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Biomedical subjects

T A Bertram

Publications and source records attributed to T A Bertram.

At least 19 recordsLinked to original sources
PubMed1997

Effects of particle exposure and particle-elicited inflammatory cells on mutation in rat alveolar epithelial cells.

To investigate mechanisms underlying development of lung adenomas and carcinomas in rats exposed to poorly soluble particles the relationships between particle exposure, inflammation and mutagenesis in rat alveolar type II cells were characterized. Rats were exposed to saline or saline suspensions of 10 and 100 mg/kg of alpha-quartz, carbon black or titanium dioxide by intratracheal instillation. Fifteen months after exposure, bronchoalveolar lavage (BAL) cells were characterized as to number and type and lung histopathology performed. The alveolar type II cells were isolated and cultured in 6 thioguanine (6TG) containing media to select for mutation in the hprt gene. The potential contribution of lung inflammatory cells to in vivo mutagenic responses, were evaluated by co-culturing BAL cells with the rat alveolar epithelial cell line, RLE-6TN for 24 h and the RLE-6TN cells selected for 6TG resistance. Neutrophilic inflammation was detected in all rats exposed to 10 and 100 mg/kg of alpha-quartz and carbon black and 100 mg/kg titanium dioxide; epithelial hyperplasia was observed in rats exposed to 10 and 100 mg/kg of alpha-quartz and 100 mg/kg carbon black. Hprt mutation frequency was increased in alveolar type II cells from rats exposed to 10 and 100 mg/kg of alpha-quartz, 100 mg/kg carbon black and 100 mg/kg titanium dioxide. In vitro exposure of RLE-6TN cells to BAL cells from rats treated with 10 and 100 mg/kg of alpha-quartz or 100 mg/kg carbon black increased hprt mutant frequency. Both macrophage and neutrophil enriched BAL cell populations were mutagenic to RLE-6TN cells, however, the mutagenic activity appeared greatest for neutrophils. Addition of catalase to BAL cell:RLE-6TN co-cultures inhibited the increase in hprt mutation frequency. These studies demonstrate exposure of rats to doses of particles producing significant neutrophilic inflammation is associated with increased mutation in rat alveolar type II cells. The ability of particle-elicited macrophages and neutrophils to exert a mutagenic effect on epithelial cells in vitro supports a role for these inflammatory cells in the in vivo mutagenic effects of particle exposure. The inhibition of BAL cell-induced mutations by catalase implies a role for cell-derived oxidants in this response.

Animals↗
PubMed1996

Evaluation in rats of the dose-response relationship among colonic mucosal growth, colonic fermentation, and dietary fiber.

The dose-response relationship among dietary fiber, colonic fermentation, fecal weight, and mucosal growth were evaluated in this study. The morphometric parameter of total mucosal volume was used to assess diet-induced differences in colonic mucosal growth. Dietary fibers with a wide range of fermentability and that have previously been shown to inhibit the development of colonic neoplasia in rats were used. Sprague-Dawley rats were fed Purina Rodent Chow, AIN-76a fiber-free diet, or an AIN-76a diet supplemented with three different dietary fibers, (cellulose, guar gum, or wheat bran) at 2, 5, 10, or 15% of the diet. Diets were fed for 28 days. Total colonic mucosal volume was determined using stereologic principles and computerized image analysis; 48-hr fecal weight was measured; and the concentration of short-chain fatty acids (SCFA) in colonic contents was determined at study termination. Each type of fiber induced a dose-dependent increase in total mucosal volume of the colon and fecal weight. Mucosal volume and fecal weight were closely correlated (R2 > 0.95). Total mucosal volume was not correlated with the concentration of total SCFA or butyrate in the colon. These results indicate that diet-induced change in colonic mucosal growth, as measured by total mucosal volume, is positively correlated with fecal weight and not related to alterations in colonic fermentation. Enhanced colonic mucosal growth occurs in rats fed dietary fibers that have previously been shown to inhibit the development of genotoxin-induced colonic neoplasia in rats.

Animals↗
PubMed1994

Fatty acid-mediated gastroprotection does not correlate with prostaglandin elevation in rats exposed to various chemical insults.

This study involved a comparison of activity of several long-chain fatty acids (arachidonic acid, dihomo-[gamma]-linolenic acid, linoleic acid, and oleic acid) for protection against gastric mucosal damage elicited by taurocholic acid, acidified aspirin, and ethanol in rats. Each damaging agent induced gastric mucosal lesions in the corpus. Mucosal damage was induced by all agents, and all fatty acids protected the gastric mucosa; however, ethanol and arachidonic acid were the most potent damaging and protecting agents, respectively. Maximally protective doses for prevention of taurocholic acid-induced damage by arachidonic, dihomo-[gamma]-linolenic, linoleic, and oleic acids were 50, 200, 100, and 200 mg/kg, respectively; however, 10 mg/kg arachidonic acid reduced lesion length by > 50%, whereas minimally effective doses of the other fatty acids were > or = 50 mg/kg. Similar potency differences were observed for fatty acid protection against acidified aspirin-induced gastric damage. Although all the fatty acids reduced macroscopic damage, histologic studies showed they did not totally eliminate surface mucosal damage. Microscopic analysis showed that treatment with dihomo-[gamma]-linolenic acid or oleic acid attenuated depletion of neutral and acidic glycoproteins from the mucus neck cells of the gastric mucosa in response to exposure to taurocholic acid. Despite having similar gastroprotective activity, arachidonic, dihomo-[gamma]-linolenic, linoleic, and oleic acids had very dissimilar abilities to elevate gastric mucosal E-series prostaglandins. Both arachidonic and dihomo-[gamma]-linolenic acids elevated E-series prostaglandins, but arachidonic acid had 2-5-fold greater gastroprotective potency. Furthermore, oleic and linoleic acids, which had protective potency similar to that dihomo-[gamma]-linolenic acid, did not significantly elevate prostaglandins. These studies failed to demonstrate an absolute correlation between prostaglandin elevation and gastroprotection. The results of this investigation suggest that prostaglandin elevation, although associated with gastroprotection, does not appear to be the sole mechanism for fatty acid-mediated protection of rat gastric mucosa.

Analysis of Variance↗
PubMed1993

A 91-day feeding study in rats with caprenin.

Caprenin, a randomized triglyceride primarily comprising caprylic (C8:0), capric (C10:0), and behenic (C22:0) acids, was administered in a semi-purified diet to weanling Sprague-Dawley rats (25/sex/group) at dose levels of 5.23, 10.23 or 15.00% (w/w) for 91 days. Corn oil was added at 8.96, 5.91 and 3.00%, respectively, to provide essential fatty acids and digestible fat calories. Corn oil alone (12.14%) and a blend of medium-chain triglyceride (MCT) oil plus corn oil (11.21 and 3.13%, respectively) served as controls. All diets were formulated to provide about 4000 kcal/kg of diet and 26.8% of digestible calories from fat by assuming that corn oil, MCT oil, and caprenin provided 9, 7 and 5 kcal/g, respectively. Survival, clinical signs, body weight, feed consumption, feed efficiency, organ weights, organ-to-body-weight ratios, organ-to-brain-weight ratios, haematological values and clinical chemistry parameters were evaluated in all groups. Histopathology of a full complement of tissues was evaluated in the corn oil and MCT oil control groups as well as the high-dose caprenin group. Additional rats (n = 5/sex/group) were included in the study to determine whether there was marked storage of C22:0 in heart, liver or perirenal fat at the end of the 91-day feeding period. No significant differences in body weight gain were measured with the balanced caloric diets, although feed conversion efficiency was reduced in the high-dose caprenin group. No adverse effects from the ingestion of caprenin were detected, nor were significant amounts of C22:0 present in the fat extracted from the selected fat depot sites. These results establish a no-observable-adverse-effect level (NOAEL) of more than 15% (w/w) caprenin in the diet (or more than 83% of total dietary fat), which is equal to a mean exposure level of more than 13.2 g/kg/day for male rats and more than 14.6 g/kg/day for female rats.

Adipose Tissue↗
PubMed1992

Colonic epithelial cell proliferation in a rat model of nongenotoxin-induced colonic neoplasia.

BACKGROUND: The effect on colonic cell proliferation of poligeenan, a nongenotoxic polysaccharide that induces colon tumors in rats, was compared with guar gum and carrageenan. EXPERIMENTAL DESIGN: Fischer 344 rats were fed a basal diet supplemented with carrageenan and poligeenan fibers for up to 91 days. The quantitative levels of proliferation, location of the proliferating cells, and the ability of the mucosa to readapt by removing the experimental fibers from the diet were tested. RESULTS: The mucosal epithelium exhibited a 5-fold increase in thymidine kinase activity in both the carrageenan and poligeenan groups. Proliferating cells appeared at the luminal surface only in the poligeenan-treated rats, and the number of proliferating cells in the upper third of the crypt increased 35-fold. A second and third set of animals were fed one of the three test diets for either 28 or 64 days, followed by a 28-day recovery period. Proliferation in the guar- and carrageenan-treated groups returned to basal levels. In poligeenan-treated rats, thymidine kinase levels, and proliferating cells in the upper third of the crypt remained 2- and 11-fold, respectively, above controls. CONCLUSIONS: The difference in recovery time between the poligeenan group and the others, and the luminal location of proliferating cells may prove useful as markers in understanding early events in the carcinogenic process induced by a nongenotoxin.

Administration, Oral↗
PubMed1991

Gastritis associated with infection by Helicobacter pylori in humans: geographical differences.

Previous studies have indicated that infection rates of Helicobacter pylori are influenced by geographical factors. The present studies evaluate the characteristics of gastritis, associated with infection by H. pyrlori, and demonstrate relationships between different geographical locations and the extent of inflammatory cell accumulation in the gastric mucosa. Gastric biopsy specimens were obtained from patients infected with H. pylori at three clinical sites (two from North America and one from South America). Gastric inflammation was evaluated by quantitative histomorphometric techniques. Patients from South America had a more severe gastritis than did those from North America. Additionally, in South American patients the neutrophil was the predominant inflammatory cell type in the gastric mucosa. In contrast, the lymphocyte was the primary cell composing the mucosal infiltrate of infected North American subjects. Eosinophil infiltration into the mucosa correlated with the extent of mucosal atrophy; however, there were no differences between the North and South American patient populations in the extent of mucosal atrophy present in the specimens. We conclude that the characteristics (severity and cell type) of gastritis associated with infection by H. pylori are influenced by geographical factors that may be similar to those that modify infection rates for different geographical locations.

Adult↗
PubMed1991

Relationship between gastric inflammatory response and symptoms in patients infected with Helicobacter pylori.

The relationship between the histologic severity of gastritis and associated symptoms was examined in 19 adult patients infected with Helicobacter pylori. At the time of gastrointestinal endoscopy, symptoms of dyspepsia were assessed by means of a linear analog scale. Gastric inflammation was quantitated with histomorphometric techniques. Symptoms such as epigastric pain, burping/belching, and nausea correlated with the degree of inflammation. These positive correlations suggest that the severity of the histologic gastritis contributes to the severity of symptoms. Therefore, utilization of a linear analog scale to assess symptoms may be a useful technique in evaluating the outcome of therapeutic trials of patients with symptomatic H. pylori infection.

Adult↗
PubMed1990

Actinobacillus pleuropneumoniae: molecular aspects of virulence and pulmonary injury.

Contributions made by several laboratories in the area of Actinobacillus pleuropneumoniae virulence and its relationship to pulmonary disease will be reviewed briefly. Lung injury and subsequent disease, after infection with A. pleuropneumoniae, can be related to various bacterial toxins and host factors. Similar to other gram-negative bacteria. A. pleuropneumoniae has cell wall lipopolysaccharides which have been incriminated in a wide variety of toxic and tissue damaging processes. Virulent isolates of A. pleuropneumoniae have been shown to have a thick capsule whereas some avirulent isolates have a thin and easily removed capsule. The capsule of A. pleuropneumoniae is a linear unbranched polysaccharide composed of repeating dissaccharide subunits that bestow antiphagocytic properties to the bacterium but are also immunogenic. In addition, A. pleuropneumoniae has several chemically defined exotoxins. These toxins have generally been shown to be proteinaceous molecules that are hemolytic, cytotoxic, or edemogenic. Some of these toxins are proteolytic and others have the putative activity of being lytic for secretory IgA. Several of these molecules are capable of inducing lesions that are similar to those observed in natural infections and disease. Endogenous host factors have also been implicated in the development of lung lesions after infection by A. pleuropneumoniae Coagulation and inflammatory pathways have been demonstrated to be pivotal in the early phases of lesion development. In addition, the immune status of the animal is clearly related to the severity and ultimate outcome of A. pleuropneumoniae infection. To adequately treat and prevent this disease, we must understand the distinguishable interactions that occur between the host and the various molecular virulence attributes of A. pleuropneumoniae.

Actinobacillus↗
PubMed1989

Comparison of arachidonic acid metabolism by pulmonary intravascular and alveolar macrophages exposed to particulate and soluble stimuli.

Pulmonary intravascular macrophages, as prominent components of the pulmonary mononuclear phagocyte system, could be significant mediators of lung inflammation. We have shown that intravascular and alveolar macrophages metabolize exogenous arachidonic acid to its inflammatory metabolites via the lipoxygenase and cyclooxygenase pathways after exposure to the calcium ionophore A23187. In this study, we compare the metabolism of endogenous arachidonic acid by porcine intravascular and alveolar macrophages after exposure to soluble and particulate stimuli. Since intravascular and alveolar macrophages are exposed to various stimuli in vivo, it is essential to know the range of inflammatory mediators that these cells can generate. Alveolar macrophages attached to plastic and exposed to the various stimuli produced prostaglandin F2 alpha, 12-hydroxyheptade-catrienoic acid (HHT), hydroxyeicosatetraenoic acids (HETE), and leukotriene B4. In contrast, adherent and stimulated intravascular macrophages produced several cyclooxygenase products and lipoxygenase products including 5-HETE, 12-HETE, and leukotriene B4. Both macrophages released large amounts of arachidonic acid upon exposure to each stimulant. Intravascular macrophages that were adherent to plastic or were stimulated with glass, asbestos, or A23187 released significantly (p less than 0.05) more metabolized arachidonic acid than similarly treated alveolar macrophages. The major cyclooxygenase metabolite released by alveolar macrophages was prostaglandin 2 alpha, whereas HHT was the primary metabolite of intravascular macrophages. The major lipoxygenase metabolite released by both macrophage types was 5-HETE, but intravascular macrophages also released substantial amounts of 12-HETE and leukotriene B4. In both macrophage preparations, lipoxygenase products composed most released metabolites. After exposure to iron, asbestos, and A23187 intravascular macrophages released significantly more (p less than 0.05) lipoxygenase metabolites than alveolar macrophages. However, in alveolar macrophages, chrysotile asbestos induced greater activity by the cyclooxygenase pathway than by the lipoxygenase pathway. Both asbestos and iron spheres induced release of arachidonic acid and its metabolites, but the most potent stimulants in both macrophage preparations were A23187, zymosan, and lipopolysaccharide. We conclude that stimulated intravascular macrophages use both cyclooxygenase and lipoxygenase pathways to metabolize endogenous arachidonic acid, that these macrophages are metabolically more active than alveolar macrophages, and that both macrophage types are induced to metabolize arachidonic acid by various particulate and soluble stimuli. Furthermore, we have shown that intravascular macrophages predominantly utilize the lipoxygenase rather than cyclooxygenase pathways to metabolize endogenous arachidonic acid.

Animals↗
PubMed1988

Isolation and preliminary in vitro characterization of the porcine pulmonary intravascular macrophage.

Porcine intravascular macrophages were isolated by perfusion of the pulmonary vasculature with 0.1% collagenase solution. The isolated cells formed intercellular adhesion plaques with endothelial cells when incubated with porcine pulmonary artery, aorta, and corneal cups. Intercellular adhesion plaques were focal junctionlike membrane specializations consisting of paired submembranous amorphous densities subjacent to 15-20 nm gaps between parallel apposing cell membranes. The intermembranous space was filled with moderately electron dense, finely granular material. Adhesion plaques formed in 4-8 hours and resembled the adhesion plaques formed between pulmonary intravascular macrophages and endothelium in vivo. Alveolar macrophages and peripheral blood monocytes did not form intercellular adhesion plaques with endothelial cells. Intravascular macrophages had histologic and ultrastructural features of macrophages, were alpha naphthyl butyrate esterase positive, adhered to plastic coverslips after 1 hour of incubation, and were smaller than alveolar macrophages and endothelial cells. The formation of intercellular adhesion plaques in vivo and in vitro by cells with morphologic and histochemical features of macrophages distinguishes intravascular macrophages from monocytes and alveolar macrophages.

Animals↗
PubMed1988

Pulmonary intravascular macrophages metabolize arachidonic acid in vitro. Comparison with alveolar macrophages.

Pulmonary intravascular macrophages are a recently identified component of the pulmonary mononuclear phagocyte system. It has been shown that alveolar macrophages are capable of metabolizing arachidonic acid (AA) to its biologically active inflammatory metabolites via the lipoxygenase and cyclooxygenase pathways. In this study, we have compared the ability of swine intravascular macrophages and alveolar macrophages to metabolize AA in vitro. Alveolar macrophages attached to a plastic substrate produced at least five identified AA metabolites including prostaglandin (PG)F2 alpha, hydroxyheptadecatrienoic acid (HHT), 5-hydroxyeicosatetraenoic acid (HETE), 12-HETE, and 15-HETE. In contrast, adherent intravascular macrophages produced eight identified metabolites including thromboxane (TX)B2, PGF2 alpha, PGD2, PGE2, HHT, 5-HETE, 12-HETE, and 15-HETE. The major lipoxygenase metabolite produced by both macrophage types was 5-HETE. The major cyclooxygenase metabolite produced by alveolar macrophages was PGF2 alpha, whereas the major metabolite produced by intravascular macrophages was HHT. Both macrophage populations treated with calcium ionophore (A23187) exhibited increased production of PGs, TXB2, leukotriene (LT)B4, 5-HETE, 12-HETE, and 15-HETE, but the most striking increase occurred in metabolism through the lipoxygenase pathway. The major lipoxygenase metabolite generated by ionophore-stimulated macrophages was 5-HETE, and in intravascular macrophages 12-HETE was also produced. Preincubation of macrophages with indomethacin and nordihydroguaiaretic acid attenuated the yield of cyclooxygenase metabolites and lipoxygenase metabolites, respectively. Studies of leukotriene formation demonstrated that both macrophage types produce LTC4 and LTB4 from the leukotriene precursor LTA4. Thus, we show that the pulmonary intravascular macrophage is capable of metabolizing AA and LTA4 to their inflammatory and vasoactive metabolites by the cyclooxygenase and lipoxygenase pathways.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Morphological and biochemical comparison of virulent and avirulent isolates of Haemophilus pleuropneumoniae serotype 5.

Capsular structure and biochemical composition varied between two isolates (virulent and avirulent) of Haemophilus pleuropneumoniae serotype 5. The presence of capsule was determined by transmission electron microscopy with glutaraldehyde-osmium, ruthenium red, alcian blue, and phosphotungstic acid staining procedures. The virulent isolate of H. pleuropneumoniae had a distinct, adherent capsule. The avirulent isolate had a fragile, easily removed capsule. Capsular material (CM) and a lipopolysaccharide (LPS) were isolated from each bacterial isolate and were compared biochemically and biologically. CM from both isolates contained carbohydrates, no detectable protein, and no detectable to trace amounts of lipid A. Each LPS contained heptose, hexose, galactose, glucosamine, 2-keto-3-deoxyoctonate, and lipid A. Biological responses to CM and LPS from both isolates were demonstrated in the proclotting enzyme of Limulus polyphemus amebocyte lysate activation and in serological cross-reactions by immunofluorescence and immunodiffusion precipitation. The virulent isolate contained approximately 10 mg of LPS per g more on an original dry weight basis than the avirulent isolate. LPS from the virulent isolate contained approximately 13 times more galactose than LPS from the avirulent isolate. The differences of capsular structure and biochemical composition may contribute to the role of CM in porcine H. pleuropneumoniae infections.

Animals↗
PubMed1986

Preferential inhibition of primary granule release from bovine neutrophils by a Brucella abortus extract.

A low-molecular-weight Brucella abortus extract (a nucleotidelike material) inhibited zymosan-elicited neutrophil degranulation and trichloroacetic acid-precipitable protein iodination (a measure of myeloperoxidase and H2O2 release from neutrophilic leukocytes). Inhibition of neutrophil function was directly related to the concentration of the Brucella extract. The extract preferentially inhibited degranulation of primary (azurophilic or peroxidase positive) granules and had limited inhibition of secondary (specific or peroxidase negative) granule release but did not inhibit opsonized zymosan ingestion. Inhibition of protein iodination closely paralleled that of primary granule release but was unrelated to inhibition of secondary granule release. These results suggest that B. abortus has a component which is capable of inhibiting release of myeloperoxidase by dose-dependent preferential inhibition of primary granule release from bovine neutrophilic leukocytes.

Animals↗
PubMed1986

Intravascular macrophages in lungs of pigs infected with Haemophilus pleuropneumoniae.

Pigs were inoculated intratracheally with a virulent or an avirulent isolate of Haemophilus pleuropneumoniae serotype 5 and sacrificed during the first 24 hours post-inoculation. Intravascular macrophages were examined by electron microscopic and morphometric techniques. Samples of lung were taken from regions with no macroscopic lesions (Zone 0), 2.5 to 3.0 cm from lesions (Zone 1), and from the immediate edge of lesions (Zone 2). Those pigs inoculated with the avirulent isolate did not develop lesions. Pigs given the virulent isolate consistently developed necrohemorrhagic lesions in the dorsolateral aspect of the caudal and middle lung lobes. Relative volumes of intravascular macrophages in Zones 1 and 2 increased with increased time post-inoculation; in pigs given the avirulent isolate, intravascular macrophage volume decreased with increased time post-inoculation. Cytoplasmic volume to nuclear volume ratios for macrophages in Zone 2 from pigs with necrohemorrhagic lesions progressively increased with increased time post-inoculation. Enlarged intravascular macrophages had large nuclei, prominent nucleoli, and abundant cytoplasm. Increased cytoplasmic volume was the result of increased numbers of lysosomes, phagosomes, rough and smooth endoplasmic reticulum, and large Golgi complexes. Pigs inoculated with the virulent bacteria had IV macrophages with large phagosomes that contained necrotic cell debris and fibrin. Macrophages with phagosomes were more frequent in the 6-, 9-, and 24-hour sample periods of pigs with lesions than in any other group. Intercellular adhesion plaques (ICAP) were present between IV macrophages and subjacent endothelial cells. ICAP's increased in length with increased time post-inoculation in Zones 1 and 2 from pigs with necrohemorrhagic lesions. In later sample periods, multiple closely associated and interlacing IV macrophages formed a discontinuous layer over endothelial cells in Zone 2 samples near necrohemorrhagic lesions. These results suggest that the intravascular macrophage population changes from immature macrophages to mature macrophages or immature epithelioid cells within 24 hours after inhalation of a virulent Haemophilus pleuropneumoniae. Furthermore, intravascular macrophages likely function to clear cellular and acellular debris from the blood in pneumonic conditions.

Animals↗
PubMed1985

Pathology of an ulcerative dermatitis in Belgian Landrace sows.

Chronic ulcers of the skin were observed in three Belgian Landrace sows. Lesions were located on ears, limbs, and in the mammary region and were resistant to treatment that included corticosteroid therapy. Major histologic changes were located at the dermo-epidermal junction. Ulcers were deep, and the adjacent epidermis had marked hyperkeratosis, acanthosis, and intracellular edema. Dermatitis was prominent, essentially located in the superficial dermis. By electron microscopy, basal lamina appeared disrupted. Dermo-epidermal separation occurred beneath the basal lamina. Collagen was morphologically normal. Desmosomes, hemidesmosomes, and anchorage fibers were present in areas adjacent to lesions. Ulcerative dermatitis of sows is morphologically similar to pemphigus, pemphigoid, systemic lupus erythematosus, epidermolysis bullosa simplex, erythema multiforme, toxic epidermal necrolysis, and drug eruption. However, significant differences exist between ulcerative dermatitis and these conditions.

Animals↗
PubMed1985

Quantitative morphology of peracute pulmonary lesions in swine induced by Haemophilus pleuropneumoniae.

Twenty-seven six-week-old cesarean-derived, colostrum-deprived pigs were inoculated intratracheally with an isolate of Haemophilus pleuropneumoniae serotype 5 (principles) of high virulence (I-200) or low virulence (B-8) or phosphate buffered saline (controls). Pigs given I-200 had severe serofibrinous pleuropneumonia at three hours after inoculation; two of three pigs were dead by 24 hours after inoculation. Interalveolar septa in the caudal lung lobes were 41% thicker than septa from control pigs at three hours after inoculation and 79% thicker by 24 hours after inoculation. Interalveolar septal capillaries in caudal lung lobes were 10.2% larger than control capillaries at three hours after inoculation and 25.6% larger by 24 hours after inoculation. Interalveolar septal capillary platelet volume was greater than the platelet volume of controls; 70% of these platelets were aggregated. There was severe diffuse alveolar, interalveolar septal, and interlobular septal edema at three hours after inoculation with fibrin, neutrophils, and macrophages present in later samples. Thirty-three percent of the lung parenchyma was necrotic at 24 hours after inoculation. Endothelial cell degeneration was generally mild, but necrotic in regions of pulmonary infarction. Pigs inoculated with the B-8 isolate did not develop marked macroscopic lesions at any sampling time. Interalveolar septa were 18% thicker than controls nine hours after inoculation and 5% thicker at six and 24 hours after inoculation. Capillary platelet volume was greatest at nine hours after inoculation with 50% of these platelets aggregated; 30% of the platelet volume was aggregated at the 24-hour sample period. Moderate diffuse pulmonary and interlobular septal edema was present at three, six, and nine hours after inoculation, but absent 24 hours after inoculation. Intravascular macrophages were present in the six, nine, and 24-hour lung samples in both B-8 and I-200 inoculated pigs. These cells were adherent to interalveolar septal capillary endothelial cells and contained phagocytized cellular debris and fibrin. These results indicate the early effects of H. pleuropneumoniae infection involve macrophage and platelet activation, and a marked increase in interalveolar septal capillary permeability.

Animals↗