Disease relevance of Acute Disease

• In this report we show that lupus-prone NZB x NZW F(1) mice given three injections of anti-CD137 (4-1BB) mAb's between 26 and 35 weeks of age reversed acute disease, blocked chronic disease, and extended the mice's lifespan from 10 months to more than 2 years [1].
• Anti-CD154 antibody treatment at either the peak of acute disease or during remission effectively blocked clinical disease progression and CNS inflammation [2].
• An inherited deficiency of porphobilinogen deaminase [porphobilinogen ammonia-lyase (polymerizing), EC 4.3.1.8] in humans is responsible for the autosomal dominant disease acute intermittent porphyria [3].
• CRP treatment of NZB/NZW mice during acute disease rapidly decreased proteinuria, and the treated mice remained aproteinuric for at least 10 weeks [4].
• Both of these cause acute disease (whooping cough), whereas their progenitor, B. bronchiseptica, is of variable virulence in a wide variety of animals [5].

High impact information on Acute Disease

• Effect of acute disease and ACTH on serum zinc proteins [6].
• In the absence of IL-2, the acute disease is mild because of reduced T cell effector function, but a chronic and progressive disease develops late and is associated with a failure to generate FoxP3(+) regulatory T (T reg) cells in the periphery [7].
• Furthermore, induction of tolerance to intact PLP (which inhibits responses to both the initiating PLP139-151 epitope and to the PLP178-191 epitope) after the acute disease episode is sufficient to prevent relapsing disease [8].
• These experiments demonstrate that IL-10 is produced during infection with a protozoan parasite and suggest a regulatory role for this cytokine in the mediation of susceptibility to acute disease [9].
• In all individuals tested, IL-10 mRNA production was increased in lymph nodes taken during acute disease over that observed in postacute samples [10].

Chemical compound and disease context of Acute Disease

• More importantly, induction of myelin-specific tolerance to relapse-associated epitopes, by i.v. injection of ethylene carbodiimide-fixed peptide-pulsed APCs, either before disease initiation or during remission from acute disease effectively blocks the expression of the initial disease relapse [11].
• Bactericidal faecal concentrations were present in all patients with acute disease receiving oral or intravenous metronidazole, and all responded to therapy [12].
• In contrast to findings in acute diseases associated with muscle wasting, we found increased muscle glutamine (GLN) levels in our patient group (mean +/- SEM = 10,782 +/- 770 versus 7,844 +/- 293 micromol/kg wet weight, p < 0. 01) [13].
• A virus with a threonine-to-valine substitution (T81V) did not cause any changes in the pattern or extent of disease seen in mice, whereas a virus with a tryptophan substitution at this position (T81W) produced a similar acute disease but was attenuated for the development of the chronic disease [14].
• Furthermore, malaria recrudesced in Nu/Nu mice after the termination of acute disease by treatment with clindamycin [15].

Biological context of Acute Disease

• These results indicate that myosin-specific autoimmunity, while a potentially important inflammatory mechanism in acute and chronic T. cruzi infection, is not essential for inflammation in acute disease [16].
• In vivo administration of recombinant IFN-gamma induces macrophage activation, and prevents acute disease, immune suppression, and death in experimental Trypanosoma cruzi infections [17].
• A diabetic syndrome closely resembling human IDDM has been induced in rats of specific pathogen-free origin by a combination of thymectomy and irradiation, with an overall incidence (10 wk postirradiation) in female rats of 34% for acute disease and 47% for islet lesions [18].
• We investigated the role of p53 in the apoptosis of BM cells (BMC) during the development of acute disease and found that at least one copy of the p53 gene is necessary for depletion of BM and subsequent lethality in host animals [19].
• While immunization with WT spinal cord homogenate (SCH) resulted in a progressive EAE phenotype, MOG(-/-) SCH induced a mild self-limiting acute disease [20].

Anatomical context of Acute Disease

• To determine the immunopathogenesis of the persistent symptoms of patients with eosinophilia-myalgia syndrome (EMS) induced by L-tryptophan, we performed immunocytochemical studies on 10 muscle and fascia biopsy specimens obtained during the acute disease and the chronic persistent connective tissue sclerosis [21].
• We conclude that during acute disease the steroidogenic capacity selectively increases in the zones that secrete cortisol and DHEAS (only in infants < 3 months) but not in the zona glomerulosa that secretes aldosterone [22].
• To examine steroidogenic responses of the different zones of the adrenal cortex to acute disease we determined the basal and adrenocorticotropin (ACTH)-stimulated levels of cortisol, dehydroepiandrosterone (DHEAS) and aldosterone in 16 infants aged 1-4 months with acute bronchiolitis [22].
• Significant differences between normal and diseased conjunctiva were found for TGF-beta and for proliferating cells, which were both increased in the acute disease group [23].
• Although there were some variations in the levels of monokine release, macrophages of patients with acute disease secreted significantly higher spontaneous levels of TNF alpha than did a nonfarming control group (p = 0.0002) [24].

Gene context of Acute Disease

• To address whether additional oncogenic events are required for progression to acute disease, we crossed hMRP8p210BCR/ABL mice to apoptosis-resistant hMRP8BCL-2 mice [25].
• In contrast, uPAR-/- mice had a delayed, less acute disease reflected in delayed infiltration of inflammatory cells [26].
• In contrast, a substantial level of monocyte chemotactic protein (MCP)-1 expression was not observed until late in acute disease and continued to be evident in the relapsing phase of the disease [27].
• The best correlation with acute disease activity was given by TNF-alpha, IL-6, IL-8, and LTB4 [28].
• In a study designed to evaluate the concept of inherited susceptibility to sarcoid arthritis (SA), 42 patients with histologically proved acute disease underwent typing of HLA-A, -B, -C and -DR antigens [29].

Analytical, diagnostic and therapeutic context of Acute Disease

• In the five patients who survived the acute disease and underwent plasma exchange (three with HUS and two with chronic relapsing TTP), subunits and fragments returned to normal values, and supranormal multimers were no longer detected in plasma [30].
• The new ELISA test with p22 may therefore have a useful diagnostic role in acute disease [31].
• METHODS: A cross-sectional analysis of 308 consecutive Type 2 diabetic patients (mean age 66+/-11.3 years) previously treated with metformin on an outpatient basis and admitted to a German general hospital during the period from 1 January 1995 to 31 May 1998 because of acute disease or in order to optimize their diabetes management [32].

References