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PubMed1977

Development of cell-mediated immunity to Epstein-Barr herpesvirus in infectious mononucleosis as shown by leukocyte migration inhibition.

Eight patients with infectious mononucleosis, aged between 8 and 24, were studied for cell-mediated immunity by the in vitro leukocyte migration inhibition test at acute and convalescent stages. Follow-up studies were also carried out at up to 4 months after clinical illness. Cell-mediated immunity to Epstein-Barr virus (EBV) in the peripheral leukocytes from these patients was absent or incipient in all cases during the acute phase, although it was present in lymphocytes from a biopsied lymph node obtained from one of the patients. In contrast, cell-mediated immunity to EBV was detected readily in peripheral leukocytes obtained during convalescence and in the follow-up studies. A blocking factor that abrogated leukocyte migration inhibition induced by EBV antigen was detected in acute and convalescent sera obtained from six of eight patients, whereas serum antinuclear autoantibodies were detected in the two patients whose sera failed to block leukocyte migration inhibition. When sera were fractionated, this blocking effect was observed only in the serum immunoglobulin G fractions. In follow-up studies, neither the blocking factor nor the antinuclear autoantibodies were found in the sera collected.

Adolescent↗
PubMed1982

Electrophoretic analysis of polypeptides immune precipitated from cytomegalovirus-infected cell extracts by human sera.

Serodiagnosis of cytomegalovirus (CMV) infection by complement fixation tests depends on showing a fourfold rise in antibody titer from acute- to convalescent-phase sera. Freeze-thaw and glycine-extracted, infected cell culture antigens used for these tests give markedly different titers in reactions with the same sera. In this study, we characterized the CMV-infected cell polypeptides contained in freeze-thaw and glycine-extracted antigens and identified the proteins precipitated by 23 pairs of human acute and convalescent sera. Our results were as follows. First, freeze-thaw and glycine-extracted antigens prepared from infected cells radiolabeled with [35S]methionine and subjected to electrophoresis in sodium dodecyl sulfate-polyacrylamide gels yielded similar patterns, and the bulk of the label was contained in late structural proteins and glycoproteins. Glycine-extracted preparations contained a greater proportion of soluble 66,000- and 50,000-molecular-weight proteins than did freeze-thaw antigens. Second, convalescent sera precipitated proteins migrating with apparent molecular weights of 150,000, 130,000, 110,000, 96,000, 74,000, 66,000, 50,000, 34,000, 32,000, and 25,000. Of these the 130,000-, 110,000-, 96,000-, 66,000-, 50,000-, and 25,000-molecular-weight proteins comigrated with glucosamine-labeled polypeptides. Both immunoglobulin G and M antibodies in human sera precipitated these proteins from CMV-infected cell preparations. Implications of the results for serodiagnosis of CMV infections are discussed.

Antibodies, Viral↗
PubMed1982

Antibody response of infants to cell surface-exposed outer membrane proteins of Haemophilus influenzae type b after systemic Haemophilus disease.

The immune response of nine infants with Haemophilus influenzae type b meningitis was examined by using a radioimmunoprecipitation procedure designed to detect antibodies directed against cell surface-exposed outer membrane proteins of this pathogen. Using intrinsically or extrinsically radiolabeled intact H. influenzae type b cells with acute- and convalescent-phase human sera in this radioimmunoprecipitation system, we found that all of the infants produced an antibody response directed against several different H. influenzae type b outer membrane proteins. Anti-H. influenzae type b outer membrane protein antibodies present in convalescent sera, but not found in acute sera, were directed against cell surface-exposed H. influenzae type b outer membrane proteins. In contrast, both acute and convalescent sera contained antibody activity directed against numerous H. influenzae type b outer membrane proteins whose antigenic determinants were apparently inaccessible to antibody on intact H. influenzae type b cells. The ability of infants to develop an antibody response to cell surface-exposed, antibody-accessible H. influenzae type b outer membrane proteins indicates that these proteins may have vaccinogenic potential.

Antibodies, Bacterial↗
PubMed1984

Human antibody response to outer membrane proteins of Campylobacter jejuni during infection.

Two techniques were used to isolate outer membrane proteins from Campylobacter jejuni, EDTA-lysozyme extraction and sodium-N-lauroylsarcosinate (Sarkosyl) solubilization. The protein profiles of the two preparations were similar, with a few additional bands in the EDTA-lysozyme preparations. The major outer membrane protein was 43,000 (43K) daltons, and there were 8 to 10 minor bands ranging from 92K to 14K daltons. There was no difference in the protein profile of a strain causing an infection (strain 17) and the resulting stool isolate (strain 17J). Sera collected before the infection and during the acute and convalescent stages were used with Western blotting and immunoautoradiographic techniques to determine the antigenicity of outer membrane proteins. A number of antigenic proteins were detected before the infection by their reaction with preinfection serum (61K, 51K, 43K, 40K, 34K, and 31K daltons), and three additional bands appeared during the infection when acute and convalescent sera were used (92K, 56K, and 19K daltons). Furthermore, an area of the gel at less than 14.4K daltons that did not stain with Coomassie brilliant blue became visible in the immune blots when the convalescent serum was used.

Antibody Formation↗
PubMed1986

Molecular characterization of proteins from porcine spirochetes.

Sonicated preparations of Treponema hyodysenteriae and Treponema innocens were subjected to sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blot analysis. Treponemal proteins were electrophoresed on a 10% polyacrylamide slab gel in a discontinuous Tris-glycine system and either stained with Coomassie blue dye or transferred electrophoretically at 20 mA for 16 h and 30 mA for 3 h to nitrocellulose paper. Staining of the gels revealed at least 42 distinct T. hyodysenteriae and T. innocens proteins, with molecular sizes ranging from greater than 100 to 14 kilodaltons (kDa). Each species contained 12 to 16 major protein bands; five of the proteins were common to both species. Fourteen major antigens were identified in T. hyodysenteriae isolate B204 by using serum specimens from pigs in the acute stage of swine dysentery. Twelve additional antigens were detected in isolate B204 when convalescent-phase serum specimens were reacted to the blot. A wide band at 16 kDa was identified with convalescent-phase serum specimens in T. hyodysenteriae but not in T. innocens. This 16-kDa antigen was also identified in T. hyodysenteriae with colonic secretions from convalescent pigs.

Animals↗
PubMed1990

Study of epitopes of cholera enterotoxin-related enterotoxins by checkerboard immunoblotting.

Checkerboard immunoblotting, a versatile new technique for examining multiple antigen and antibody interactions simultaneously, was applied in studies of epitopes in the cholera enterotoxin (CT)-related heat-labile enterotoxin (LT) family. The purified antigens used included the following: the B-subunit proteins from two CTs (CT-B-1 and CT-B-2), from classical and El Tor biotype strains of Vibrio cholerae, respectively; human LT-B-1 (H-LT-B-1) and porcine LT-B (P-LT-B) derived from LTs produced by Escherichia coli strains of human (H) and porcine (P) origins, respectively; and genetically engineered chimeric P-LT-Bs with amino acid substitutions from H-LT-B-1. The antigens were used in native, partially denatured, and CNBr-fragmented forms. The antisera included a variety of mouse monoclonal antibodies against these proteins as well as polyclonal hyperimmune sera and sera from adult American volunteer vaccinees or convalescents from induced cholera. Rabbit antisera against synthetic peptides of the CT-B-1 subunit were also used. In some instances, the effect of GM1 ganglioside on antibody binding was evaluated. The reactivity of the monoclonal antibodies was directed primarily against conformational epitopes: some were specific for homologous antigen; some were promiscuously reactive; and some recognized particular related proteins. Individual amino acids (most notably amino acid 46) exerted a dominant effect on epitope formation--in some instances, in a complementary fashion. Epitope expression was also affected by distant amino acid residues (polar effects). Some reactions were blocked by GM1 treatment of the immobilized antigen, indicating that the epitope was involved in or affected by GM1 binding. Polyclonal antibody responses varied within and among animal species. Human serum antitoxic responses were higher in convalescents from induced cholera than in recipients of a genetically engineered live vaccine, and the convalescent sera (from El Tor biotype cholera patients) generally preferred CT-B-2 to CT-B-1. The results demonstrate the potential significance of the differences among these immunologically related enterotoxins and may help provide direction to further vaccine development.

Amino Acid Sequence↗
PubMed1991

Antibody recognition and isoelectrofocusing of antigens of the malaria parasite Plasmodium yoelii.

Inbred BALB/c mice were either immunized with Triton X-100-extracted antigens of blood-stage Plasmodium yoelii or infected with P. yoelii and cured in three successive schedules. Whereas the immunized BALB/c became only partially protected from subsequent challenge infection with blood-stage P. yoelii, the convalescent mice acquired total immunity. When total P. yoelii antigen extract was resolved by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, transferred to nitrocellulose, and immunoblotted with anti-P. yoelii serum, five major protein bands of 150, 84, 40, 19, and 16 kDa were recognized by the sera of fully protected convalescent mice but not by the sera of partially protected mice. The utility of comparing reactivities of sera from fully protected and partially protected malaria hosts and the possibility that antigens uniquely recognized by the convalescent mouse sera may contribute to immunity against P. yoelii infection are discussed. Although previously reported to be an effective adjuvant for immunization against P. yoelii infection in (BALB/c x C57BL)F1 hybrid mice, saponin did not promote protection any better than did Freund adjuvant in BALB/c mice immunized with detergent-extracted P. yoelii antigen. Most of the P. yoelii proteins (14 to 250 kDa) found in Triton X-100 extracts of P. yoelii-parasitized erythrocytes isoelectrofocused as a single peak in the pH region 4.4 to 4.6, suggesting a rationale for previous findings that the most anti-P. yoelii protective and T-helper activities are induced by antigens isoelectrically focused in a fraction of similar pH.

Animals↗
PubMed1992

Phagocytosis and killing of Actinobacillus pleuropneumoniae by alveolar macrophages and polymorphonuclear leukocytes isolated from pigs.

To study the cellular response of phagocytic cells to Actinobacillus pleuropneumoniae, we investigated whether porcine alveolar macrophages (AM) and polymorphonuclear leukocytes (PMN) are able to phagocytize and intracellularly kill A. pleuropneumoniae in vitro. Bacterial cultivation methods of A. pleuropneumoniae were used to assess in vitro phagocytosis and the ability to kill. A specific-pathogen-free pig was killed, blood was collected, and PMN were isolated and counted. The AM were isolated by lung lavage of the same animal and counted. In addition, convalescent-stage serum was collected from a specific-pathogen-free pig that was infected with A. pleuropneumoniae. Both porcine AM and porcine PMN effectively phagocytized A. pleuropneumoniae in the presence of convalescent-stage pig serum. PMN killed 90 to 99% of the bacteria intracellularly, whereas AM did not. Because A. pleuropneumoniae produces exotoxins that kill porcine AM and porcine PMN, we incubated equal amounts of bacteria and phagocytic cells and tested the viability of the cells 120 min later. In the presence of convalescent-stage pig serum, A. pleuropneumoniae was toxic to AM but not to PMN. Probably in porcine AM, intracellular released toxins of A. pleuropneumoniae lessen the ability of the cell to kill the bacterium. Consecutive lysis of AM and release of viable A. pleuropneumoniae may initiate the characteristic porcine pleuropneumonia.

Actinobacillus pleuropneumoniae↗
PubMed1996

Number of specific antibody-secreting cells in the peripheral blood among children with mycoplasma pneumonia.

Mycoplasma pneumoniae-specific antibody-secreting cells (ASCs) in the peripheral blood were enumerated with an enzyme-linked immunospot assay in 12 children with mycoplasma pneumonia. Those cells were detected in the acute phases and declined in number in the convalescent stage. The maximum numbers of M. pneumoniae-specific ASCs ranged from 0 to 478 for immunoglobulin G (IgG), 13 to 1,992 for IgM, and 0 to 53 for IgA per 106 peripheral blood mononuclear cells, whereas the total numbers (i.e., including both specific and nonspecific) of immunoglobulin-secreting cells (IgSCs) were as high as 4,000 for both IgG and IgM and 1,000 for IgA per 106 peripheral blood mononuclear cells. Such a great increase in the numbers of total IgSCs in comparison with that in M. pneumoniae-specific ASCs suggests that the majority of the IgSC increase in the course of mycoplasmal infection was nonspecific to M. pneumoniae. The serum level of M. pneumoniae antibody measured by enzyme-linked immunosorbent assay remained high in the convalescent phase, while the number of specific ASCs decreased. Whereas this observation may be explained by declined degeneration or consumption of the antibody in the convalescent phase, it may be suggestive of the source of M. pneumoniae antibody other than ASCs in the peripheral blood.

Adolescent↗
PubMed1997

In situ characterization of inflammatory responses in the rectal mucosae of patients with shigellosis.

Shigella species cause bacillary dysentery in humans by invading epithelial cells of the colonic mucosa leading to colonic epithelial cell destruction and inflammation. For further analysis of local gut inflammation, morphological changes and the potential involvement of mediators in regulatory mechanisms of cell activation and cell proliferation were studied immunohistochemically in rectal mucosal biopsies taken from patients during the acute phase of shigellosis and at convalescence. Rectal biopsies from 25 Shigella dysenteriae-1 and 10 Shigella flexneri-infected patients and from 40 controls were studied. The frequencies of proliferative cells (Ki67-positive cells), p53-immunostaining cells, and cells coexpressing Ki67 with CD3 or with p53 were analyzed. Immunostaining for the inducible nitric oxide synthase (iNOS) and the endothelial NOS was assessed. In addition, the frequencies of apoptotic cells and CD68+ cells that engulf apoptotic cells were assessed. By morphological grading, 20% of the patients had advanced inflammation (grade 3) in the acute phase; mild inflammation (grade 1) was seen in 37% of the patients at convalescence as well as in 10% of the controls. The findings in the present study suggest that in the acute phase of shigellosis inflammation is characterized by increased cell turnover in the lamina propria (LP) and the epithelium, increased iNOS expression in the surface epithelium, and apoptosis, which seems to be associated with LP macrophages. The findings also suggest that neither p53 nor iNOS are important factors for the induction of apoptosis in shigellosis. Expression of p53 may be related to early cell activation in crypt epithelium. Moreover, there is an indication of an active, low-level inflammatory process at convalescence. The results thus indicate that Shigella-induced inflammation is associated with a complex series of cellular reactions in the rectal gut mucosa which persist long after clinical symptoms have resolved.

Adult↗
PubMed1998

Molecular analysis of Shiga toxigenic Escherichia coli O111:H- proteins which react with sera from patients with hemolytic-uremic syndrome.

Western blot analysis was used to assess the reactivity of convalescent-phase sera from patients who were associated with an outbreak of hemolytic-uremic syndrome (HUS) caused by fermented sausage contaminated with Shiga toxin-producing Escherichia coli (STEC). The predominant STEC isolated from HUS patients belonged to serotype O111:H-, and reactivity to O111:H- whole-cell lysates, treated or untreated with proteinase K, was examined. As expected, all five serum samples demonstrated a marked anti-lipopolysaccharide response, but several protein bands were also immunoreactive, particularly one with an apparent size of 94 kDa. One convalescent-phase serum sample was subsequently used to screen an O111:H- cosmid bank and 2 of 900 cosmid clones were found to be positive, both of which contained a similar DNA insert. Western blot analysis of one of these clones identified three major immunoreactive protein bands of approximately 94, 70, and 50 kDa. An immune response to the three proteins was detectable with all five convalescent-phase serum samples but not with healthy human serum. Immunoreactive 94- and 50-kDa species were produced by a deletion derivative of the cosmid containing a 7-kb STEC DNA insert. Sequence analysis of this region indicated that it is part of the locus for enterocyte effacement, including the eaeA gene which encodes intimin. The deduced amino acid sequence of the O111:H- intimin was 88.6% identical to intimin from O157:H7 STEC, and the most divergent region was the 200 residues at the carboxyl terminus, which were only 75% identical. Such variation may be antigenically significant as serum from a HUS patient infected only with the O111:H- STEC reacted with intimin from an enteropathogenic E. coli O111 strain, as well as several other eaeA-positive STEC isolates, but not with an eaeA-positive STEC belonging to serotype O157:H-. Sera from two of the other HUS patients also failed to react with intimin from this latter strain. However, intimin from O157:H- STEC did react with serum from a patient infected with both O111:H- and O157:H- STEC.

Adhesins, Bacterial↗
PubMed1999

Human opsonins induced during meningococcal disease recognize outer membrane proteins PorA and PorB.

Human opsonins directed against specific meningococcal outer membrane structures in sera obtained during meningococcal disease were quantified with a recently developed antigen-specific, opsonin-dependent phagocytosis and oxidative burst assay. Outer membrane vesicles (OMVs) and PorA (class 1) and PorB (class 3) proteins purified from mutants of the same strain (44/76; B:15:P1.7. 16) were adsorbed to fluorescent beads, opsonized with acute- and convalescent-phase sera from 40 patients with meningococcal disease, and exposed to human leukocytes. Flow cytometric quantitation of the resulting leukocyte phagocytosis products (PPs) demonstrated that disease-induced serum opsonins recognized meningococcal OMV components and both porins. The PPPorA and PPPorB values induced by convalescent-phase sera correlated positively with the PPOMV values. However, the PPPorB values were higher than the PPPorA values in convalescent-phase sera (medians [ranges] of 754 [17 to 1,057] and 107 [4 to 458], respectively) (P < 0.0001) and correlated positively with higher levels of immunoglobulin G against PorB than against PorA as evaluated by enzyme-linked immunosorbent assay. Extensive individual variations in the anti-OMV and antiporin serum opsonic activities between patients infected by serotypes and serosubtypes homologous and heterologous to the target antigens were observed. Simultaneously measured oxidative burst activity correlated with the opsonophagocytosis, an indication that both of these important steps in the in vitro phagocytic elimination of meningococci are initiated by opsonins directed against OMV components, including PorA and PorB. In conclusion, human patient opsonins against meningococcal OMV components and in particular PorB epitopes were identified by this new method, which might facilitate selection of opsonin-inducing meningococcal antigens for inclusion in future vaccines.

Adolescent↗
PubMed1973

Fate of intravenously injected Mycoplasma arthritidis in rodents and effect of vaccines.

Virulent Mycoplasma arthritidis strain 158 P10 was rapidly eliminated from the peripheral circulation of rats and mice during the first 2 h after intravenous injection of the organisms. Characteristically after this time, the numbers of viable organisms remained remarkably constant through 48 to 72 h. The inability to clear the remaining mycoplasmas was not due to reticuloendothelial blockade but appeared to indicate the presence of a certain number of cells which were resistant to the clearance mechanism. Rat blood was usually devoid of mycoplasmas at 6 days and mouse blood was sterile by 14 days. An occasional transient mycoplasmemia occurred after these times. Avirulent M. arthritidis strain H606 was cleared more rapidly from rats in which it is non-arthritogenic. Different, but characteristic, clearance curves were obtained in mice using M. hominis, M. bovirhinis, and M. pulmonis. Active immunization procedures resulted in enhanced clearance of virulent M. arthritidis from rats. These procedures were less successful in mice. The results of passive immunization of normal rats and mice using convalescent serum indicated the presence of a serum factor which greatly enhanced clearance from rats but had only minimal effects in mice. This serum factor could not be correlated with metabolic-inhibiting antibody. Lymphocytes taken from convalescent rats enhanced the clearance rates of recipient rats. Mouse convalescent lymphocytes were without effect. The results indicated that mice are less able to control long-term infection by M. arthritidis than are rats.

Animals↗
PubMed2002

Apoptosis in acute shigellosis is associated with increased production of Fas/Fas ligand, perforin, caspase-1, and caspase-3 but reduced production of Bcl-2 and interleukin-2.

Shigella dysenteriae type 1-induced apoptotic cell death in rectal tissues from patients infected with Shigella dysenteriae type 1 was studied by the terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) technique and annexin V staining. Expression of proteins and cytokines participating in the apoptotic process (caspase-1, caspase-3, Fas [CD95], Fas ligand [Fas-L], perforin, granzyme A, Bax, WAF-1, Bcl-2, interleukin-2 [IL-2], IL-18, and granulocyte-macrophage colony-stimulating factor) in tissue in the acute and convalescent stages of dysentery was quantified at the single-cell level by in situ immunostaining. Apoptotic cell death in the lamina propria was markedly up-regulated at the acute stage (P < 0.05), where an increased number of necrotic cells were also seen. Phenotypic analysis of apoptotic cells revealed that 43% of T cells (CD3), 10% of granulocytes (CD15), and 5% of macrophages (CD56) underwent apoptosis. Increased activity of caspase-1 persisted in the rectum up to 1 month after onset. More-extensive expression of Fas, Fas-L, perforin, caspase-3, and IL-18, but not IL-2, at the acute stage than at the convalescent stage was observed. Increased expression of caspase-3 and IL-18 in tissues with severe inflammation compared to expression in those with mild inflammation was evident, implying a possible role in the perpetuation of inflammation. Significantly reduced cell death during convalescence was associated with a significant up-regulation of Bcl-2, Bax, and WAF-1 expression in the rectum compared to that in the acute phase of infection. Thus, induction of apoptosis at the local site in the early phase of S. dysenteriae type 1 infection was associated with a significant up-regulation of Fas/Fas-L and perforin and granzyme A expression and a down-regulation of Bcl-2 and IL-2, which promote cell survival.

Acute Disease↗
PubMed2004

Antibody-mediated neutralization of pertussis toxin-induced mitogenicity of human peripheral blood mononuclear cells.

Antibody-mediated neutralization of pertussis toxin-induced proliferation of human peripheral blood mononuclear cells (PBMC) was assessed using alamarBlue and compared with results from the Chinese hamster ovary (CHO) cell assay using sera from vaccinated adults and convalescent children. Neutralization values for the CHO assay were similar for vaccinated and convalescent subjects; however. the convalescent group had higher titers in the PBMC assay. Results for pertussis toxin neutralization with the CHO assay appear to be distinct from those with the PBMC assay.

Animals↗
PubMed1992

Cloning and sequencing of a gene encoding a 21-kilodalton outer membrane protein from Bordetella avium and expression of the gene in Salmonella typhimurium.

Three gene libraries of Bordetella avium 197 DNA were prepared in Escherichia coli LE392 by using the cosmid vectors pCP13 and pYA2329, a derivative of pCP13 specifying spectinomycin resistance. The cosmid libraries were screened with convalescent-phase anti-B. avium turkey sera and polyclonal rabbit antisera against B. avium 197 outer membrane proteins. One E. coli recombinant clone produced a 56-kDa protein which reacted with convalescent-phase serum from a turkey infected with B. avium 197. In addition, five E. coli recombinant clones were identified which produced B. avium outer membrane proteins with molecular masses of 21, 38, 40, 43, and 48 kDa. At least one of these E. coli clones, which encoded the 21-kDa protein, reacted with both convalescent-phase turkey sera and antibody against B. avium 197 outer membrane proteins. The gene for the 21-kDa outer membrane protein was localized by Tn5seq1 mutagenesis, and the nucleotide sequence was determined by dideoxy sequencing. DNA sequence analysis of the 21-kDa protein revealed an open reading frame of 582 bases that resulted in a predicted protein of 194 amino acids. Comparison of the predicted amino acid sequence of the gene encoding the 21-kDa outer membrane protein with protein sequences in the National Biomedical Research Foundation protein sequence data base indicated significant homology to the OmpA proteins of Shigella dysenteriae, Enterobacter aerogenes, E. coli, and Salmonella typhimurium and to Neisseria gonorrhoeae outer membrane protein III, Haemophilus influenzae protein P6, and Pseudomonas aeruginosa porin protein F. The gene (ompA) encoding the B. avium 21-kDa protein hybridized with 4.1-kb DNA fragments from EcoRI-digested, chromosomal DNA of Bordetella pertussis and Bordetella bronchiseptica and with 6.0- and 3.2-kb DNA fragments from EcoRI-digested, chromosomal DNA of B. avium and B. avium-like DNA, respectively. A 6.75-kb DNA fragment encoding the B. avium 21-kDa protein was subcloned into the Asd+ vector pYA292, and the construct was introduced into the avirulent delta cya delta crp delta asd S. typhimurium chi 3987 for oral immunization of birds. The gene encoding the 21-kDa protein was expressed equivalently in B. avium 197, delta asd E. coli chi 6097, and S. typhimurium chi 3987 and was localized primarily in the cytoplasmic membrane and outer membrane. In preliminary studies on oral inoculation of turkey poults with S. typhimurium chi 3987 expressing the gene encoding the B. avium 21-kDa protein, it was determined that a single dose of the recombinant Salmonella vaccine failed to elicit serum antibodies against the 21-kDa protein and challenge with wild-type B. avium 197 resulted in colonization of the trachea and thymus with B. avium 197.

Amino Acid Sequence↗
PubMed1969

Immunological responses of the rat to Mycoplasma arthritidis.

Arthritis was produced in rats by the intravenous injection of Mycoplasma arthritidis. Metabolic inhibiting antibody and indirect hemagglutinating antibody could not be detected in the sera of arthritic or convalescent animals. Nonmurine species of mycoplasma were capable of inducing metabolic inhibiting antibody in the rat. A hypothesis based upon the possible occurrence of heterogenetic antigens common to M. arthritidis and rat tissue was brought forward to explain these findings. Complement-fixing antibody to M. arthritidis was detected 3 to 4 days after injection and subsequently rose to high levels, depending upon the severity of arthritis and number of organisms injected. Animals that had recovered from intravenous or subcutaneous inoculation with M. arthritidis were resistant to subsequent infections by the organism. Immunity could be passively transferred by the intravenous injection of convalescent serum. Adsorption of the convalescent serum with antigen greatly reduced the complement fixation titer but did not significantly alter the protective properties of the serum. The presence of complement-fixing antibody could not be related to the development of immunity. An avirulent strain of M. arthritidis and a strain previously classified as M. hominis type 2 were capable of inducing resistance to subsequent injection by virulent M. arthritidis.

Animals↗
PubMed1982

Detection of Japanese encephalitis virus immunoglobulin M antibodies in serum by antibody capture radioimmunoassay.

An assay for detecting human immunoglobulin M (IgM) antibodies to Japanese encephalitis (JE) virus was developed by using the antibody capture solid-phase radioimmunoassay approach (JE IgM ACRIAAA). Heavy-chain-specific goat antihuman IgM was first bound to the wells of a polyvinyl microtiter plate, and successive steps involved sequential binding of test sample IgM, acetone-extracted mouse brain JE antigen, and (125)I-labeled flavivirus hyperimmune human IgG. Among 20 patients hospitalized in Bangkok with clinical diagnoses of acute encephalitis, and with acute flavivirus infections proven by hemagglutination inhibition (HAI) serology, 16 had detectable (positive/negative [P/N] ratio, greater than 3.0) JE IgM ACRIA antibodies in the acute-phase serum specimen, and 19 had such antibodies in the convalescent-phase serum specimen. Convalescent patient sera regularly had higher P/N values than the corresponding acute-phase sera (mean +/- 1 standard deviation = 13.0 +/- 9.3 with acute-phase sera and 25.8 +/- 19.6 with convalescent-phase sera). JE virus-infected patients with HAI serological responses indicative of a primary flavivirus infection had higher JE IgM ACRI P/N responses than did those patients whose serological response indicated past exposure to other flaviviruses. None of 70 serum specimens from healthy Thai adults and children with serum JE HAI antibodies had detectable JE IgM ACRIA activity (P/N ratios all less than or equal to 3.0). Biological false-positives with low P/N ratios (range, 3 to 15) were found in sera from patients with acute or recent infections with flaviviruses other than JE virus but could be differentiated by the fact that these sera gave higher P/N ratios with homologous antigens than with JE virus. False-positive reactions with low P/N ratios (range, 3 to 6) due to serum rheumatoid factor activity were differentiated by testing with control antigen. The JE IgM ACRIA technique permits a rapid, accurate diagnosis of acute JE virus infections in both patients with and those without previous exposure to other flaviviruses.

Antibodies, Viral↗