Biomedical subjects
Publications and source records attributed to K Krawczyński.
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The excretion of hepatitis A virus (HAV) in stools from 30 patients with clinically overt hepatitis A infection on the day of their admission to the hospital was determined and compared with the dynamics and values of biochemical indices of hepatocyte injury as well as with the immune response to HAV. Virus was found in 16 out of 30 stools (53%) collected within 1 week after the appearance of clinical symptoms. In sera obtained on the day of hospitalization both IgM and IgA anti-HAV were detected in all of the 30 patients, while IgG anti-HAV were found in 20 (67%). There was a correlation between HAV excretion and increasing SGPT upon admission to hospital, while the level of SGPT or bilirubin as well as presence or absence of IgG anti-HAV did not correlate with excretion of HAV. HAV from stools was characterized morphologically and physicochemically. The majority of particles visualized by immune electron microscopy had electrondense appearance, while electron-lucid particles were only occasionally encountered. Isopycnic banding of HAV in CsCl revealed a broad range of densities with HAV activity. Rebanding of pooled fractions containing HAV revealed peak amounts of the virus in fractions with densities 1.32-1.33 gm/cm3.
The anti-HAV humoral immune response in the IgM, IgA, and IgG classes was analyzed weekly in 35 patients with clinically overt hepatitis A during the time of their hospitalization and 2-3 years afterward. In parallel, the dynamics of total immunoglobulins and complement C3 component (C3) levels were determined. The results suggest that the appearance of class-specific anti-HAV is compatible with the course of primary humoral immune response, with IgM and IgA anti-HAV, providing immunity in the early and intermediate phases of the infection, and IgG anti-HAV, providing immunity in the later phase. The overall appearance of anti-HAV, total immunoglobulins, and C3, do not support the view that liver injury is mediated by the humoral immune mechanisms. Instead, the hepatocyte damage is probably caused by direct viral cytotoxicity. This hypothesis is supported by a case of hepatitis A in a patient under immunosuppressive treatment.
The ability of protein A from Staphylococcus aureus to interact with Fc fragments of IgG was used to estimate the antithyroid plasma membrane antibodies in sera of patients with Graves' disease. The results were expressed as an antithyroid plasma membrane antibodies (ATMA) index. The ATMA index estimated in 60 healthy blood donors varied from 0.57 to 1.28, with a mean value of 0.99, SD theta 0.20. The ATMA index in hyperthyroid untreated Graves' disease varied from 1.80 to 8.0, with a mean value of 4.7. Autoantibody binding to thyroid plasma membranes could be inhibited by (Fab)2 fragments obtained from the serum of patients with Graves' disease but not by (Fab)2 fragments obtained from the serum of healthy blood donors. The influence of rabbit antithyroglobulin and antimicrosomal antibodies on the ATMA index estimation has been evaluated. The ATMA index estimation was compared with the thyrotrophin binding inhibiting immunoglobulins (TBII) index and with the adenyl cyclase stimulating activity of immunoglobulins obtained from 92 hyperthyroid Graves' patients. The ATMA index was positive in 97%, the TBII index in 62% and TSI in 35% of cases. This method using protein A could also be used for estimation of ATMA in other autoimmune thyroid disorders.
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Mesenteric lymph nodes obtained at surgery from 36 patients with gastrointestinal tract cancer were studied by immunofluorescence for the presence of carcinoembryonic antigen (CEA). Granular deposits of CEA in a homogenous mixture with immunoglobulins and complement were detected in the activated germinal centers in 12 lymph nodes from 8 investigated cases. Identification of CEA in germinal centers was confirmed by blocking and absorbtion procedures. Successful elution of immunoglobulins and part of CEA content with a buffer known to dissociate antigen-antibody bonds suggested that these deposits represent CEA immune complexes.
A close correlation between the presence of hepatitis B surface antigen and albumin in the cytoplasm of hepatocytes infected with hepatitis B virus was established by immunofluorescence and immunoelectron microscopy in 52 liver biopsy specimens of various forms of hepatitis and liver cirrhosis. Albumin deposits usually accompanied cytoplasmic content of hepatitis B surface antigen, but were less frequently observed together with hepatitis B antigen localized in or on the membranes. Ultrastructural observations demonstrated albumin on the tubular and spherical forms of hepatitis B surface antigen in the endoplasmic reticulum. The hepatocytes with the content of hepatitis B surface antigen and albumin showed the ability of binding with the fluorescein-labeled preparation of polymerized human serum albumin. The affinity of polymerized albumin to hepatitis B surface antigen was considerably increased after preincubuation of liver sections with 2-mercaptoethanol that removed most of the originally present albumin. This may be indicative for the role of disulfide bonds in the formation of hepatitis B surface antigen-albumin complexes. These results justify the hypothesis that albumin may be incorporated into the viral coat protein during its synthesis in the cytoplasm of infected hepatocytes.
Direct immunofluorescence, immunoelectron microscopy, and special immunohistochemical procedures including guinea pig complement fixation, differential elution, and in situ antigen binding were employed in an immunomorphologic analysis of kidney biopsy specimens from 98 children with clinically diagnosed nephrotic syndrome and/or glomerulonephritis (GN). Glomerular deposits of hepatitis B virus (HBV) antigens, immunoglobulins, and complement were detected in specimens from 24 children, all seropositive for hepatitis B surface antigen (HBsAg) and antibody to hepatitis B core antigen (HBcAg). Of these, 21 cases were diagnosed as membranous glomerulopathy (MGN), 1 as membranoproliferative GN, and 2 as diffuse mesangial proliferative GN. HBaAg was identified as the only HBV antigen in about a third of the cases of MGN, whereas in another third it was accompanied by HBsAg. HBsAg was the only HBV antigenic component detected in the glomerular deposits in the remaining third of the cases of this GN form. The results of this study indicate that apart from, or in addition to, HBsAg immune complexes, HBcAg immune complexes may also participate in the pathogenesis of a significant number of MGN cases in children subclinically infected with HBV. A possibility that these complexes include nonparticulate, presumably low-molecular-weight HBaAg components and that they are found in an environment of antibody-excess is discussed.
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Specimens of liver tissue obtained by biopsy from five patients and at necropsy from seven patients with postnecrotic liver cirrhosis and hepatocellular carcinoma were examined for the presence of hepatitis B surface antigen (HBs Ag) and hepatitis B core antigen (HBc Ag) by direct immunofluorescence. In all cases, samples of serum were tested for HBs Ag and antibody to HBs Ag (anti-HBs) by immunoelectroosmophoresis and for antibody to HBc Ag (anti-HBc) by indirect immunofluorescence. Of these 12 representative cases of the main histological types of hepatocellular carcinoma, six were found to be seropositive for anti-HBc, and three of them were negative for HBs Ag. HBs Ag was detected in the cytoplasm of hepatocytes in the cirrhotic nodules in one seronegative patient and in three of the seropositive cases. In the latter cases, HBs Ag was identified in the cytoplasm of cells in well-differentiated hepatocellular carcinoma. HBc Ag was not found in any of the specimens examined.
Measles antibodies were determined, in the course of measles, in sera and nasal secretions of 54 and 27 children, respectively. The examinations were performed on the 3rd or 4th day (1st period) and between the 10th and 14th day (2nd period) after onset of rash in both sera and nasal secretions and after 25 to 60 days (3rd period) in sera only. Geometric mean titres of antibodies in sera determined by haemmagglutination inhibition (HI) and neutralization tests in the 1st period were 126.3 and 115.3 respectively. For the 2nd period the respective figures were 318.4 and 396.1 and for the 3rd period--388.0 and 445.6. Fractionation on Sephadex G-200 of sera from the 1st period revealed HI and neutralizaing antibodies associated mainly with the IgM serum globulin class. Measles HI and neutralizing antibodies were also found in nasal secretions of all 27 children, but their titres were much lower than in serum. The antibodies determined by indirect immunofluorescence in nasal secretions were associated with IgA in 26 and with IgG immunoglobulin in 15 of the 27 subjects. No IgM antibodies were found.
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The markers d, IST, EA1(OH)3 and rct at sub- and supraoptimal temperatures as well as neurovirulence (PMic) for monkeys was determined for strains isolated from children vaccinated with Leon 12a1b vaccine, their contacts and from paralytic cases. The strains were isolated at early and late phases of excretion. The changes concerned mainly rct determined at supraoptimal temperatures, d and PMic markers, especially in strains isolated at the late phase of excretion. The passage through the human alimentary tract did not change such markers as IST and EA1(OH)3. Some degree of correlation was observed between the rct 40.3, d and PMic markers.
Markers d, IST, EA1(OH)3, rct (at sub- and supraoptimal temperatures) and neurovirulence were determined for clones isolated from two lots (S2 and S3) of vaccines containing poliovirus strain Leon 12a1b. Changes of markers rct, d and neurovirulence were observed in several clones isolated from S2 vaccine. No changes were observed in IST and EA1(OH)3 markers.
Lung tissue, lymph nodes, and spleen from infants 4-15 weeks old who died of Pneumocystis carinii pneumonia were studied by immunofluorescence and immunoelectron microscopy. The results strongly suggest that antibodies to P. carinii synthetized in lungs by inflammatory infiltrates and in regional lymph nodes are essential in the elimination of P. carinii from infected lungs through their opsonization of the P. carinii organisms. Disintegration of P. carinii conglomerates subsequent to the binding of complement preceded their phagocytosis by lung alveolar macrophages. The immunomorphologic findings strongly supported the hypothesis that the replication of P. carinii at the rate leading to clinical symptoms is due to impaired and delayed synthesis both of antibodies to P. carinii and of complement.
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