Biomedical subjects

Rie Yanagisawa

Publications and source records attributed to Rie Yanagisawa.

At least 19 recordsLinked to original sources

PubMed2007

Pulmonary exposure to diesel exhaust particles enhances fatty change of the liver in obese diabetic mice.

In epidemiological studies, exposure to ambient particulate matter (PM) has been reported to be positively associated with mortality in subjects with diabetes mellitus. Diesel exhaust particles (DEP) are major constituents of atmospheric PM. However, there is no experimental evidence for the relation of DEP to diabetes mellitus and its complications. We investigated the effects of DEP inoculated intratracheally on diabetic changes and nonalcoholic fatty liver disease (NAFLD) in diabetic obese and control mice. db/db mice and the corresponding nondiabetic db/+m mice received exposure to vehicle or DEP every two weeks. Animals were examined with biochemistry, histology, and immunohistochemistry for hexanoyl-lysine (HEL) in the liver. In the db/+m mice, pulmonary exposure to DEP did not increase levels of aspartate aminotransferase (AST) or alanine aminotransferase (ALT) compared to that to vehicle. In the db/db mice, however, the exposure to DEP increased the levels of AST and ALT compared to that to vehicle. Only in the db/db mice, DEP enhanced the magnitude of steatosis and formation of HEL, a marker of oxidative stress, in the liver compared to vehicle. These results suggest that pulmonary exposure to DEP, PM, enhances steatosis in the liver of obese diabetic subjects possibly via enhanced oxidative stress.

Alanine Transaminase↗

PubMed2006

Suppression of Th1 and Th2 immune responses in mice by Sinomenine, an alkaloid extracted from the chinese medicinal plant Sinomenium acutum.

The present study was designed to investigate the effect of sinomenine (SIN), an alkaloid extracted from Sinomenium acutum, on Th1 and Th2 immune responses in mice. For this investigation, mice were S. C. immunized with ovalbumin (OVA) emulsified with complete Freund's adjuvant (day 0). Varying doses of SIN were orally administered daily over a period of 21 days, commencing on day 0. On day 21, anti-OVA IgG and proliferative responses of spleen cells to the antigen were measured. Anti-OVA IgG2a and IFN-gamma were measured as indicators of Th1 immune responses and anti-OVA IgG1, IgE, and IL-5 as those of Th2 responses. TGF-beta was measured as an indicator of Th3 immune responses. The results showed that treatment with SIN was followed by decreases in anti-OVA IgG and the antigen-specific splenocyte proliferation. Production of all isotypes of antibodies including anti-OVA IgG2a, IgG1 and IgE as well as secretion of cytokines such as IFN-gamma and IL-5 was suppressed by SIN, although the suppression of anti-OVA IgG2a and IFN-gamma by the alkaloid appeared to be greater than that of anti-OVA IgG1, IgE, and IL-5. In addition, SIN enhanced the secretion of TGF-beta. These results suggest that SIN appears to have suppressive effects on both Th1 and Th2 immune responses. The results also suggest that Th1 responses may be more preferentially suppressed by the Sinomenium acutum-derived alkaloid compared to Th2 responses. TGF-beta may at least in part contribute to the suppression of Th1 as well as Th2 immune responses.

Administration, Oral↗

PubMed2006

Effects of nano particles on cytokine expression in murine lung in the absence or presence of allergen.

Particulate matter (PM) can exacerbate allergic airway diseases. Health effects of PM with a diameter of less than 100 nm, called nano particles, have been focused. We have recently demonstrated that carbon nano particles (14, 56 nm) exaggerate allergic airway inflammation in mice. In the present study, we investigated the effects of repeated pulmonary exposure to carbon nano particles on the expression of a variety of cytokines in the absence or presence of allergen in mice. ICR mice were divided into six experimental groups. Vehicle, two sizes of carbon nano particles, ovalbumin (OVA), and OVA + nano particles were administered intratracheally. Nano particles increased the lung protein levels of thymus and activation-regulated chemokine (TARC), macrophage inflammatory protein (MIP)-1alpha, and granulocyte-macrophage colony-stimulating factor (GM-CSF) in the absence or presence of allergen. The enhancement was more prominent with 14 nm of nano particles than with 56 nm of nano particles in overall trend. 14 nm nano particle exposure significantly enhanced the lung expressions of interleukin (IL)-2 and IL-10 in the presence of allergen as compared with allergen exposure. These results suggest that pulmonary exposure to nano particles can induce the lung expression of TARC, MIP-1alpha, GM-CSF in the absence of allergen and can enhance that of TARC, MIP-1alpha, GM-CSF, IL-2, and IL-10 in the presence of allergen. The enhancing effects are more prominent with smaller particles.

Allergens↗

PubMed2006

Effects of organic chemicals derived from ambient particulate matter on lung inflammation related to lipopolysaccharide.

The effects of components of ambient particulate matter (PM) on individuals with predisposing respiratory disorders are not well defined. We have previously demonstrated that airway exposure to diesel exhaust particles (DEP) or organic chemicals (OC) extracted from DEP (DEP-OC) enhances lung inflammation related to bacterial endotoxin (lipopolysaccharide, LPS). The present study aimed to examine the effects of airway exposure to OC extracted from urban PM (PM-OC) on lung inflammation related to LPS. ICR mice were divided into four experimental groups that intratracheally received vehicle, LPS (2.5 mg/kg), PM-OC (4 mg/kg), or PM-OC + LPS. Lung inflammation, lung water content, and lung expression of cytokines were evaluated 24 h after intratracheal administration. LPS challenge elicited lung inflammation evidenced by cellular profiles of bronchoalveolar lavage fluid and lung histology, which was further aggravated by the combined challenge with PM-OC. The combination with PM-OC and LPS did not significantly exaggerate LPS-elicited pulmonary edema. LPS instillation induced elevated lung expression of interleukin-1beta, macrophage inflammatory protein-1alpha, macrophage chemoattractant protein-1, and keratinocyte chemoattractant, whereas the combined challenge with PM-OC did not influence these levels. All the results were consistent with our previous reports on DEP-OC. These results suggest that the extracted organic chemicals from PM exacerbate infectious lung inflammation. The mechanisms underlying the enhancing effects are not mediated via the enhanced local expression of proinflammatory cytokines.

Air Pollutants↗

PubMed2006

Enhancement of mite allergen-induced eosinophil infiltration in the murine airway and local cytokine/chemokine expression by Asian sand dust.

Data on the effects of sand dust toward allergic asthma produced by indoor allergens, such as house dust mites, are not currently available. This study was undertaken to clarify the role of Asian sand dust on mite allergen, Dermatophagoides farinae (D. farinae)-induced eosinophilic inflammation in the murine lung, using sand dusts from the Maowusu Desert (Inner Mongolia) (SD-1) and the Tengger Desert (China) (SD-2). ICR mice were intratracheally administered saline; SD-1 alone; SD-2 alone; D. farinae alone; D. farinae + SD-1; and D. farinae + SD-2, 4 times at 2-wk intervals. The two sand dusts enhanced infiltration of eosinophil in the airway, along with goblet-cell proliferation related to D. farinae. The degree of eosinophil infiltration induced with SD-2 was greater than with SD-1. The SD-1, which contained higher amounts of beta-glucan, increased the expression of interferon (IFN)-gamma in bronchoalveolar lavage fluids (BALF) with or without D. farinae, but SD-2 did not. Synergistically or cumulatively elevated levels of interleukin (IL)-5, eotaxin, and monocyte chemotactic protein in BALF related to D. farinae were higher with D. farinae + SD-2 than with D. farinae + SD-1. These results suggest that increased cytokine and chemokines in BALF play an important role in the enhancement of eosinophil infiltration in the airway induced by D. farinae + sand dusts. The reduced eosinophil infiltration in the SD-1-treated mice could be due to suppression of Th-2 cytokine and eotaxin via interferon-gamma induced by microbial materials, such as beta-glucan.

Animals↗

PubMed2006

Role of interleukin-6 in fibrinolytic changes induced by lipopolysaccharide in mice.

We have recently demonstrated that interleukin (IL)-6 is protective against coagulatory and hemostatic disturbance and subsequent pulmonary hemorrhage induced by bacterial endotoxin, at least partly, via the inhibition of proinflammatory cytokines and chemokines using IL-6-null [IL-6(-/-)] mice and corresponding wild-type mice. Its role in fibrinolytic systems remains undefined, however. The present study elucidated the role of IL-6 in the activity of alpha(2)-plasmin inhibitor, an inhibitor of fibrinolysis, during inflammation induced by intraperitoneal administration of lipopolysaccharide in IL-6(-/-) and wild-type mice. Both IL-6(-/-) and wild-type mice were injected with vehicle or lipopolysaccharide (1 mg/kg). Seventy-two hours later, blood samples were collected and alpha(2)-plasmin inhibitor activity was examined. Lipopolysaccharide challenge induced significant enhancement of alpha(2)-plasmin inhibitor activity as compared with vehicle challenge in wild-type mice, but not in IL-6(-/-) mice. In the presence of lipopolysaccharide, the activity was significantly lower in IL-6(-/-) mice than that in wild-type mice. These results indicate that IL-6 can, at least partly, inhibit the lipopolysaccharide-enhanced fibrinolysis via the enhanced alpha2-plasmin inhibitor activity.

Animals↗

PubMed2006

Effects of volatile constituents of rosemary extract on lung inflammation induced by diesel exhaust particles.

Epidemiological and experimental studies have implicated that diesel exhaust particles are involved in increases in morbidity and mortality from lung diseases. Recently, we have demonstrated that rosmarinic acid, a polyphenolic liquid component in perilla, inhibits lung inflammation induced by diesel exhaust particles in vivo, partly through its antioxidative property. We have also shown the antioxidative activities of volatile constituents of rosemary extract, the gaseous component in perilla, in vitro. The purpose of this study was to evaluate the effects of intratracheal administration of volatile rosemary extract on lung inflammation induced by diesel exhaust particles. ICR mice were treated with intratracheal administration of volatile rosemary extract before intratracheal exposure to diesel exhaust particles. Twenty-four hr later, diesel exhaust particles exposure elicited lung inflammation characterized by the infiltration of neutrophils and eosinophils, which was confirmed by cellular profile of bronchoalveolar lavage fluid and histological examination. Diesel exhaust particles enhanced the protein expressions of interleukin-1beta, macrophage inflammatory protein-1alpha, macrophage chemoattractant protein-1, and keratinocyte chemoattractant in the lung. Pretreatment with rosemary extract significantly inhibited the diesel exhaust particles-induced lung inflammation. Rosemary extract treatment also suppressed the diesel exhaust particles-enhanced lung expression of macrophage inflammatory protein-1alpha, macrophage chemoattractant protein-1, and keratinocyte chemoattractant. These results suggest that intratracheal administration of rosemary extract can prevent lung inflammation induced by diesel exhaust particles. The preventive effect is mediated, at least partly, through the inhibition of the enhanced lung expressions of macrophage inflammatory protein-1alpha, macrophage chemoattractant protein-1, and keratinocyte chemoattractants.

Administration, Inhalation↗

PubMed2006

Effects of diesel exhaust on lung inflammation related to bacterial endotoxin in mice.

We have previously shown that intratracheal instillation of diesel exhaust particles enhances lung inflammation and lung expression of proinflammatory cytokines and chemokines related to bacterial endotoxin (lipopolysaccharide) in mice. The present study was designed to elucidate the effects of inhalation of diesel exhaust on lung inflammation related to lipopolysaccharide. ICR mice were exposed for 12 hr to clean air or diesel exhaust at a soot concentration of 0.3, 1.0, or 3.0 mg/m(3) after intratracheal challenge with 125 microg/kg of lipopolysaccharide. Lung inflammation and lung expression of proinflammatory chemokines such as macrophage chemoattractant protein-1 and keratinocyte chemoattractant were evaluated 24 hr after intratracheal administration. Diesel exhaust inhalation decreased lipopolysaccharide-elicited inflammatory cell recruitment into the bronchoalveolar lavage fluid as compared with clean air inhalation. Histological study demonstrated that exposure to diesel exhaust did not affect lipopolysaccharide-enhanced neutrophil recruitment into the lung parenchyma. Lipopolysaccharide instillation elevated lung expression of macrophage chemoattractant protein-1 and keratinocyte chemoattractant under clean air or diesel exhaust inhalation. However, diesel exhaust exposure did not influence but rather did suppress these levels in the presence of lipopolysaccharide. These results suggest that short-term exposure to diesel exhaust did not exacerbate lung inflammation related to bacterial endotoxin.

Air Pollutants↗

PubMed2006

Pulmonary exposure to diesel exhaust particles enhances coagulatory disturbance with endothelial damage and systemic inflammation related to lung inflammation.

Pulmonary exposure to diesel exhaust particles (DEP) enhances lung inflammation related to bacterial endotoxin (lipopolysaccharide [LPS]) in mice. Severe lung inflammation can reportedly induce coagulatory abnormalities and systemic inflammation. This study examined the effects of components of DEP on lung inflammation, pulmonary permeability, coagulatory changes, systemic inflammatory response, and lung-to-systemic translocation of LPS in a murine model of lung inflammation. ICR mice were divided into six experimental groups that intratracheally received vehicle, LPS (2.5 mg/kg), organic chemicals in DEP (DEP-OC; 4 mg/kg) extracted with dicloromethane), residual carbonaceous nuclei of DEP (washed DEP: 4 mg/kg), DEP-OC + LPS, or washed DEP + LPS. Both DEP components exacerbated lung inflammation, vascular permeability, and the increased fibrinogen and E-selectin levels induced by LPS. With overall trends, the exacerbation was more prominent with washed DEP than with DEP-OC. Washed DEP + LPS significantly decreased activated protein C and antithrombin-III and elevated circulatory levels of interleukin (IL)-6, keratinocyte chemoattractant (KC), and LPS as compared with LPS alone, whereas DEP-OC + LPS elevated IL-6, KC, and LPS without significance. These results show that DEP components, especially washed DEP, amplify the effects if LPS on the respiratory system and suggest that they contribute to the adverse health effects of particulate air pollution on the sensitive populations with predisposing vascular and/or pulmonary diseases, including ischemic vascular diseases and respiratory infection.

Animals↗

PubMed2006

Effects of airway exposure to nanoparticles on lung inflammation induced by bacterial endotoxin in mice.

BACKGROUND: Although adverse health effects of particulate matter with a diameter of < 100 nm (nanoparticles) have been proposed, molecular and/or experimental evidence for their facilitation of lung inflammation in vivo is not fully defined. OBJECTIVE: In the present study we investigated the effects of nanoparticles on lung inflammation related to bacterial endotoxin [lipopolysaccharide (LPS) ] in mice. RESULTS: We intratracheally administered vehicle, two sizes (14 nm, 56 nm) of carbon black nanoparticles (4 mg/kg) , LPS (2.5 mg/kg) , or LPS plus nanoparticles and evaluated parameters for lung inflammation and coagulation. Nanoparticles alone induced slight lung inflammation and significant pulmonary edema compared with vehicle. Fourteen-nanometer nanoparticles intensively aggravated LPS-elicited lung inflammation and pulmonary edema that was concomitant with the enhanced lung expression of interleukin-1beta (IL-1beta) , macrophage inflammatory protein-1alpha (MIP-1alpha) , macrophage chemoattractant protein-1, MIP-2, and keratinocyte chemoattractant in overall trend, whereas 56-nm nanoparticles did not show apparent effects. Immunoreactivity for 8-hydroxyguanosine, a marker for oxidative stress, was more intense in the lungs from the LPS + 14-nm nanoparticle group than in those from the LPS group. Circulatory fibrinogen levels were higher in the LPS + plus 14-nm nanoparticle group than in the LPS group. CONCLUSIONS: Taken together, evidence indicates that nanoparticles can aggravate lung inflammation related to bacterial endotoxin, which is more prominent with smaller particles. The enhancement may be mediated, at least partly, via the increased local expression of proinflammatory cytokines and via the oxidative stress. Furthermore, nanoparticles can promote coagulatory disturbance accompanied by lung inflammation.

Air Pollutants↗

PubMed2006

Di-(2-ethylhexyl) phthalate enhances atopic dermatitis-like skin lesions in mice.

Di-(2-ethylhexyl) phthalate (DEHP) has been widely used in polyvinyl chloride products and has become ubiquitous in the developed countries. DEHP reportedly displays an adjuvant effect on immunoglobulin production. However, it has not been elucidated whether DEHP is associated with the aggravation of atopic dermatitis. We investigated the effects of DEHP on atopic dermatitis-like skin lesions induced by mite allergen in NC/Nga mice. NC/Nga male mice were injected intradermally with mite allergen on their right ears. In the presence of allergen, DEHP (0, 0.8, 4, 20, or 100 microg) was administered by intraperitoneal injection. We evaluated clinical scores, ear thickening, histologic findings, and the protein expression of chemokines. Exposure to DEHP at a dose of 0.8-20 microg caused deterioration of atopic dermatitis-like skin lesions related to mite allergen; this was evident from macroscopic and microscopic examinations. Furthermore, these changes were consistent with the protein expression of proinflammatory molecules such as macrophage inflammatory protein-1alpha (MIP-1alpha) and eotaxin in the ear tissue in overall trend. In contrast, 100 microg DEHP did not show the enhancing effects. These results indicate that DEHP enhances atopic dermatitis-like skin lesions at hundred-fold lower levels than the no observed adverse effect level determined on histologic changes in the liver of rodents. DEHP could be at least partly responsible for the recent increase in atopic dermatitis.

Animals↗

PubMed2005

Role of metallothionein in coagulatory disturbance and systemic inflammation induced by lipopolysaccharide in mice.

Although metallothionein (MT) can be induced by inflammatory mediators, its roles in coagulatory disturbance during inflammation are poorly defined. We determined whether MT protects against coagulatory and fibrinolytic disturbance and systemic inflammation induced by intraperitoneal administration of lipopolysaccharide (LPS) in MT-I/II null (-/-) and wild-type (WT) mice. As compared with WT mice, MT (-/-) mice revealed significant prolongation of prothrombin and activated partial thromboplastin time, a significant increase in the levels of fibrinogen and fibrinogen/fibrin degradation products, and a significant decrease in activated protein C, after LPS treatment. LPS induced inflammatory organ damages in the lung, kidney, and liver in both genotypes of mice. The damages, including neutrophil infiltration, were more prominent in MT (-/-) mice than in WT mice after LPS treatment. In both genotypes of mice, LPS enhanced protein expression of interleukin (IL)-1beta, IL-6, granulocyte/macrophage-colony-stimulating factor, macrophage inflammatory protein (MIP)-1alpha, MIP-2, macrophage chemoattractant protein-1, and keratinocyte chemoattractant in the lung, kidney, and liver and circulatory levels of IL-1beta, IL-6, MIP-2, and KC. In overall trends, however, the levels of these proinflammatory proteins were greater in MT (-/-) mice than in WT mice after LPS challenge. Our results suggest that MT protects against coagulatory and fibrinolytic disturbance and multiple organ damages induced by LPS, at least partly, via the inhibition of the expression of proinflammatory proteins.

Animals↗

PubMed2005

The role of toll-like receptor 4 in airway inflammation induced by diesel exhaust particles.

Although several studies have demonstrated that airway exposure to diesel exhaust particles (DEP) induces lung inflammation, the signaling pathways involved in the pathogenesis remain unclear. Toll-like receptors (TLRs) are generally accepted to be pathogen recognition receptors in mammalians. In the present study, we investigated the role of TLR-4 in DEP-induced lung inflammation and cytokine expression in the lung in TLR-4 point mutant (C3H/HeJ) mice and corresponding control (C3H/HeN) mice. Both the types of mice were randomized into four experimental groups that received vehicle or DEP (12 mg/kg body weight) by intratracheal instillation (n = 8-10 in each group). Cellular profile of bronchoalveolar lavage (BAL) fluid, expressions of cytokines and chemokines in the lung, and circulatory fibrinogen levels were evaluated 24 h after the instillation.DEP challenge revealed a significant increase in the numbers of total cells and neutrophils in the BAL fluid as compared to vehicle challenge, however, the numbers were less in C3H/HeJ mice than in C3H/HeN mice. DEP exposure significantly induced the lung expression of interleukin (IL)-1beta, keratinocyte chemoattractant (KC), and macrophage inflammatory protein (MIP)-1alpha when compared to vehicle challenge in both genotypes of mice. In the presence of DEP, the level of MIP-1alpha was significantly lower in C3H/HeJ mice than in C3H/HeN mice, however, the levels of IL-1beta, KC, and fibrinogen showed opposite findings. These results suggest that TLR-4 is one of recognition receptors against DEP in the airways.

Animals↗

PubMed2005

Effects of nano particles on antigen-related airway inflammation in mice.

BACKGROUND: Particulate matter (PM) can exacerbate allergic airway diseases. Although health effects of PM with a diameter of less than 100 nm have been focused, few studies have elucidated the correlation between the sizes of particles and aggravation of allergic diseases. We investigated the effects of nano particles with a diameter of 14 nm or 56 nm on antigen-related airway inflammation. METHODS: ICR mice were divided into six experimental groups. Vehicle, two sizes of carbon nano particles, ovalbumin (OVA), and OVA + nano particles were administered intratracheally. Cellular profile of bronchoalveolar lavage (BAL) fluid, lung histology, expression of cytokines, chemokines, and 8-hydroxy-2'-deoxyguanosine (8-OHdG), and immunoglobulin production were studied. RESULTS: Nano particles with a diameter of 14 nm or 56 nm aggravated antigen-related airway inflammation characterized by infiltration of eosinophils, neutrophils, and mononuclear cells, and by an increase in the number of goblet cells in the bronchial epithelium. Nano particles with antigen increased protein levels of interleukin (IL)-5, IL-6, and IL-13, eotaxin, macrophage chemoattractant protein (MCP)-1, and regulated on activation and normal T cells expressed and secreted (RANTES) in the lung as compared with antigen alone. The formation of 8-OHdG, a proper marker of oxidative stress, was moderately induced by nano particles or antigen alone, and was markedly enhanced by antigen plus nano particles as compared with nano particles or antigen alone. The aggravation was more prominent with 14 nm of nano particles than with 56 nm of particles in overall trend. Particles with a diameter of 14 nm exhibited adjuvant activity for total IgE and antigen-specific IgG1 and IgE. CONCLUSION: Nano particles can aggravate antigen-related airway inflammation and immunoglobulin production, which is more prominent with smaller particles. The enhancement may be mediated, at least partly, by the increased local expression of IL-5 and eotaxin, and also by the modulated expression of IL-13, RANTES, MCP-1, and IL-6.

Air Pollutants↗

PubMed2005

Pulmonary exposure to diesel exhaust particles induces airway inflammation and cytokine expression in NC/Nga mice.

Although several studies have reported that diesel exhaust particles (DEP) affect cardiorespiratory health in animals and humans, the effect of DEP on animal models with spontaneous allergic disorders has been far less intensively studied. The Nc/Nga mouse is known to be a typical animal model for human atopic dermatitis (AD). In the present study, we investigated the effects of repeated pulmonary exposure to DEP on airway inflammation and cytokine expression in NC/Nga mice. The animals were randomized into two experimental groups that received vehicle or DEP by intratracheal instillation weekly for six weeks. Cellular profiles of bronchoalveolar lavage (BAL) fluid and expressions of cytokines and chemokines in both the BAL fluid and lung tissues were evaluated 24 h after the last instillation. The DEP challenge produced an increase in the numbers of total cells, neutrophils, and mononuclear cells in BAL fluid as compared to the vehicle challenge (P<0.01). DEP exposure significantly induced the lung expressions of interleukin (IL)-4, keratinocyte chemoattractant (KC), and macrophage inflammatory protein (MIP)-1alpha when compared to the vehicle challenge. These results indicate that intratracheal exposure to DEP induces the recruitment of inflammatory cells, at least partially, through the local expression of IL-4 and chemokines in NC/Nga mice.

Animals↗

PubMed2005

Diesel exhaust affects immunological action in the placentas of mice.

We investigated the effect of diesel exhaust (DE) on pregnancy and fetal development in mice at day 14 postcoitum (pc) with a special focus on the placenta. The number of absorbed fetuses increased in groups exposed to DE, and congestion was observed in histological sections of placentas. During placental absorption expression of CYP1A1 mRNA decreased to undetectable levels, whereas expression of TNF alpha mRNA increased approximately twofold over that of the control. Levels of CYP1A1 mRNA in normal placentas from DE-exposed mice were unchanged. mRNA levels of inflammatory cytokines IL-2, IL-5, IL-12 alpha, IL-12 beta, and GM-CSF increased in placentas exposed to DE (0.3 and 3.0 mg diesel exhaust particles (DEP)/m3). Expression of IL-5 mRNA was markedly increased in DE-exposed placentas, although levels were barely detectable in control placentas. IL-6 mRNA expression was increased approximately 10-fold in placentas exposed to DE (3.0 mg DEP/m3). It has been reported that expression of mRNA encoding proteins involved in immune function in the placenta is increased during fetal absorption in mice. In the present study, expression of such mRNA by the placenta was increased by DE exposure. Because it is believed that expression of mRNA in the placenta also affects fetal development, DE may promote fetal absorption. These findings suggest that in mice exposure to DE affects fetal absorption and placental function by modifying expression of immune-related genes during early gestation and expression of endocrine-related genes during late gestation.

Animals↗

PubMed2005

Asian sand dust enhances ovalbumin-induced eosinophil recruitment in the alveoli and airway of mice.

Asian sand dust (ASD) containing sulfate (SO4(2-)) reportedly causes adverse respiratory health effects but there is no experimental study showing the effect of ASD toward allergic respiratory diseases. The effects of ASD and ASD plus SO4(2-) toward allergic lung inflammation induced by ovalbumin (OVA) were investigated in this study. ICR mice were administered intratracheally with saline; ASD alone (sample from Shapotou desert); and ASD plus SO4(2-) (ASD-SO4); OVA+ASD; OVA+ASD-SO4. ASD or ASD-SO4 alone caused mild nutrophilic inflammation in the bronchi and alveoli. ASD and ASD-SO4 increased pro-inflammatory mediators, such as Keratinocyte chemoattractant (KC) and macrophage inflammatory protein (MIP)-1 alpha, in bronchoalveolar lavage fluids (BALF). ASD and ASD-SO4 enhanced eosinophil recruitment induced by OVA in the alveoli and in the submucosa of the airway, which has a goblet cell proliferation in the bronchial epithelium. However, a further increase of eosinophils by addition of SO4(2-) was not observed. The two sand dusts synergistically increased interleukin-5 (IL-5) and monocyte chemotactic protein-1 (MCP-1), which were associated with OVA, in BALF. However, the increased levels of IL-5 were lower in the OVA+ASD-SO4 group than in the OVA+ASD group. ASD caused the adjuvant effects to specific-IgG1 production by OVA, but not to specific-IgE. These results suggest that the enhancement of eosinophil recruitment in the lung is mediated by synergistically increased IL-5 and MCP-1. IgG1 antibodies may play an important role in the enhancement of allergic reaction caused by OVA and sand dust. However, extra sulfate may not contribute to an increase of eosinophils.

Animals↗

PubMed2005

Effects of 15-deoxy-Delta12,14-prostaglandin J2 on the expression of Toll-like receptor 4 and 2 in the murine lung in the presence of lipopolysaccharide.

1. Previously, we have demonstrated that 15-deoxy-Delta12,14-prostaglandin J2 (15d-PGJ2) enhances acute lung injury induced by lipopolysaccharide (LPS) in mice. The enhancement in acute lung injury by 15d-PGJ2 was concomitant with the enhanced expression of several pro-inflammatory cytokines in the lung. However, other underlying mechanisms of this enhancement remain to be elucidated. The present study investigated the effects of 15d-PGJ2 on the expression of Toll-like receptor (TLR) 4 and 2 in the lung in the absence or presence of LPS. 2. In the present study, ICR mice were divided into four experimental groups that received (intratracheally) vehicle, LPS (125 microg/kg), 15d-PGJ2 (1 mg/kg) or 15d-PGJ2 + LPS. The mRNA expression of both TLR4 and 2 in the lung was evaluated 4 h after intratracheal administration. 3. 15-Deoxy-Delta12,14-prostaglandin J2 enhanced the mRNA expression of both TLR4 and 2 in the presence of LPS. 4. These results suggest that the enhancing effects of 15d-PGJ2 on LPS-induced acute lung injury may be explained, at least in part, by its effect on the lung expression of TLR4 and 2.

Animals↗