Inflammatory response induced by Helicobacter pylori infection in lung.

Helicobacter pylori is a microorganism that in the last years has been associated with extragastric disorders such as respiratory diseases, however, its impact on lung is partially understood. The aim of this work was to study infection impact of H. pylori on the inflammatory markers expression at the pulmonary level using an animal model. Infection was performed by BALB/c wild type (WT) mice orotracheal instillation with 20 µl of 1 × 108H. pylori reference strain suspension once per day throughout 3 days. Inflammatory response was evaluated at 3, 7, 14, 21 and 30 days post infection. Lung was aseptically removed and pulmonary edema index values showed a significant change at 30 days of infection. Hematoxylin-Eosin (H-E) stain allowed to visualizing H. pylori presence in lung samples at 3 days of infection near the phagocytic cells or in the alveoli lumen. Bronchoalveolar lavage (BAL) was used for inflammatory response evaluation. Lactate dehydrogenase values showed a gradual increase in infected animals along infection time. Protein concentrations in mg/ml from BAL increased significantly at 7 days in infected animals. Macrophages viability obtained from BAL, decreased at the first moment of infection, maintaining constant values along contamination time. Results obtained demonstrate an inflammatory response in lung after orotracheal H. pylori infection and suggest that the pathogenic mechanism is strongly evidenced by tissue damage, endothelial dysfunction inflammatory mediators and markers expression at the pulmonary level.

Diet-Induced Pulmonary Inflammation and Incipient Fibrosis in Mice: a Possible Role of Neutrophilic Inflammation.

Chicken fat and fructose are added into food-processing to reduce costs and enhance acceptability; however, these additives turn food into unhealthy and hypercaloric meals. Herein we have hypothesized that chronic feeding with chicken fat and fructose, together or by separate, can cause pulmonary redox and inflammatory changes. These changes are particularly related to neutrophils and myeloperoxidase, with consequent changes in the organ histophysiology. To test this hypothesis, we fed mice for 16 weeks with either control food (low-fat diet, LFD) or control food supplemented with 22% chicken fat and with or without 10% fructose in the drinking water. At the end of the feeding regimen, we measured redox and inflammatory changes in the lung with particular emphasis on neutrophil accumulation/activation and molecular-histological markers of fibrosis. Our results suggest that a diet supplemented with chicken fat and fructose causes additive effects on pulmonary oxidative stress, inflammation, and a pro-fibrotic status. Neutrophilic inflammation may play a critical role in pulmonary pathology associated with metabolic syndrome.

Study of Helicobacter pylori infection on lung using an animal model.

Helicobacter pylori infection has been reported to be associated with extra-digestive disorders such as respiratory diseases; however, the impact of H. pylori on lung is incompletely understood. Inflammatory response is mediated by the release of cytokines, interferon, and enzymes such as metalloproteinases (MMPs). This may contribute to collagen accumulation during the early phase of infection. MMP expression is an important factor for the proliferation and infiltration of lung cells in the process of fibrosis formation. The aim of this work was to study the impact of the infection with H. pylori on lung using a mouse model. We looked for histological lesions of lung infected with the microorganism as well as the expression of inflammatory and of endothelial dysfunction markers. C57BL/6 wild type (WT) mice were infected by orotracheal instillation with 20 µl of 1 × 108H. pylori reference strain suspension once per day for 3 days. Animals infected and controls were sacrificed at 3, 7, 14, 21 and 30 days. The lung from mice were stained with Hematoxylin-Eosin (H-E), Masson's Trichromic and Periodic Acid Schifft (PAS) for histological study. Also, lipid hydroperoxides and enzime catalase (CAT) activity were determined. Expression level of multiple markers implicated in inflammation (tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, IL-4, IL-6, IL-8, IL-10; metalloproteinase MMP-9) and markers of endothelial dysfunction (I-CAM and V-CAM) was determined from lung tissues mRNA using RT-PCR. Results showed that H. pylori induced morphological changes in the lung tissue with recruitment of inflammatory cells and lung parenchymal cell degradation. The mRNA of IL-1ß and TNF-α; MMP-9, I-CAM and V-CAM increased at 3-7 days infections. Also, iNOS, IL-8 and Phosphocholine cytidyltransferase (CCT) increased with lung injury. Anti-inflammatory interleukin as: IL-4, and IL-10 increased at 7 and 14 days post infection respectively. The results obtained suggest that the pathogenic mechanism of H. pylori on lung could be strongly associated with lung injury as indicate the expression increased of inflammatory mediators and markers of endothelial dysfunction.

A unified degree day model describes survivorship of Copitarsia corruda Pogue & Simmons (Lepidoptera: Noctuidae) at different constant temperatures.

Predictions of survivorship are critical to quantify the probability of establishment by an alien invasive species, but survival curves rarely distinguish between the effects of temperature on development versus senescence. We report chronological and physiological age-based survival curves for a potentially invasive noctuid, recently described as Copitarsia corruda Pogue & Simmons, collected from Peru and reared on asparagus at six constant temperatures between 9.7 and 34.5 degrees C. Copitarsia spp. are not known to occur in the United States but are routinely intercepted at ports of entry. Chronological age survival curves differ significantly among temperatures. Survivorship at early age after hatch is greatest at lower temperatures and declines as temperature increases. Mean longevity was 220 (+/-13 SEM) days at 9.7 degrees C. Physiological age survival curves constructed with developmental base temperature (7.2 degrees C) did not correspond to those constructed with a senescence base temperature (5.9 degrees C). A single degree day survival curve with an appropriate temperature threshold based on senescence adequately describes survivorship under non-stress temperature conditions (5.9-24.9 degrees C).

Interleukin-12p40 contributes to protection against lung injury after oral Yersinia enterocolitica infection.

OBJECTIVE: The impact of Yersinia enterocolitica on lung is incompletely understood, so we studied the inflammatory effects of Yersinia oral infection and the influence of IL-12p40 deficiency. METHODS: Wild-type (WT) and IL-12p40-/- (KO) mice were orally infected with Y. enterocolitica 0:3. After 3 and 21 days, cell viability in bronchoalveolar lavage (BAL) fluid, inflammatory reactions, lipid hydroperoxides, antioxidant enzyme expression and histological changes were studied. RESULTS: An effect on the lung was demonstrated by changes in lactate dehydrogenase, total protein (p <0.001), nitrosative stress and increase numbers of lymphocyte in the BAL fluid. All of these appeared to be IL-12 - independent since statistically significant changes in response to infection (at 21 days) did not differ between WT and KO groups. However, a protective role of IL-12 after infection was suggested by a decrease in cell viability, histopathological changes, different cell populations, higher lipid peroxidation and a decrease in antioxidant enzymes - glutathione peroxidase, superoxide dismutase-2 (p <0.05). The main changes were detected at day 21 suggesting a chronic effect of Yersinia infection and that IL-12 could play a role in the protection against chronic sequelae in the lung. CONCLUSIONS: These results demonstrate that Y. enterocolitica infection may induce inflammatory response in lung and that IL-12p40 could contribute to protection against lung injury.

Influence of a protein concentrate from Amaranthus cruentus seeds on lipid metabolism.

It is widely known that elevated cholesterol and triglycerides levels favor the development of heart disease. In this paper we studied the effect of a protein concentrate from Amaranthus cruentus (Ac) on the lipid content in serum and liver tissue of male Wistar rats. The animals were separated into two groups, each group with 16 rats. The control diet had casein as protein source (CD), and the experimental one had Ac protein concentrate (PCAcD). The diets contained 1% cholesterol. Parameters of oxidative stress in liver with CD and PCAcD were also evaluated. No significant differences were observed in serum total cholesterol, whereas LDL decreased and HDL increased (P < 0.001), and the amount of triglycerides decreased in PCAcD as compared to CD. In liver, a decrease of total cholesterol and triglycerides (P < 0.001) was observed in the experimental group in relation to control. Fatty acid synthase (FAS) activity decreased significantly in the experimental group. The mRNA of HMG-CoA reductase did not change, and mRNA of FAS decreased in rat liver fed with PCAcD compared with CD. The excretion of total lipids in feces increased with PCAcD compared to CD (P < 0.001). The activity of reactive substances to thiobarbituric acid in liver showed no significant differences between the control and experimental diets. However, total glutathione and reduced glutathione increased in PCAcD compared to CD (P < 0.001). It can be concluded that PCAcD has a hypotriglyceridemic effect, affects the metabolism of liver lipids, and increases parameters of antioxidant protection in male Wistar rats.

Lung lipid composition in zinc-deficient rats.

There have been a limited number of studies investigating surfactant lipid changes in lung with trace elements. The present investigation was designed to examine the effect of moderate zinc deficiency on the lipid metabolism in rat lung. We also evaluated whether zinc deficiency, which is a wide-spread problem, could play a role in adult respiratory distress syndrome (ARDS). For that purpose, adult male Wistar rats were fed two diets differing in zinc concentration. The rats were divided into two groups. One group was fed a zinc-deficient diet containing 3 mg Zn/kg, and the other group received a zinc-adequate control diet with 30 mg Zn/kg according to AIN 93-M. After 2 mon of treatment, we observed that in the zinc-deficient group (i) total lipids, phospholipids, and cholesterol increased whereas TG decreased in whole lung; (ii) phospholipid (PC) concentration increased in lamellar bodies and alveolar macrophages and decreased in extracellular surfactant but did not change in microsomes; (iii) protein concentration decreased in whole lung, extracellular surfactant, lamellar bodies, and macrophages; (iv) the incorporation of [Me-14C]choline into PC (phospholipids) of lung slices increased; and (v) the activity of CTP/phosphocholine cytidylyltransferase bound to the microsomes increased in the lung. These results suggest that the lipid concentration in the lung (especially the phospholipids) is modified directly or indirectly by a zinc-deficient diet. In a zinc-deficient diet, the lung changes the pattern of PC for an adaptive or recovery stage. Therefore, zinc deficiency implications are important for the design of therapies and public health interventions involving targeted zinc supplementation for high-risk groups or groups with certain diseases, such as ARDS.

Morphologic and biochemical changes in male rat lung after surgical and pharmacological castration.

The morphology of the rat lung was studied by light microscopy in different situations: after surgical and pharmacological castration and after administration of testosterone to the castrated rat to determine if the androgen is required to maintain the normal morphology of the lung. We also determined the effect of flutamide on the phospholipid composition of both the surfactant and microsomes of the lung. Rats were separated into five groups: I - control non-castrated rats, II - castrated rats sacrificed 21 days after castration, III - castrated rats that received testosterone daily from day 2 to day 21 after castration, IV - castrated rats that received testosterone from day 15 to day 21 after castration, and V - control rats injected with flutamide for 7 days. The amount of different phospholipids in the surfactant and microsomes of the lung was measured in group I and V rats. At the light microscopy level, the surgical and pharmacological castration provoked alterations in the morphology of the lung, similar to that observed in human lung emphysema. The compositions of surfactant and microsomes of the lung were similar to those previously reported by us for the surgically castrated rats. These results indicate that androgens are necessary for the normal morphology as well as for some metabolic aspects of the lung.

Morphologic and biochemical changes in male rat lung after surgical and pharmacological castration

The morphology of the rat lung was studied by light microscopy in different situations: after surgical and pharmacological castration and after administration of testosterone to the castrated rat to determine if the androgen is required to maintain the normal morphology of the lung. We also determined the effect of flutamide on the phospholipid composition of both the surfactant and microsomes of the lung. Rats were separated into five groups: I - control non-castrated rats, II - castrated rats sacrificed 21 days after castration, III - castrated rats that received testosterone daily from day 2 to day 21 after castration, IV - castrated rats that received testosterone from day 15 to day 21 after castration, and V - control rats injected with flutamide for 7 days. The amount of different phospholipids in the surfactant and microsomes of the lung was measured in group I and V rats. At the light microscopy level, the surgical and pharmacological castration provoked alterations in the morphology of the lung, similar to that observed in human lung emphysema. The compositions of surfactant and microsomes of the lung were similar to those previously reported by us for the surgically castrated rats. These results indicate that androgens are necessary for the normal morphology as well as for some metabolic aspects of the lung.