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PubMed1992

Cotrimoxazole therapy of Toxoplasma gondii encephalitis in AIDS patients.

Twenty-four consecutive HIV-positive patients affected by Toxoplasma gondii encephalitis received trimethoprim-sulfamethoxazole (cotrimoxazole) as acute-phase treatment. Two dosage regimens of cotrimoxazole were used: 40 mg/kg/day (12 patients) or 120 mg/kg/day (12 patients) of total compound (trimethoprim plus sulfamethoxazole). Clinical and radiological responses to treatment were evaluated, and the product-limit method for survival data analysis was used. Eighteen of 24 patients showed both a clinical and radiological response (75% response rate). There were no differences in response rates between patients receiving the two dosage regimens of cotrimoxazole. Adverse reaction consisted of leukopenia (two cases) and skin rash (three cases) which led to the discontinuation of the drug in one case. These results suggest that a randomized, controlled clinical trial should be carried out comparing cotrimoxazole versus sulfadiazine-pyrimethamine in AIDS patients with Toxoplasma gondii encephalitis.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Agarose gel filtration of concentrated fecal extracts containing virus-like particles associated with hepatitis A.

Virus-like particles shown to be associated with hepatitis A infection were recently visualized by immune electron microscopy in human and chimpanzee acute-phase fecal extracts. Agarose gel filtration of concentrated chimpanzee fecal extracts containing those 27-nm diameter particles separated more than 99% of the high molecular weight fecal impurities into two major peaks as determined by absorbance at 280 and 260 nm. The hepatitis A-associated particles were found between these two peaks by both immune electron microscopy and a new immunoradiometric assay.

Animals↗
PubMed2024

Systematic Proteome Profiling of Maternal Plasma for Development of Preeclampsia Biomarkers.

Preeclampsia (PE) is a hypertensive disorder of pregnancy with various clinical symptoms. However, traditional markers for the disease including high blood pressure and proteinuria are poor indicators of the related adverse outcomes. Here, we performed systematic proteome profiling of plasma samples obtained from pregnant women with PE to identify clinically effective diagnostic biomarkers. Proteome profiling was performed using TMT-based liquid chromatography-mass spectrometry (LC-MS/MS) followed by subsequent verification by multiple reaction monitoring (MRM) analysis on normal and PE maternal plasma samples. Functional annotations of differentially expressed proteins (DEPs) in PE were predicted using bioinformatic tools. The diagnostic accuracies of the biomarkers for PE were estimated according to the area under the receiver-operating characteristics curve (AUC). A total of 1307 proteins were identified, and 870 proteins of them were quantified from plasma samples. Significant differences were evident in 138 DEPs, including 71 upregulated DEPs and 67 downregulated DEPs in the PE group, compared with those in the control group. Upregulated proteins were significantly associated with biological processes including platelet degranulation, proteolysis, lipoprotein metabolism, and cholesterol efflux. Biological processes including blood coagulation and acute-phase response were enriched for down-regulated proteins. Of these, 40 proteins were subsequently validated in an independent cohort of 26 PE patients and 29 healthy controls. APOM, LCN2, and QSOX1 showed high diagnostic accuracies for PE detection (AUC >0.9 and p&#xa0;<&#xa0;0.001, for all) as validated by MRM and ELISA. Our data demonstrate that three plasma biomarkers, identified by systematic proteomic profiling, present a possibility for the assessment of PE, independent of the clinical characteristics of pregnant women.

Humans↗
PubMed1992

[The pathogenesis of psoriasis--new results].

A great deal of new immunological, biochemical, and cell biological information has been published on the pathogenesis of psoriasis. Many of these findings must be considered to be epi-phenomena of the inflammatory reaction (clinical correlate--erythema) and hyperproliferation of keratinocytes (scaling). The mechanisms of the psoriatic inflammatory reaction and of the specific neutrophil infiltration can now be more readily understood following the discovery of adhesion molecules, and the identification of new mediators--in particular NAP-1/IL-8. Proliferation-promoting factors for keratinocytes in vitro, that is, possible mediators of psoriatic scaling, are listed, and currently known changes in expression and concentration in psoriatic lesions are discussed.

Acute-Phase Proteins↗
PubMed1978

The in vitro interactions of rat pancreatic elastase and normal and inflammatory ray serum.

The partition of labelled rat pancreatic elastase (EC 3.4.21.11) between the different protease inhibitors of rat plasma was studied at different levels of saturation of the inhibitors of rat plasma was studied at different levels of saturation of the inhibitor capacity of plasma with the enzyme. The reaction mixtures were analysed by immunoelectrophoretic methods utilizing specific antisera against the different inhibitors and by gel filtration on Sephadex G-200. Rat serum was shown to contain four elastase binding proteins. alpha 1-antitrypsin, alpha 1-macroglobulin and alpha 2-acute phase protein and alpha 1-inhibitor 3 which exhibits immunologic cross-reaction with human inter-alpha-trypsin inhibitor and is of similar molecular weight. With minute amounts of labelled elastase the partition among the binding protein was alpha 1-macroglobulin 60%, alpha 1-antitrypsin 24% and alpha 1-I3 16%. The 60% value of alpha 1-M bound radioactivity in normal serum corresponds to the sum of alpha 1-M and alpha 2-AP labelling in inflammatory serum.

Acute-Phase Proteins↗
PubMed1979

Effect of human cord and postoperative serum on experimental inflammation in the rat.

Human cord and postoperative serum depressed the oedema provoked by mediators of the inflammatory reaction such as bradykinin, histamine, serotonin and prostaglandin E2 and also the experimental inflammation caused by carrageenin. Normal human and pregnancy serum did not have such an effect. In two cases of open neural tube defect, one of anencephaly and another of spina bifida, human amniotic fluid also had a strongly depressing effect on the experimental oedema provoked by serotonin. Human amniotic fluid from normal pregnancies did not inhibit this experimental inflammation. A protein-fraction of mol. wt 30,000--100,000 has been isolated from the inhibiting sera and shows the anti-inflammatory activity to be dose-related towards all the oedema-provoking substances used. Immunological studies showed that the inhibiting factor could be a protein in the pre-albuminic region, while alpha-foetoprotein did not appear to be responsible for the anti-inflammatory activity. Our conclusion is that human serum contains a protein of foetal origin with an acute-phase character and strong anti-inflammatory activities analogous to rat alpha 2-macrofoetoprotein.

Amniotic Fluid↗
PubMed1992

Evidence for lipopolysaccharide binding in human granulosa-luteal cells.

We investigated whether human granulosa-luteal (GL) cells exhibited lipopolysaccharide (LPS)-binding protein, and the response of follicular aspirate cells to LPS in vitro. Follicular aspirates taken from a human in-vitro fertilization and gamete intra-fallopian-tube transfer programme were subjected to Percoll gradients in order to isolate an enriched population of GL cells. GL cells exhibited specific LPS-binding protein, detected by autoradiography of the cellular lysate on SDS-PAGE after the cells were specifically labelled with a radioiodinated, photoactivable and reducible LPS derivative. LPS binding to the cells was also detected by the appearance of immunofluorescence associated with the cellular membrane when incubated with a fluorescent conjugated LPS receptor antibody. Ninety-four per cent of the cells exhibiting immunofluorescent LPS-binding protein were also positive for the steroidogenic enzyme 3 beta-hydroxysteroid dehydrogenase, as detected by cytochemistry. In order to detect a response to LPS, the enriched population of GL cells were cultured in vitro in the presence or absence of LPS; after 16 h of culture, tumour necrosis factor-alpha (TNF) mRNA was detected by reverse transcription-polymerase chain reaction and Southern blot analysis of the amplified cDNA. The expression of TNF mRNA was enhanced when the cells were cultured in the presence of LPS, which also significantly enhanced TNF secretion into the media during the 16-h period. These results reveal that GL cells exhibit LPS-binding protein and thus increased TNF secretion occurs in response to LPS in follicular aspirate cells. The source of ovarian TNF may be leukocytes, macrophages and/or GL cells.

3-Hydroxysteroid Dehydrogenases↗
PubMed1976

Conformational flexibility of the serum amyloid precursor SAA.

SAA is a normal acute-phase serum protein and is thought to be the precursor of amyloid protein AA which is deposited as insoluble beta-pleated sheet fibrils in secondary amyloidosis. Native SAA has a molecular weight of 160,000 and has not been isolated; it has been most frequently purified as a species (designated SAAL) of 12,500 mol. wt. by gel filtration in dissociating solutions. The conformational properties of SAA proteins in patients with and without amyloidosis have been compared in an effort to determine the factors involved in the induction of the beta-pleated sheet conformation in the amyloid SAA protein prior to fibril deposition. Amyloid and nonamyloid SAA proteins are similar in that they readily undergo conformational changes which result in the formation of heterogenous mol. wt. SAA species and in an increased exposure of antigenic determinants which cross-react with AA fibril proteins. Amyloid and nonamyloid SAA are different, however, in that amyloid SAA is more resistant to dissociation to SAAL. Amyloid SAAL, while similar to nonamyloid SAAL in immunoreactivity, shows a greater tendency toward aggregation. The relative resistance of both amyloid SAA and SAAL to complete dissociation may play an important role in amyloid fibril formation from these precursors.

Amyloid↗
PubMed1977

Acute-phase proteins from the liver and enzymes from myocardial infarction; a quantitative relationship.

In 14 patients with acute myocardial infarction (M.I.) not having any other disease, the possible quantitative relationship between enzymes from M.I. and changes in concentration of acute phase reactants coming from the liver were studied. The patients were followed up until 1 1/2 years after M.I. and comparison of baseline-protein values took place using a control group of 18 healthy individuals. Quantitation of protein changes was done by planimetric determination of the area under the concentration curve and by taking peak values. The myocardial infarction was quantitatively estimated by mathematical analysis of the time course of alpha-hydroxybutyrate dehydrogenase (alpha-HBDH) plasma concentrations and by taking peak values. A quantitative relationship with enzymatic infarct size was found for haptoglobin, alpha1-acid glycoprotein, alpha1-antitrypsin, C-reactive protein, fibrinogen and E.S.R. Albumin and transferrin did not show a negative quantitative relationship with enzymatic infarct size. Humoral factors originating from the site of tissue injury and evoking in proportion a positive acute phase reaction by the liver are probably the basis for this observed quantitative relationship.

Acute Disease↗
PubMed1992

Interleukin-6 and its receptor in autoimmunity.

Interleukin-6 (IL-6) is a multifunctional cytokine which acts on a wide variety of cells, regulating immune response, acute phase reaction and hematopoiesis. In accordance with its pleiotropic functions, IL-6 is indicated to be involved in the pathogenesis of several diseases including autoimmunities, lymphoid malignancies and inflammations. An elevated level of IL-6 is demonstrated in patients with rheumatoid arthritis and cardiac myxoma, which can explain symptoms of these diseases, such as autoantibody production and increase in acute phase proteins. Therefore, inhibitors of IL-6 production or IL-6 receptor-mediated signal transduction may be used for treatment of IL-6-related diseases. The IL-6 receptor system consists of two membrane proteins, a ligand-binding chain (IL-6R) and a non-ligand-binding signal transducer, gp130, both of which belong to the cytokine receptor family. Binding of IL-6 to IL-6R triggers the association of IL-6R and gp130, and gp130 in turn transduces the signal. A nuclear factor for controlling IL-6 gene expression (NF-IL6) is also involved in the transcriptional regulation of various acute-phase protein genes. IL-6-stimulation of hepatocytes, through modification of pre-existing NF-IL6 protein, leads to binding of NF-IL6 to IL-6-responsive elements and activation of acute-phase protein genes. NF-IL6 is shown to recognize the enhancer core sequence of several viruses, suggesting a possible relationship of virus infection and IL-6 expression.

Acute-Phase Proteins↗
PubMed2026

Saliva versus lesion swabs for PCR diagnosis of acute-phase clade Ib mpox in Uganda: a prospective matched hospital cohort study.

BACKGROUND: As clade Ib mpox expands through HIV-affected populations in east and central Africa, diagnostic specimen selection should balance accuracy, accessibility, and operational feasibility in outbreak settings. Here, we aimed to compare the diagnostic performance of matched plasma, saliva, genital, anal, and skin specimens during the acute rash phase of clade Ib mpox to identify clinically practical and high-yield sampling approaches for outbreak response and clinical care. METHODS: We conducted a prospective cohort study of 155 adults (median age 30 years, IQR 25-36) hospitalised at Uganda's national mpox referral hospital. The specimens were collected between March 3 and April 10, 2025, during the clade Ib outbreak. All participants were admitted with suspected mpox and were subsequently confirmed by MPXV PCR. We collected 836 clinical specimens (acid citrate dextrose plasma, saliva, genital swabs, anal swabs, and skin swabs) during the acute phase (visit 1; 14 days [SD 2] after systemic symptom onset) and at approximately 3 months (visit 2). A matched acute-phase subset (n=80) provided concurrent plasma, saliva, genital, and skin specimens for within-participant comparisons. MPXV DNA was quantified by F3L real-time quantitative PCR, and cycle threshold (Ct) values were compared using paired Wilcoxon signed-rank tests. Whole-genome sequencing of selected acute specimens confirmed clade assignment. FINDINGS: In the matched subset at visit 1, PCR positivity was high in saliva (78 [98%] of 80), skin swabs (78 [98%] of 80), and genital swabs (77 [96%] of 80). Results for the saliva closely mirrored genital and skin swab results, supporting saliva as a high-yield alternative when lesion sampling is painful, operationally difficult, or unacceptable. Plasma had substantially lower sensitivity (34 [43%] of 80) and showed poor agreement with mucocutaneous compartments. At 3 months, persistent MPXV DNA was rare (ten [9%] of 109) and clustered among people with HIV, including the only two participants with persistent plasma positivity. All sequenced genomes clustered within clade Ib. INTERPRETATION: During the established rash phase (14 days [SD 2] after onset), saliva provides diagnostic yield similar to that provided by lesion swabs for clade Ib mpox in this hospitalised cohort. These findings are restricted to this sampling window; further studies are needed to define performance in prodromal, pre-rash, and asymptomatic infection. FUNDING: CEPI through its Centralised Laboratory Network.

Adult↗
PubMed1978

Hepatitis "C" antigen in non-A, non-B post-transfusion hepatitis.

Evidence for a new hepatitis-specific antigen has been obtained from double immunodiffusion assays between acute and convalescent sera obtained from patients with non-A, non-B post-transfusion hepatitis. The designation hepatitis C (HC) antigen is proposed. HC was found in the acute-phase sera of all 13 non-A, non-B post-transfusion hepatitis patients with longer incubation and duration periods (type 2) tested, but only transiently in 4 out of 10 acutephase sera obtained from patients with type 1 non-A, non-B hepatitis, with shorter incubation and duration periods. The antigen was also detected in 2 out of 16 single specimens obtained during the acute phase from acute hepatitis patients who had not received a blood-transfusion. This suggests presence of a carrier state. No patients with alcoholic hepatitis and no healthy blood-donor carried HC antigen. The antigen seems distinct from those of hepatitis A and B (surface and core). It migrated in the serum beta-globulin region and had a buoyant density of 1.30 and a molecular weight between 100 000 and 300 000. Antibodies against HC antigen were found in only 30% of the type-2 non-A, non-B post-transfusion hepatitis patients and did not persist for long. However, these antibodies were directed specifically against HC antigen and moved in a manner similar to 7S globulin on rate-zonal centrifugation.

Acute Disease↗
PubMed1975

Cell-mediated immunity to Epstein-Barr-virus-transformed lymphoblastoid cells in acute infectious mononucleosis.

Mononuclear peripheral blood leukocytes from 21 patients with infectious mononucleosis and 16 healthy controls were tested in a 51Cr-release assay for cytotoxicity against two human lymphoblastoid cell lines derived from the same donor. One line contained the Epstein-Barr virus (EBV); the other did not. Acute-phase leukocytes were significantly more cytotoxic against the EBV-infected cell line than were control leukocytes. Mean (+/- S.E.) lysis at a leukocyte-target-cell ratio of 100:1 was 10.6 +/- 1.6 per cent for patients and 3.4 +/- 0.6 per cent for controls (P less than 0.0005). Cytotoxicity correlated with the percentage of atypical lymphocytes. Cells of three patients with acute mononucleosis-like illnesses failed to show killing activity above those of normal controls. Cytotoxicity against the EBV-negative line was not significantly different for each group. The finding of cytotoxic cells in infectious-mononucleosis patients with atypical lymphocytes suggests that these cells operate in vivo to limit the proliferation of altered EBV-transformed B lymphoblasts.

Acute Disease↗
PubMed1992

Transient immunoglobulin M antibody response to hepatitis C virus capsid antigen in posttransfusion hepatitis C: putative serological marker for acute viral infection.

The development of serological assays for hepatitis C virus (HCV) has made specific diagnosis possible. However, markers useful in indicating acute-phase HCV infection have not been identified. By an immunoblotting method, we characterized the IgM and IgG antibody response against HCV capsid antigen in patients with HCV infection. Among 88% of patients with acute posttransfusion hepatitis C recruited in a prospective study, there was a transient IgM antibody response. The IgM antibody appeared shortly after onset of hepatitis (average 3.7 weeks), persisted for several months (average 18 weeks), and then disappeared. In contrast, the IgG antibody persisted long-term once it appeared. Among patients with chronic hepatitis C with milder disease activities (serum aminotransferase increase above normal levels of less than 4-fold), the IgM antibody was negative in the majority (72%). In those with acute exacerbations (aminotransferase increase of greater than 10-fold), about 55% were negative for the IgM antibody. The reactivity of the IgM antibody in the rest was weaker or became negative upon further dilution of serum. The results suggest that IgM anti-capsid antibody may serve as a marker indicating acute or active HCV infection.

Acute Disease↗
PubMed1978

Localization of hepatitis A antigen in marmoset organs during acute infection with hepatitis A virus.

Twelve marmosets (Saguinus mystax) were inoculated intravenously (iv) with hepatitis A virus (HAV). One died early (day 12); seven were sacrificed at the time of elevation in level of alanine aminotransferase (serum glutamic-pyruvic transaminase), and four without elevation were not sacrificed but seroconverted. In the seven marmosets sacrificed during the acute stage of illness, hepatitis A antigen (HA Ag) was detected in the liver by immunofluorescence in all cases, by immune electron microscopy in four, and by enzyme-linked immunosorbent assay (ELISA) in three. The HA Ag appeared by immunofluorescence as very fine granules in the cytoplasm of hepatocytes and Kupffer cells. The HA Ag could not be detected by immunofluorescence in biopsy specimens taken from the duodenum, jejunum, ileum, or transverse colon in any of eight marmosets in which necropsy was performed during the acute or preacute stage of illness. These findings suggest that the gut is not involved during the acute phase of HAV infection following iv inoculation into marmosets. The ELISA results showed that only three of 12 marmoset livers obtained during the acute phase of HAV infection could be used as an antigen source in serologic testing for antibody to HA Ag. Thus, marmoset livers were no better as a source of HA Ag than acute-phase stools from patients with type A hepatitis.

Acute Disease↗
PubMed1978

Enzyme-linked immunosorbent assay for detection of hepatitis A antigen in stool and antibody to hepatitis A antigen in sera: comparison with solid-phase radioimmunoassay, immune electron microscopy, and immune adherence hemagglutination assay.

Previously described techniques for detection of hepatitis A antigen (HA Ag) and antibody (anti-HA) have required purified HA Ag and expensive equipment. Herein is described an enzyme-linked immunosorbent assay (ELISA) for specific detection of HA Ag in human stool filtrates and of anti-HA in sera by using selected HA Ag-containing human stool filtrates as the antigen source. Because human stools often react nonspecifically in serological tests for HA Ag, blocking with preexposure and hyperimmune anti-HA sera from a chimpanzee inoculated with hepatitis A virus was used to confirm specific detection of HA Ag. The sensitivity of ELISA was found to be comparable to that of solid-phase radioimmunoassay (SPRIA) and immune electron microscopy (IEM). Of 37 acute-phase stools collected from nine patients, 16 were positive for HA Ag by ELISA. In 13 of these, HA Ag particles were found by IEM, and an additional 3 stools negative by ELISA contained HA Ag particles by IEM. Eight control stools were negative by both ELISA and IEM. Anti-HA was measured in sera by demonstrating its ability to block binding of the enzyme conjugate to HA Ag in a stool without detectable nonspecificity. This test (blocking ELISA) was as sensitive and specific as blocking SPIRA, IEM, and immune adherence hemagglutination and, like SPRIA and IEM, detected early-developing antibody. The ELISA is simple to perform and requires only a minimum of equipment. It is useful for screening stools for HA Ag and for monitoring HA Ag during purification, as well as for detecting early and late anti-HA in sera.

Acute Disease↗
PubMed1992

The value of acute phase protein measurements in clinical practice.

There is clearly a role for the measurement of acute phase proteins and other indices of the acute phase reaction but it is equally clear that no one laboratory test is suitable for use in all clinical situations. The choice of acute phase protein measurement depends on the diagnostic sensitivity and specificity of the measurement in the particular clinical situation. The choice of measurement must also include a decision on time of sampling and whether single or serial sampling would be more appropriate. In most situations where acute phase measurement is useful CRP is the assay of choice with alpha 1-antichymotrypsin also being useful in inflammatory bowel disease and other situations where a wider time window is required. The ESR or plasma viscosity can be useful to screen for disease. Cytokine and enzyme-inhibitor complex measurements may be important assays in the future.

Acute-Phase Proteins↗
PubMed1992

Observations on the interleukin-6 and acute phase protein profiles in the disease course of patients with lupus erythematosus.

In vitro models have shown that interleukin-6 (IL-6) is the main dominator of the stimulation of the full spectrum of acute phase proteins. This study describes IL-6 levels in relation to levels of acute phase proteins in 15 systemic lupus erythematosus (SLE) patients, with special attention given to those patients with increased serum levels of IL-6. Three episodes with elevated levels of IL-6 were observed in a period shortly after a flare-up of SLE, in three of the 15 patients. In one of these three patients a clear increase in the C-reactive protein (CRP) level, preceded by an IL-6 increase, was observed. In the other two patients, CRP levels remained unchanged. It is speculated that, next to IL-6, another signal is operative or needed for the start of an acute phase reaction. However, influences of the disease itself or of the administered therapy cannot be excluded as the cause of the described discrepancy between IL-6 and acute phase protein profiles in these two SLE patients.

Acute-Phase Proteins↗