland (SMG) of C3H/HeN mice but not that of C3H/HeJ mice, a mutant strain for Toll-like receptor-4 (TLR-4(-) mutant). The mRNA levels of these cytokines in the SMG of the wild-type mice increased as early as 3 hr after injection, peaked at 3-6 hr, and had decreased again by 24 hr. In this study, we particularly focused on IL-1beta, and induction by this endotoxin was investigated in detail. Denervation of the superior cervical trunk and chorda tympani nerve did not diminish the LPS-induced elevation of IL-1beta mRNA in the SMG, indicating the irrelevance of the central nervous system in this induction. TLR-4 mRNA and protein were shown to be strongly expressed in the SMG, suggesting the direct action of LPS on this gland. IL-1beta proteins were localized in the secretory granules of granular convoluted tubular (GCT) cells, and their molecular weights in the gland were 17.5 and 20 kDa. IL-1beta of the same size appeared in the saliva 6 hr after LPS injection in C3H/HeN but not in C3H/HeJ mice. The present study thus suggests that IL-1beta, an inflammation cytokine, is induced and secreted into the saliva in response to endotoxin injected intraperitoneally.

Animals↗

PubMed1995

Effect of oleanolic acid on complement in adjuvant- and carrageenan-induced inflammation in rats.

The present work was aimed at evaluating the influence of oleanolic acid on complement-related inflammation. In adjuvant-induced arthritis and carrageenan-induced paw oedema in rats, oleanolic acid was found to possess significant anti-inflammatory and complement-inhibitory activities. The intraperitoneal injection of oleanolic acid (60 mg kg-1, twice a day), before and after Freund's Complete Adjuvant challenge and thereafter repeated for several days, significantly reduced foot-pad thickness of experimental animal models and simultaneously reduced complement activity. Oleanolic acid also produced marked reduction in complement levels and inflammatory effects on carrageenan-induced paw oedema in rats when injected intraperitoneally (60 mg kg-1, twice a day).

Animals↗

PubMed1975

[Effects of staphylococcal leucocidin in mice (author's transl)].

After intraperitoneal injections of mice with paraffin-oil and sodium caseinate the numbers of macrophages and granulocytes increased respectively as well in their peritoneal exsudate as in their blood. On the other hand, cyclophosphamide markedly decreased the numbers of leucocytes. All mice were more susceptibel to infections with leucocidin (PVL-R)-positive staphylococci than to those with leucodidin-negative staphylococci of comparable hemolytic properties. Generally, mice with increased numbers of leucocytes were relatively more resistant to the staphylococcal infections. Concentrated PVL-R-leucocidin injected intraperitoneally into mice caused a temporary decrease in the number of leucocytes, especially granulocytes and their phagocytic activity.

Animals↗

PubMed2006

In vivo administration of D609 leads to protection of subsequently isolated gerbil brain mitochondria subjected to in vitro oxidative stress induced by amyloid beta-peptide and other oxidative stressors: relevance to Alzheimer's disease and other oxidative stress-related neurodegenerative disorders.

Tricyclodecan-9-yl-xanthogenate (D609) has in vivo and in vitro antioxidant properties. D609 mimics glutathione (GSH) and has a free thiol group, which upon oxidation forms a disulfide. The resulting dixanthate is a substrate for glutathione reductase, regenerating D609. Recent studies have also shown that D609 protects brain in vivo and neuronal cultures in vitro against the potential Alzheimer's disease (AD) causative factor, Abeta(1-42)-induced oxidative stress and cytotoxicity. Mitochondria are important organelles with both pro- and antiapoptotic factor proteins. The present study was undertaken to test the hypothesis that intraperitoneal injection of D609 would provide neuroprotection against free radical-induced, mitochondria-mediated apoptosis in vitro. Brain mitochondria were isolated from gerbils 1 h post injection intraperitoneally (ip) with D609 and subsequently treated in vitro with the oxidants Fe(2+)/H(2)O(2) (hydroxyl free radicals), 2,2-azobis-(2-amidinopropane) dihydrochloride (AAPH, alkoxyl and peroxyl free radicals), and AD-relevant amyloid beta-peptide 1-42 [Abeta(1-42)]. Brain mitochondria isolated from the gerbils previously injected ip with D609 and subjected to these oxidative stress inducers, in vitro, showed significant reduction in levels of protein carbonyls, protein-bound hydroxynonenal [a lipid peroxidation product], 3-nitrotyrosine, and cytochrome c release compared to oxidant-treated brain mitochondria isolated from saline-injected gerbils. D609 treatment significantly maintains the GSH/GSSG ratio in oxidant-treated mitochondria. Increased activity of glutathione S-transferase, glutathione peroxidase, and glutathione reductase in brain isolated from D609-injected gerbils is consistent with the notion that D609 acts like GSH. These antiapoptotic findings are discussed with reference to the potential use of this brain-accessible glutathione mimetic in the treatment of oxidative stress-related neurodegenerative disorders, including AD.

Alzheimer Disease↗

PubMed1997

Specific and long-lasting suppression of rat adjuvant arthritis by low-dose Mycobacterium butyricum.

We have tested the therapeutic effect of intraperitoneal injections of Mycobacterium butyricum on the development of adjuvant arthritis in rats and we have explored the specificity and the duration of effectivity of this treatment. Rats with induced arthritis were injected intraperitoneally with the causative antigen, Mycobacterium butyricum, at concentrations 10 times lower than the inducing one, on the 3rd and 10th day after arthritis induction. The severity of the disease was assessed on the basis of physical (arthritis index, paw swelling) and biochemical (serum interleukin-6) parameters. The treatment with Mycobacterium butyricum led to a significant suppression of adjuvant-induced arthritis. This therapeutic effect was both antigen-specific, because intraperitoneal aspecific inflammation did not prevent the disease, and long-lasting. The results obtained in this model confirm the possibility of modulating the autoimmune process even when the immunological response is already triggered, suggesting new therapeutic strategies, more suitable than preventive vaccination, in human autoimmune diseases.

Animals↗