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T R Schoeb

Publications and source records attributed to T R Schoeb.

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

Vitamin A deficiency impairs some aspects of the host response to influenza A virus infection in BALB/c mice.

We examined the impact of vitamin A deficiency on the host response to an acute, viral infection of the respiratory tract by infecting BALB/c mice with a mouse-adapted strain of influenza A virus. Several indicators of the severity of infection were examined, including the rate of virus clearance from the lungs, the extent of inflammatory lesions, and percentage of survival. None of these was affected by vitamin A deficiency. Following the acute phase of infection, however, the regeneration of normal, respiratory epithelium was impaired and adenomatoid, metaplastic lesions developed within inflammatory foci in the lungs of deficient animals. The antibody response to infection was also characterized: the influenza A-specific immunoglobulin A (IgA) response in the respiratory tract was markedly decreased by vitamin A deficiency, but tracheal and lung lavage IgG titers were not affected. The serum IgM and IgG responses, and the serum hemagglutination-inhibition response, were also diminished by vitamin A deficiency. Decreased mucosal IgA titers and impaired regeneration of normal respiratory epithelium could impair recovery from a primary infection and increase susceptibility to opportunistic secondary infections.

Animals↗
PubMed1993

Cultivation of cilia-associated respiratory bacillus in artificial medium and determination of the 16S rRNA gene sequence.

Cilia-associated respiratory (CAR) bacillus, an unclassified gliding bacterium associated with respiratory disease in rats, mice, and rabbits, has previously been cultivated only in embryonated chicken eggs, cell culture, or cell culture medium supplemented with conditioned medium from cultured tracheas. A reference strain of CAR bacillus, originally isolated in eggs, grew in cell culture flasks as adherent individual bacilli and ropy, whorled fascicles in cell culture media supplemented only with fetal calf serum. Using Dulbecco's minimal essential medium, we isolated CAR bacillus from naturally infected rats and a naturally infected rabbit and from experimentally inoculated mice and rats. Isolates were maintained for up to 20 passages. Isolates from rats were similar in morphology to the reference strain, but most were more actively motile and formed pincushion-like aggregates. The rabbit bacilli were smaller and formed fewer aggregates. DNAs of rat isolates differed only slightly in restriction fragment patterns from that of the reference strain, whereas that of the rabbit isolate was distinctly different. Cultures of CAR bacilli of all strains from rats contained Mycoplasma fermentans, Mycoplasma pulmonis, or both, and cultures of the CAR bacillus from the rabbit contained an unidentified arginine-utilizing mycoplasma. The sequence of the 16S rRNA gene of the reference strain was determined by amplification by polymerase chain reaction, cloning of the product, and sequencing by the dideoxynucleotide chain termination method. Comparison of the sequence with sequences in the GenBank data base indicated that CAR bacillus is a unique organism most closely related to Flavobacterium ferrugineum and Flexibacter sancti.

3T3 Cells↗
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

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↗
PubMed1991

Mouse hepatitis virus strain UAB infection enhances resistance to Salmonella typhimurium in mice by inducing suppression of bacterial growth.

We have previously shown that intranasal infection of mice with mouse hepatitis virus (MHV) strain UAB (MHV-UAB) increases their resistance to Salmonella typhimurium injected intravenously 6 days later. To study how salmonella resistance was induced, BALB/cAnNCr mice were infected with salmonella strains carrying specific genetic alterations. One set of studies compared the effect of MHV infection on subsequent salmonella infections with AroA- (avirulent) and Aro+ (virulent) salmonellae. Unlike its effect on Aro+ salmonellae, MHV failed to reduce the number of AroA- salmonellae recovered from mice. Because AroA- S. typhimurium shows almost no growth in vivo, this failure indicated that the effect of MHV on salmonella resistance required growth of the infecting salmonellae. In other studies, the effect of MHV infection on both growth and killing were monitored simultaneously in mice with growing salmonellae carrying a single copy of the temperature-sensitive pHSG422 plasmid, which is unable to replicate in vivo. MHV infection reduced salmonella growth but caused no increase in salmonella killing. MHV infection of mice given wild-type salmonellae also resulted in no increase in salmonella killing 4 h after salmonella challenge. These studies demonstrate that MHV-UAB infection increases host resistance to salmonellae by enhancing suppression of bacterial growth instead of by increasing the amount of salmonella killing.

Animals↗
PubMed1991

Mycoplasma pulmonis infections cause long-lasting potentiation of neurogenic inflammation in the respiratory tract of the rat.

These experiments were done to learn whether Mycoplasma pulmonis infections of the respiratory tract of rats can potentiate "neurogenic inflammation" and whether this potentiation is amplified by factors that exacerbate the infections. Pathogen-free F344 rats were inoculated intranasally with M. pulmonis or with sterile culture medium and then lived for 4 wk in an ammonia-free atmosphere or in air containing ammonia (100 parts per million). Neurogenic inflammation was evoked by an intravenous injection of capsaicin, and 5 min later the magnitude of the response was quantified by measuring the amount of extravasation of two tracers, Monastral blue pigment and Evans blue dye. We found that vascular permeability in the tracheas of all rats was normal in the absence of capsaicin. However, a 75-micrograms/kg dose of capsaicin, which caused almost no extravasation of Evans blue in the tracheas of pathogen-free controls (17 +/- 3 ng/mg; mean +/- SE), produced extensive extravasation in the infected rats (135 +/- 18 ng/mg; P less than 0.001). Similarly, this dose of capsaicin produced 30 times as much Monastral blue extravasation in the infected rats (area density = 47 +/- 8% of surface area) as it did in the pathogen-free rats (1.6 +/- 0.5%; P less than 0.001), a difference that resulted from increases in the number of Monastral blue-labeled postcapillary venules and in the amount of labeling per venule. Exposure of the infected rats to ammonia exacerbated the infections, further increased the number of Monastral blue-labeled vessels and the amount of labeling per vessel, and made the rats so sensitive to capsaicin that a normally tolerable dose of 150 micrograms/kg i.v. caused fatal apnea. Ammonia did not have these effects in pathogen-free rats. We conclude that M. pulmonis infections of the airway mucosa cause a potent, long-lasting potentiation of neurogenic inflammation, which results in part from an increase in the number and responsiveness of mediator-sensitive postcapillary venules. These changes can be amplified by environmental factors such as ammonia which exacerbate the infections.

Ammonia↗
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↗
PubMed1990

Enterocecocolitis associated with intraepithelial Campylobacter-like bacteria in rabbits (Oryctolagus cuniculus).

We examined 28 suckling, weanling, and young adult rabbits with lethargy, inappetence, and mucinous, semifluid feces. Sixteen of the rabbits had intestinal lesions. In eight of these rabbits, the primary changes were multifocal to diffuse epithelial proliferation and accumulation of lymphocytes, macrophages, or both in the lamina propria of the small intestine, cecum, and sacculated colon. In two of these rabbits, the accumulation of macrophages in the lamina propria was extensive. The other eight rabbits had erosive and suppurative cecocolitis, and four of the rabbits with proliferative lesions also had suppurative cecocolitis. In Warthin-Starry-stained sections of affected intestine, curved or spiral bacteria were visible within degenerated or hyperplastic epithelium, in luminal exudate, or in both. Such organisms were sparse or not found in the other 12 rabbits, which did not have intestinal lesions. The bacteria ultrastructurally resembled intraepithelial Campylobacter-like bacteria previously observed in proliferative enteritis in a variety of species and in acute typhlitis in young rabbits. In immunofluorescence tests, Campylobacter-like bacteria in epithelial cells, crypt lumina, and in luminal exudates in both proliferative and erosive lesions bound monoclonal antibodies and polyclonal antisera prepared against intracellular bacteria found in proliferative enteritis in pigs, hamsters, and ferrets. These observations indicate that a condition similar to proliferative enteritis of swine, hamsters, and other species also occurs in laboratory rabbits.

Animals↗
PubMed1989

Modulation of resistance to Salmonella typhimurium infection in mice by mouse hepatitis virus (MHV).

Prior infection of mice with a field strain of mouse hepatitis virus (MHV) increased the early resistance of euthymic mice to virulent Salmonella typhimurium strain SR-11 infections (as defined by significantly fewer salmonella colony-forming units (cfu) present in spleens and livers 4 days after salmonella infection). This increase in salmonella resistance was observed when the interval between MHV and salmonella infections was 6 days, but not at 3, 10, or 14 day intervals. The mouse Ity locus, which controls the number of intracellular salmonella, had a significant effect on the ability of MHV to induce resistance to salmonella. MHV caused an increase in resistance to salmonella in Itys (salmonella susceptible) mice at all doses of salmonella tested (100 to 10,000 cfu). In the Ityr (salmonella resistant) mice tested the beneficial effect of MHV on salmonella resistance was small and when observed, was only present at salmonella doses of 10,000 cfu or greater. Neither the Lpsd nor Xid mutations affected the ability of MHV to increase resistance to salmonella infection. In contrast to euthymic mice, MHV infection greatly decreased the resistance of athymic (nude) mice to salmonella infection. Since the Nu locus does not affect the resistance of mice to salmonella (at 4 days post salmonella infection), these results indicate that MHV infection and the nude phenotype interact to increase susceptibility to salmonella. These findings re-emphasize the importance of keeping laboratory mice used in research free of MHV and other immunomodulatory pathogens.

Adjuvants, Immunologic↗
PubMed1988

Inhibition of phagocytosis and interleukin-1 production in pulmonary macrophages from rats with sialodacryoadenitis virus infection.

To test whether or not sialodacryoadenitis virus (SDAV) infection in rats affects pulmonary macrophage function, we intranasally inoculated pathogen-free F344 rats with SDAV and collected alveolar and interstitial macrophages 5 d later. We assessed Fc receptor-mediated attachment and phagocytosis by phase-contrast microscopic examination of monolayers of alveolar and interstitial macrophages incubated with zymosan, nonopsonized sheep erythrocytes, or erythrocytes opsonized with rabbit antisheep-erythrocyte IgG. Alveolar macrophages from virus-infected rats had significantly (P less than or equal to .05) lower indices of attachment and phagocytosis of opsonized erythrocytes than control macrophages, but there was no difference in attachment of zymosan particles. Interstitial macrophages were not affected. Alveolar macrophages from SDAV-infected rats produced significantly less interleukin-1 than those from control rats, as assessed by testing supernatants from lipopolysaccharide-stimulated macrophage cultures for induction of mouse thymocytes to take up tritiated thymidine. Effects of SDAV infection on lung macrophages could increase host susceptibility to other pathogens or complicate studies of respiratory tract immunity.

Acute Disease↗
PubMed1988

Promotion of Mycoplasma pulmonis growth in rat tracheal organ cultures by ammonium chloride.

During exacerbation of respiratory mycoplasmosis in rats by environmental ammonia, numbers of Mycoplasma pulmonis organisms in the respiratory tract are increased. To test whether or not exposure of respiratory epithelium to ammonia in vitro promotes growth of the organism, rat tracheal organ cultures were treated with 50 mM ammonium chloride, inoculated with M. pulmonis, and quantitatively cultured. After 48 hours, treated tracheas harbored almost 10 times more M. pulmonis colony-forming units than control tracheas. Cellular lesions in the epithelium of treated tracheas resembled those in the nasal passages of rats exposed to gaseous ammonia. To determine whether or not growth-modifying factors were released from tracheal epithelium exposed to ammonium chloride, M. pulmonis growth was assessed in medium collected from ammonium chloride-treated and control tracheas. Growth in medium from treated tracheas was greater than that in medium from untreated tracheas.

Ammonium Chloride↗
PubMed1987

Suppression of immune response induction in Peyer's patch lymphoid cells from mice infected with mouse hepatitis virus.

Multiple previous studies have demonstrated significant alterations of immunologic parameters associated with mouse hepatitis virus (MHV) infection, but effects of the virus on mucosal lymphoid cells have not been examined. Coincident with a natural outbreak of MHV at our institution, we noted alterations in immunoglobulin secretion by mature Peyer's patch B cells under an inductive stimulus provided by dendritic cells and mitogen-activated T cells (DC-T). MHV was isolated from mice affected during the outbreak, and experimental infection of mice with the isolate consistently resulted in failures of immunoglobulin secretion by cocultures of Peyer's patch DC-T and B cells. In subsequent experiments, MHV appeared to negatively affect DC-T more than B cells. Therefore, the effects of inapparent MHV infection on experimental mucosal immune responses can result from natural infection and can be experimentally reproduced.

Animals↗
PubMed1987

Exacerbation of murine respiratory mycoplasmosis by sialodacryoadenitis virus infection in gnotobiotic F344 rats.

To test the hypothesis that sialodacryoadenitis virus infection could exacerbate respiratory mycoplasmosis in rats, four groups of 40 7- to 9-week-old gnotobiotic F344/N rats were given two intranasal inoculations 7 days apart: Mycoplasma pulmonis, then sialodacryoadenitis virus; M. pulmonis followed by sterile culture medium; medium initially, then virus; or two doses of medium. Immediately and 3, 5, 10, and 20 days after the second inoculation, the nasal passages, middle ears, larynges, tracheas, lungs, and salivary and lacrimal glands of four rats from each group were prepared for histologic examination, and the respiratory organs from four other rats were collected for quantitative culture of M. pulmonis and sialodacryoadenitis virus. To test statistically the effect of virus infection on mycoplasmosis lesions, we determined indices of the severity of respiratory tract lesions by subjective scoring. In rats given both organisms, indices of nasal and tracheal lesions were significantly (P less than 0.05) greater at 3 days and after than in rats given M. pulmonis alone, and middle ear, laryngeal, and lung lesion indices were significantly greater at 5 days and after. Rats given both mycoplasma and virus had significantly more mycoplasmal colony-forming units in the nasal passages at 3 days and after, and in the larynges, tracheas, and lungs at 10 and 20 days, than rats given only mycoplasma. These results show that sialodacryoadenitis virus infection can exacerbate respiratory mycoplasmosis in rats under experimental conditions; therefore, the virus probably also contributes to expression of naturally occurring mycoplasmosis.

Animals↗
PubMed1987

Muscle necrosis in Syrian hamsters resulting from intramuscular injections of ketamine and xylazine.

To assess tissue damage resulting from intramuscular injection of mixtures of ketamine and xylazine, 48 hamsters were given 100, 150 or 200 mg/kg ketamine and 10 mg/kg xylazine in one hind leg and an equal volume of sterile physiologic saline in the other leg. Four hamsters from each group were killed 1, 3, 7 and 14 days after injection and the tissues at the injection sites were examined. There was grossly apparent muscle necrosis in most of the ketamine-xylazine injected legs. By light microscopy, 47 of 48 legs injected with ketamine-xylazine had moderate to extensive muscle necrosis with an acute to chronic inflammatory response, depending on the time elapsed since injection. Microscopic slides of the injection sites were coded, randomized and scored for severity of muscle lesions. Lesion scores for ketamine-xylazine injected legs were significantly higher than controls at all post-injection times. These findings indicate that intramuscular injection of ketamine with xylazine can cause extensive muscle necrosis in hamsters and should not be used for anesthesia in survival procedures.

Animals↗