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J K Davis

Publications and source records attributed to J K Davis.

At least 37 records · Page 2Linked to original sources
PubMed1993

IDDM patients' sera recognize a novel 30-kD pancreatic autoantigen related to chymotrypsinogen.

We have examined, by western immunoblot analysis, the sera of 16 insulin-dependent diabetes mellitus patients (IDDM) for the presence of autoantibodies against proteins extracted from islet-cell enriched preparations of normal human pancreata. A novel putative autoantigen recognized by late stage IDDM patients sera was identified, and its amino acid sequence was partially determined. Islets of Langerhans were partially purified by a modified collagenase digestion procedure, and subsequent protein extracts were fractionated by one-dimensional or two-dimensional polyacrylamide gel electrophoresis (1-D or 2-D SDS-PAGE). Immunoblot analysis revealed a 30-kD species which was recognized by 4 of 16 IDDM patients sera, but none of 16 normal sera. The 30-kD protein, appeared as a single band on 1-D SDS-PAGE, but was resolved on 2-D gel electrophoresis as several distinct protein species with different isoelectric points (pI's), ranging from 7 to 9. The amino terminal sequence of one such species was partially determined by microsequencing, and the second through the fourteenth amino acids were found to be identical to the corresponding sequence in human chymotrypsinogen. The fifteenth through the eighteenth amino acids were different from the known chymotrypsinogen sequence. This region corresponds with the site that is cleaved to activate chymotrypsinogen. Based on the size and sequence homology, this antigen appears to be related to chymotrypsinogen. We conclude that this 30-kD species may be an autoantigen in some late stage IDDM patients.

Adolescent↗
PubMed1993

Effects of viral and mycoplasmal infections, ammonia exposure, vitamin A deficiency, host age, and organism strain on adherence of Mycoplasma pulmonis in cultured rat tracheas.

Adherence to host cells is thought to be a pathogenetic mechanism in mycoplasmal diseases, thus, factors affecting adherence could affect disease expression. To determine whether factors that affect expression of Mycoplasma pulmonis respiratory disease in rats alter adherence of the organism to respiratory epithelium, we studied adherence of radiolabelled M. pulmonis in perfused whole rat tracheas. Adherence was significantly increased in tracheas from rats with sialodacryoadenitis virus infection or vitamin A deficiency (103 +/- 16% and 112 +/- 29% of control means, respectively), but Sendai virus infection, ammonia exposure, and host age (40 versus 8 weeks) were not associated with increased adherence. We also assessed the relationship between adherence and virulence of M. pulmonis strains. The virulent strain 5782C was more adherent (51 +/- 7%) than the type strain, PG34(Ash), and a polystyrene-adherent, hemadsorbing UAB CT subclone was more adherent (229 +/- 40%) than a UAB CT subclone that does not adhere to polystyrene or erythrocytes. PG34(Ash) and the UAB CT subclones caused rhinitis only; however, the adherent UAB CT subclone caused significantly more severe rhinitis than either the nonadherent subclone or PG34(Ash) as determined by scoring of histologic sections. To determine whether M. pulmonis itself induces changes in respiratory epithelium resulting in enhanced adherence, we studied adherence in tracheas from rats inoculated with M. pulmonis 3 weeks earlier. Adherence was increased 64 +/- 22%, compared with that in tracheas from control rats. Adherence in infected tracheas treated with tetracycline for 2 days was not increased, indicating that M. pulmonis-induced changes in epithelial adherence are rapidly resolved after elimination of infection.

Age Factors↗
PubMed1992

Mycoplasma pulmonis possesses a novel chemoattractant for B lymphocytes.

Mycoplasma pulmonis causes chronic murine respiratory mycoplasmosis, which is characterized by extensive peribronchial and perivascular infiltration of mononuclear cells, including B lymphocytes. B-lymphocyte recruitment into sites of inflammation is presently poorly understood but must involve directed chemotaxis of these cells in response to some external recruitment stimulus. In these studies, picogram amounts of M. pulmonis membrane protein were found to possess potent chemoattractant activity for resting rat B lymphocytes. This report is the first description of a bacterially derived chemoattractant for B lymphocytes and offers a unique opportunity to study regulation of B-lymphocyte recruitment to a site of chronic pulmonary inflammation. Furthermore, M. pulmonis membrane activation of fresh rat serum was found to produce a potent stimulus for recruitment of peritoneal and alveolar macrophages. M. pulmonis-mediated recruitment of lymphocytes and macrophages may play a significant role in the pathogenesis of murine respiratory mycoplasmosis, a role in which organisms on the bronchiolar epithelial surfaces may release proteins which can directly or indirectly promote chemotaxis of inflammatory cells from the circulation.

Animals↗
PubMed1992

Infection-induced airway fibrosis in two rat strains with differential susceptibility.

Chronic infections play a significant role in the morbidity and mortality of patients with chronic airflow limitation. By stimulating airway inflammation, persistent infection has the potential to cause airway fibrosis. However, in patient this condition is most typically found in lungs damaged by other factors, such as smoking, abnormal secretions, or barotrauma. We report the characterization of Mycoplasma pulmonis infection-induced lung fibrosis in two immunocompetent rat strains with no preexisting lung disease. The fibrosis was predominantly in the airways, as demonstrated by the findings for infected animals of increased airway inflammation, airway fibrosis, and airway wall thickness, which correlated with the collagen content of the lungs. Also, the physiological alterations were the opposite of those found in interstitial fibrosis, with a positive correlation between lung compliance and collagen content. The airway fibrosis was noted earlier and to a greater extent in Lewis rats than in Fisher rats, and this result apparently was related to regulation of the inflammatory response. Airway wall thickness, airway inflammation, and airway fibrosis are commonly reported in tissue specimens from patients with chronic airway diseases and have been shown to correlate with airflow limitation in patients with chronic obstructive pulmonary disease. Thus, this model may be useful in furthering our understanding of the role of chronic infection and airway inflammation in airflow obstruction.

Analysis of Variance↗
PubMed1992

Decreased intrapulmonary killing of Mycoplasma pulmonis after short-term exposure to NO2 is associated with damaged alveolar macrophages.

Previous studies have shown that exposure of pathogen-free C57BL/6N mice to 5 or 10 ppm NO2 increases the severity of murine respiratory mycoplasmosis and that this effect is associated with decreased intrapulmonary killing of Mycoplasma pulmonis. The purposes of the present studies were to determine the effects of doses of NO2 lower than 5 ppm on pulmonary clearance and to provide experimental links between NO2 exposure, defects in intrapulmonary killing, and alterations in alveolar macrophages. Exposure to less than 5 ppm NO2 had no effect on intrapulmonary killing of M. pulmonis. Bronchoalveolar lavage cells killed M. pulmonis in vitro only if they were allowed to associate with mycoplasmas in vivo. Prior exposure to NO2 abrogated killing in this in vivo-in vitro model. More than 95% of the BAL cells were macrophages, and more than 98% of the cell-associated mycoplasmas were on or in alveolar macrophages. Immediately after exposure, the viability of alveolar macrophages was 89 +/- 4% in the control group, 56 +/- 19% in the group receiving M. pulmonis alone, 23 +/- 7% in the group receiving 10 ppm NO2, and 16 +/- 6% in the group receiving both M. pulmonis and NO2 exposures. Viability was significantly decreased following exposure to 10 and 5 ppm NO2 but not following exposure to 2 ppm. Both viability and intrapulmonary killing were depressed at 3 days after exposure to NO2 but were normal by 7 days after exposure. The cellular target of NO2 exposure in relation to intrapulmonary killing of M. pulmonis appears to be the alveolar macrophages.

Animals↗
PubMed1992

Pulmonary clearance of Mycoplasma pulmonis in rats with respiratory viral infections or of susceptible genotype.

We sought to determine whether or not increased severity of bronchopulmonary disease due to Mycoplasma pulmonis infection in rats with respiratory viral infections and in rats of susceptible genotype could result from altered pulmonary clearance. Pathogen-free rats were exposed to aerosols of radiolabeled M. pulmonis and the numbers of M. pulmonis colony-forming units, and amounts of radiolabel in the lungs were determined immediately after exposure or 4 hours later. Intrapulmonary killing of M. pulmonis during the 4-hour interval was determined from decreases in ratios of colony-forming units to radiolabel, and physical clearance was determined from decreases in radiolabel. Neither intrapulmonary killing nor physical clearance differed between control F344 rats and F344 rats inoculated with Sendai virus or sialodacryoadenitis virus, or between F344 and LEW rats. Rates of intrapulmonary killing and physical clearance were 64 +/- 3% and 44 +/- 2%, respectively (overall means +/- standard error).

Animals↗
PubMed1992

Early experience with laser disc decompression. A percutaneous method.

A study over an 18-month period involved 40 patients with a contained HNP who underwent laser-assisted percutaneous lumbar discectomy utilizing KTP/532. Access to the disc was via an 18-gauge probe followed by dilating cannulas under fluoroscopic control. A 400 um quartz fiber was utilized. The laser power was set between 10 and 15 watts and the exposure duration at 0.5 seconds and repeated with intervals of 0.5 seconds. Two of six patients required an open conventional L4-5 discectomy; four refused additional surgery. These failures are considered probably secondary to a subligamentous location of disc. Based upon early results, laser-assisted percutaneous lumbar discectomy with KTP laser appears to be a viable alternative to automated percutaneous discectomy in selected cases and perhaps an improvement over other techniques.

Adult↗
PubMed1991

Specific and nonspecific antibody responses in different segments of the respiratory tract in rats infected with Mycoplasma pulmonis.

Murine respiratory mycoplasmosis resulting from Mycoplasma pulmonis infection in rats provides a useful model for the study of immunological and inflammatory mechanisms operative in the respiratory tract. We have previously shown that LEW rats develop more severe disease than do F344 rats. To further study the production of antibody responses in chronic respiratory disease due to M. pulmonis infection, we examined the distribution and development of M. pulmonis-specific antibody-forming cells (AFC) in different segments of the respiratory tracts of infected LEW and F344 rats. In these studies, the upper respiratory nodes were the initial site of antibody production after infection and remained the major site for recovery of AFC. Since infected LEW rats had equal or higher numbers of AFC than did infected F344 rats, these results suggest that the level of local antibody production alone is not responsible for the decreased susceptibility of F344 rats to murine respiratory mycoplasmosis. The differences in total antibody responses appear to be due to the greater numbers of cells recovered from the tissues of infected LEW rats compared with those recovered from F344 rats, suggesting that LEW rats may have greater production of chemotactic factors. Also, we demonstrate that nonspecific activation and/or recruitment of B cells occurs in the respiratory tracts of both LEW and F344 rats after infection with M. pulmonis.

Animals↗
PubMed1991

Murine respiratory mycoplasmosis: a model to study effects of oxidants.

Previous studies have shown that exposure to nitrogen dioxide at concentrations of 5 and 10 parts per million (ppm) decreases intrapulmonary killing of Mycoplasma pulmonis, and that this decrease is related to increased lung lesions and mortality. The specific objectives of the present study were to titrate the effects of nitrogen dioxide on pulmonary clearance of M. pulmonis, determine the mechanisms by which this organism is killed within the lungs, and determine the target that the nitrogen dioxide affects. Pathogen-free C57BL/6N mice were exposed to 0, 0.5, 1, 2, or 5 ppm of nitrogen dioxide (contamination with other oxides of nitrogen compounds was 5% or less) for four hours and then immediately were exposed to aerosols of viable, radiolabeled M. pulmonis strain UAB CT. One-half of the animals in each group were killed immediately after exposure to the infectious aerosols, and the rest were killed 24 hours later. The amount of radioactivity and the number of viable M. pulmonis were determined for each group. Exposure to less than 5 ppm of nitrogen dioxide had no effect on intrapulmonary killing of M. pulmonis, although exposure to 1 ppm of nitrogen dioxide did increase mechanical removal. We were unable to develop a completely in vitro mycoplasma killing method. However, we were able to demonstrate the in vitro killing of M. pulmonis that had been allowed to associate with alveolar macrophages in vivo. Thus, mouse lungs contain unidentified factors that allow cells to kill M. pulmonis. Furthermore, we obtained evidence that suggests that prior exposure to nitrogen dioxide abrogates killing in these experiments. We also have shown that exposure to nitrogen dioxide does not increase the protein content of bronchoalveolar lavage fluid. Using immunofluorescence, more than 95% of the cells recovered by lavage were macrophages; with double-label immunofluorescence, more than 98% of the cell-associated mycoplasmas were on or in alveolar macrophages. In assessing the cytological parameters of lung lavage cells from mice exposed to nitrogen dioxide, M. pulmonis, or both, we found that both insults affected the viability of recovered macrophages. Viability immediately after exposure as measured by trypan blue exclusion or by fluorescein diacetate uptake, was 89% +/- 4% and 88% +/- 4% in the control group, respectively; 56% +/- 19% and 64% +/- 11% in the group receiving M. pulmonis alone; 23% +/- 7% and 48% +/- 9% in the group receiving nitrogen dioxide alone; and 16% +/- 6% and 25% +/- 6% in the group receiving both M. pulmonis and 10 ppm nitrogen dioxide exposures.(ABSTRACT TRUNCATED AT 400 WORDS)

Air Pollutants↗
PubMed1991

The effects of three serotypes of Ureaplasma urealyticum on spermatozoal motility and penetration in vitro.

The effects of incubation of spermatozoa with three serotypes of Ureaplasma urealyticum on spermatozoal motility and penetration in vitro were investigated. Using computer-assisted video microscopy, three parameters of motility were determined: individual path lengths, individual vectorial distances, and percentage motility. Polyacrylamide gels were used as a medium for assessment of spermatozoal penetration. Ureaplasma-infected spermatozoa did have significantly greater path lengths and individual distances than did uninfected controls, but ureaplasma infection had no significant effect on percentage motility. Overall, there were no significant differences in penetration distances between ureaplasma-infected spermatozoa and their corresponding uninfected controls. Our conclusion is that the ureaplasmas did not adversely affect motility or penetration when spermatozoa were incubated with ureaplasmas for 45 minutes at ureaplasma:sperm ratios as high as 100:1.

Female↗
PubMed1990

The Sunglass Standard and its rationale.

This paper reports on the 17-year development of the current Z80.3 Sunglass Standard. The dioptric tolerances of +0.125 to -0.25 D power, 0.125 D astigmatism, 0.25 delta prism, and 0.18 D power imbalance are based on research by optometry's leaders. The traffic signal and luminous transmittance requirements are the result of study of the literature and original research. There has been much misunderstanding regarding the UV transmittance specifications. They too were exhaustively researched and discussed. That work is reviewed in detail. New equations for calculating exposures are presented with sample spectra. Graphic evaluations of severe risk exposures are presented. They show that based on the accepted criteria, for reasonable assumptions the Standard offers a 10x margin of safety. Studies of retinal risk indicate the Standard provides ample protection. Some criteria need further study. Potential problems are based on the fact that some sunglasses are too dark for driving and that use of ordinary sunglasses for sports provides inadequate protection from injuries.

Animals↗
PubMed1989

Serum antibody does not account for differences in the severity of chronic respiratory disease caused by Mycoplasma pulmonis in LEW and F344 rats.

Chronic respiratory disease in rats, resulting from Mycoplasma pulmonis infection, is useful in the study of the immunological mechanisms in similar inflammatory diseases and provides a unique opportunity to study the interactions between systemic and mucosal immune systems in a naturally occurring infection. The present study examined the serum antibody responses to M. pulmonis in strains of rats which differ in disease progression and severity; LEW rats developed more severe disease than did F344 rats. Serum antibody responses were evaluated as to their levels, isotypes, and antigens recognized. Infected LEW rats produced greater or equal levels of the major classes of serum antibody to M. pulmonis than did infected F344 rats, suggesting that development of serum antibody responses alone does not resolve lesions and is not responsible for the difference in disease severity found in LEW and F344 rats. Although LEW rats produced higher responses in all subclasses of immunoglobulin G (IgG), the specific IgG response of LEW rats was composed predominately of IgG1 and IgG2a subclasses, while IgG2b was the major component of the IgG response in F344 rats. Finally, LEW rats responded more quickly to M. pulmonis antigens than did F344 rats, and there was no difference in the antigens eventually recognized by each strain, confirming previous work which suggested that LEW rats do not exhibit an unresponsiveness to a specific antigen(s) of M. pulmonis.

Animals↗
PubMed1989

Ureaplasma urealyticum pneumonia: experimental production and demonstration of age-related susceptibility.

Two different strains of Ureaplasma urealyticum isolated in pure culture from the lungs of newborn human infants were shown to produce an acute, self-limiting, interstitial pneumonia in newborn C3H/HeN and C57BL/6 mice that were free of other respiratory pathogens. Lesion severity peaked 3 to 6 days following intranasal inoculation of ureaplasmas and was resolved by 12 days. Rhinitis and otitis also occurred but did so less frequently than pneumonia. Organisms were localized within the alveoli in areas of inflammation. In comparison with newborn mice, 14-day-old mice were less susceptible to either colonization or disease.

Age Factors↗
PubMed1989

Short-term exposure to nitrogen dioxide enhances susceptibility to murine respiratory mycoplasmosis and decreases intrapulmonary killing of Mycoplasma pulmonis.

In C57BL/6N and C3H/HeN mice known to be free of all murine pathogens and matched for age, sex, microbiologic, and environmental factors, exposure to NO2 for 4 h prior to exposure to infectious aerosols of Mycoplasma pulmonis resulted in potentiation of murine respiratory mycoplasmosis (MRM). In the C57BL/6N mice, NO2 increased the incidence of death, incidence of gross lung lesions, and incidence of microscopic lung lesions, but did not increase the incidence of infection in the lungs. Nitrogen dioxide affected the C3H/HeN mice (a strain known to be more susceptible than the C57BL/6N strain to MRM) similarly, with the exception that the incidence of death and microscopic lesions were not affected in this strain at the concentrations of M. pulmonis used. Exposure to the oxidant also increased the severity of microscopic lesions and the numbers of Mycoplasma organisms in the lungs of both mouse strains. Thus, NO2 appeared to affect host lung defense mechanisms responsible for limiting the extent of infection. The NO2 exposure level required to produce potentiation varied with the genetic background of the host, the number of Mycoplasma organisms administered, and the end point measured. In further experiments in C57BL/6N mice, exposure to 5 or 10 ppm of NO2 for 4 h prior to infection with aerosolized, radiolabeled M. pulmonis reduced clearance of these organisms from the lungs over a 72-h time period. Nitrogen dioxide exposure did not change the rate of physical removal of Mycoplasma organisms from the lung. Reduced clearance was due to impaired intrapulmonary killing of Mycoplasma organisms in NO2-exposed mice.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗