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Biomedical subjects

L A Hanson

Publications and source records attributed to L A Hanson.

At least 109 records · Page 6Linked to original sources
PubMed1995

Deletion of thymidine kinase gene attenuates channel catfish herpesvirus while maintaining infectivity.

A recombinant thymidine kinase (TK) gene deletion mutant of channel catfish herpesvirus (CCV) was constructed and compared to the parent virus for replicative ability in cell culture, for the ability to infect, replicate, and cause lethal disease in the channel catfish host, and for the ability to induce protective immunity in channel catfish fingerlings. There was no difference between parent CCV and the TK-negative mutant (CCVTK-) in viral production in cell culture. However, in immersion challenge trials, 100-fold more CCVTK- than parent CCV was required to kill similar numbers of channel catfish fingerlings. The attenuation was confirmed as a TK-associated characteristic in marker rescue; the revertant regained the pathogenic characteristic of the parent virus. When catfish were immersion challenged with equal amounts of CCVTK- or CCV, the levels of virus isolated from the posterior kidney were similar through the peak production period which occurred 4 days postinfection. Subsequently, CCVTK- levels decreased dramatically when compared to CCV levels. Exposure to CCVTK- induced protective immunity against challenge with a lethal dose of wild-type CCV. The degree of protection provided by CCVTK- was related to the dose of CCVTK- given. This study demonstrates that the genetically distant CCV retains recombination properties and TK-associated attenuation properties of herpesviruses of higher vertebrates. Additionally, the unique characteristic of CCV containing two copies of the TK gene did not prevent the use of this gene as a selectable site of homologous recombination.

Animals↗
PubMed1995

Adhesins of Escherichia coli associated with extra-intestinal pathogenicity confer binding to colonic epithelial cells.

Escherichia coli adhesins are virulence factors in intestinal and extra-intestinal infections, but their role in normal intestinal colonization has not been defined. We investigated the intestinal adherence of E. coli with Dr hemagglutinin, S fimbriae, CFA/I or CFA/II, using freshly isolated ileal or colonic enterocytes and cells from the human colonic cell line HT-29. E. coli with S-fimbrial adhesins (Sfa I or Sfa II), P or type 1 fimbriae, adhered in a non-polarized manner, and in similar numbers to colonic and ileal enterocytes. S fimbriae of the variety Sfa II (originating from a meningitis isolate), mediated a stronger binding than Sfa I (of uropathogenic origin). Strains expressing Dr hemagglutinin adhered preferentially to the brush borders, slightly better to colonic than ileal enterocytes. Strains expressing CFA/I or II adhered to colonic and ileal enterocytes, although brush border adherence was predominantly observed with ileal cells. Binding to HT-29 cells paralleled binding to colonic enterocytes for all adhesin specificities except CFA/I. The results suggest that Dr hemagglutinin, P-, type 1- and S-fimbrial adhesins mediate binding to both colonic and ileal enterocytes. These specificities may contribute to the establishment of E. coli in the intestinal microflora, which precedes their spread to extra-intestinal sites.

Adhesins, Escherichia coli↗
PubMed1995

Discrimination of ovarian steroids by rats.

Rats' ability to discriminate their hormonal states was examined by observing the effects of ovarian steroids on state-dependent learning using a drug discrimination task. A rat's entry into the correct arm (left or right) of a Y-maze terminated mild foot shock. The arm designated as correct was alternated daily, but was consistently paired with a pretrial injection of hormone or vehicle. In Experiment 1, ovariectomized rats successfully discriminated pretreatment with 4.0 or 8.0 mg/kg progesterone vs. the oil vehicle but not 2.0 or 0.5 mg/kg progesterone vs. oil, or the daily alternation schedule alone (oil vs. oil). In Experiment 2a, ovariectomized rats correctly discriminated pretreatment with progesterone (4 mg/kg) vs. oil or dihydroprogesterone (4 mg/kg) vs. oil, and the results of Experiment 2b, appear consistent with the possibility that the rats discriminated pretreatment with progesterone vs. dihydroprogesterone. In Experiment 3a, ovariectomized rats discriminated on the basis of progesterone (4.0 mg/kg) vs. oil, estrogen (6.4 micrograms/kg estradiol benzoate) vs. oil, and estrogen vs. progesterone. In Experiment 3b, the rats were adrenalectomized, and the procedure from Experiment 3a repeated. The removal of the adrenal glands failed to abolish hormonal discriminations, suggesting that the effect is not adrenally mediated. The results of these studies show that rats can discriminate relatively low doses of ovarian steroids.

20-alpha-Dihydroprogesterone↗
PubMed1995

Antibody titre and avidity in saliva and serum are not impaired in mildly to moderately undernourished children.

Avidities and titres of serum IgA, IgM, IgG, and salivary IgA antibodies for poliovirus type 3, beta-lactoglobulin and E. coli O antigens were analysed in well-nourished (n=58) and mildly to moderately undernourished (n = 18) 1-7-year-old children, living in slums in São Paulo, Brazil, with irregular water supply and no sewage system. The serum titres of antibodies in the undernourished children were not statistically different from the well-nourished ones, except for the IgA anti-beta-lactoglobulin titres which were lower in the youngest undernourished group. In respect to avidity of the serum antibodies, no statistical difference was observed, except that the youngest undernourished children presented avidities of serum IgA anti-E. coli O antigens higher than those of the well-nourished children of the same age range. With respect to salivary titres and avidities no difference was observed between well-nourished and undernourished children. The fact that the undernourished children were not deficient in antibody amount or quality, as measured in this study, suggests that in this respect their immune system was not impaired.

Antibodies, Bacterial↗
PubMed1995

Linkage of IgA deficiency to Gm allotypes; the influence of Gm allotypes on IgA-IgG subclass deficiency.

IgA deficiency (IgAD) is the most common immunodeficiency, characterized by an arrest in B cell differentiation. It has a sporadic occurrence or variable inheritance pattern, and is also linked to the HLA genes. IgA deficiency is sometimes associated with IgG subclass deficiency. In this study the Gm allotypes, as genetic characteristics of the IgG1, IgG2 and IgG3, were analysed in 83 Caucasian IgAD individuals. Half of the patients presented with IgG4 < 0.01 g/l compared with 5% (P < 0.001) in a healthy population. Three of the 83 had significantly low IgG2 and four had significantly low IgG3 levels. Gm allotype frequencies in IgAD deviated compared with a normal population. Of the 83 patients, 44 (53%) showed homozygous G2 m(",") expression on the IgG2 locus (33% in controls, P < 0.01). In IgAD the Gm(a,",g) haplotype was more frequent (43%) compared with controls (31%, P < 0.01). The Gm homozygous phenotype Gm(a,",g/a,",g) was most common, found in 20 of 83 patients (24%, P < 0.05) compared with controls (14%). On the other hand the Gm(f,n,b) haplotype of IgAD was rare (28%) compared with controls (45%, P < 0.001). The low IgG4, < 0.01 g/l, found in 50% of the patients, was even more frequent (56-69%) among the G2 m(",") phenotypes. IgG subclass levels were given for different Gm phenotypes of the IgAD group and compared with controls. Significantly low IgG4 was revealed in the Gm(a,",g/a,",g) phenotype (P < 0.01) and significantly low IgG2 in the Gm(a,",g/f,",b) phenotype (P < 0.01). The Gm(a,",g/f,",b) phenotype contained the three patients found with IgG2 levels < -2 s.d., and the four patients with IgG3 levels < -2 s.d. were present among those with the homozygous Gm(a,",g/a,",g) phenotype; both phenotypes with G2 m(",") on the IgG2 locus. The 'compensatory' increase of IgG was significant for both IgG1 and IgG3 in all Gm phenotypes, but in the Gm(a,",g/f,",b). Thus, the susceptibility of IgAD with the additional IgG antibody deficiencies, down-regulated IgG4 and IgG2/IgG3, is associated with Gm allotypes, especially the homozygous G2 m(",") expression on the IgG2 locus.

Hemagglutination Inhibition Tests↗
PubMed1995

ADCC-mediating capacity in children with cow's milk protein intolerance in relation to IgG subclass profile of serum antibodies to beta-lactoglobulin.

In a previous study sera from children with cow's milk protein intolerance (CMPI) exhibiting gastrointestinal symptoms were found to efficiently induce antibody-dependent cell-mediated cytotoxicity (ADCC) to beta-lactoglobulin-coated cells. In contrast, sera from children with coeliac disease showed a low ADCC-mediating capacity, despite high levels of IgG anti-beta-lactoglobulin antibodies. The study described here was undertaken to evaluate whether differences in IgG subclass profile of anti-beta-lactoglobulin antibodies could explain the observed variations in the ADCC-mediating capacity. Forty-eight sera from the following groups of children were investigated: CMPI with predominantly gastrointestinal symptoms, CMPI with skin symptoms of immediate-onset, children with untreated coeliac disease and healthy references. Absorption experiments indicated that primarily IgG1 antibodies were responsible for the ADCC-mediating capacity of the sera. Accordingly, the ADCC reactivity of individual sera correlated with their IgG1 antibody levels. Sera from CMPI children with gastrointestinal symptoms, most of which had a high ADCC reactivity, also demonstrated a distinctive subclass pattern of their anti-beta-lactoglobulin antibodies with higher relative proportions of IgG1 (ratios: IgG1/IgG, IgG1/IgG3 and IgG1/IgG4) than those from the other diagnostic groups. Using logistic regression analysis, the diagnostic potential of ADCC as well as of different IgG subclass variables for the recognition of gastrointestinal symptoms caused by CMPI was evaluated. The ADCC reactivity of sera was found to be the best predictor in this model.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1995

Role of Escherichia coli P fimbriae in intestinal colonization in gnotobiotic rats.

Adherence via P fimbriae is associated with long-term persistence of Escherichia coli in the human large intestine, but a causal relationship has not been proven. In the present study, germfree rats were colonized with a mixture of two isogenic E. coli strains, one P fimbriated and the other type 1 fimbriated. Both types of fimbriae conferred adherence to rat colonic epithelial cells. With two mutant strains from a pyelonephritogenic isolate of serotype O75:K5:H-, the P-fimbriated strain 824 attained much higher numbers than its type 1-fimbriated counterpart when colonized in vivo for 2 weeks (10(10) versus 10(6) bacteria per g, respectively; P < 0.0001). The expression of P fimbriae by 824 was also retained during colonization. With transformant isogenic strains obtained from a normal fecal isolate incapable of phase variation, no benefit of P fimbriae was seen and most bacteria lost their plasmids during in vivo colonization. When the pyelonephritogenic mutant and fecal transformant strains were combined, the former colonized at high levels while the latter were suppressed. In contrast, no suppression was seen when the transformant E. coli strains colonized in combination with Lactobacillus acidophilus or Peptostreptococcus sp. The results indicate that P fimbriae, but also other bacterial traits linked to uropathogeneicity, could play an important role for persistence in the gut normal microbiota. Neither P nor type 1 fimbriae seemed to contribute to the ability to translocate to the mesenteric lymph nodes.

Animals↗
PubMed1995

Increased translocation of Escherichia coli and development of arthritis in vitamin A-deficient rats.

We studied the immune response and the colonization pattern in vitamin A-deficient rats that were colonized with the Escherichia coli O6 K13 pOmp 21 strain, which is genetically manipulated to produce ovalbumin and to be resistant to ampicillin. In the vitamin A-deficient rats, the number of bacteria per gram of feces was about five times higher than in the paired fed control rats 4 weeks after colonization. In the control rats, the colon and the lower part of the ileum were colonized, while in the vitamin A-deficient rats all parts of the small intestine, as well as the colon, were heavily inhabited by bacteria. Furthermore, in 75% of the vitamin A-deficient rats, the E. coli bacteria were found in the mesenteric lymph nodes, and in 50% of the rats E. coli were found in the kidneys. These animals also developed severe arthritis. The levels of serum immunoglobulin G (IgG), IgM, IgE, and biliary IgA antibodies against the bacterial antigens were significantly higher in the vitamin A-deficient rats than in the control rats. The number of IgA-producing cells in the lamina propria of the small intestine was significantly lower in the vitamin A-deficient rats than in the control rats; however, there was an increase in the number of CD8+ cells and transforming growth factor beta-producing cells in the lamina propria of the vitamin A-deficient rats. Disturbances in T-cell function were demonstrated, since spleen cells from the vitamin A-deficient rats produced more gamma interferon and interleukin-2 in vitro than control spleen cells. In summary, vitamin A deficiency led to a decrease in the ability to control the localization of intestinal bacteria and an increase in translocation, which was followed by development of arthritis regardless of substantial levels of antibacterial antibodies. The bacterial invasion made the animals hyperresponsive to the bacterial antigens, despite the fact that vitamin A deficiency is normally associated with suppressed antibody production, as previously shown by us and others.

Animals↗