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Jianguo Xu

Publications and source records attributed to Jianguo Xu.

At least 37 records · Page 2Linked to original sources
PubMed2005

Pentoxifylline reduces indirect lung injury of fresh water drowning in canis.

BACKGROUND: Previous studies have suggested that pentoxifylline (PTX) exerts multiple beneficial effects on the inflammatory cascade, particularly on the function of neutrophils. We investigated whether continuous infusion of PTX could reduce indirect lung injury (ILI) caused by fresh water drowning and if so, what is the possible molecular mechanism. METHODS: Twenty 4 male canis were divided randomly into control group, fresh water drowning group (right lung), drowning treated with PTX group and PTX alone group. At different time points after drowning, the changes of hemodynamic parameters and wet/dry weight of indirect lung (left lung) tissues were compared among these 4 groups. Other measures included lung histopathology, PMN infiltration assessed by immune staining, CD11b, ICAM-1 mRNA and TNF-alphamRNA in left lung detected by RT-PCR. NF-kappaB activation in blood neutrophils and lungs were measured with electrophoretic mobility shift assay (EMSA). RESULTS: Animals treated with PTX showed a significant reduction in lung injury. PTX suppressed drowning-induced ICAM-1 and TNF-alphamRNA elevation and inhibited NF-kappaB activation in blood neutrophils and lungs. CONCLUSIONS: Continuous infusion of PTX reduces ILI caused by fresh water drowning. PTX decreases expression of ICAM-1 and TNF-alpha, possibly via inhibition of NF-kappaB.

Animals↗
PubMed2005

Bone marrow-derived mesenchymal stem cells in repair of the injured lung.

We sought to determine whether an intact bone marrow is essential to lung repair following bleomycin-induced lung injury in mice, and the mechanisms of any protective effects conferred by bone marrow-derived mesenchymal stem cell (BMDMSC) transfer. We found that myelosupression increased susceptibility to bleomycin injury and that BMDMSC transfer was protective. Protection was associated with the differentiation of engrafted BMDMSC into specific and distinct lung cell phenotypes, with an increase in circulating levels of G-CSF and GM-CSF (known for their ability to promote the mobilization of endogenous stem cells) and with a decrease in inflammatory cytokines. In vitro, cells from injured, but not from normal, mouse lung produced soluble factors that caused BMDMSC to proliferate and migrate toward the injured lung. We conclude that bone marrow stem cells are important in the repair of bleomycin-injured lung and that transfer of mesenchymal stem cells protects against the injury. BMDMSC localize to the injured lung and assume lung cell phenotypes, but protection from injury and fibrosis also involves suppression of inflammation and triggering production of reparative growth factors.

Animals↗
PubMed2005

Lung infection with gamma-herpesvirus induces progressive pulmonary fibrosis in Th2-biased mice.

Idiopathic pulmonary fibrosis (IPF) is a progressive, fibrotic lung disease of unknown etiology. A viral pathogenesis in IPF has been suggested since >95% of IPF patients have evidence of chronic pulmonary infection with one or more herpesviruses. To determine whether pulmonary infection with herpesvirus can cause lung fibrosis, we infected mice with the murine gamma-herpesvirus 68 (MHV68). Because IPF patients have a T helper type 2 (Th2) pulmonary phenotype, we used IFN-gammaR-/-, a strain of mice biased to develop Th2 responses. Chronic MHV68 infection of IFN-gammaR-/- mice resulted in progressive deposition of interstitial collagen as shown by light and electron microscopy. A significant decrease in tidal volume paralleled the collagen deposition. Five features typically seen in IPF, increased transforming growth factor-beta expression, myofibroblast transformation, production of Th2 cytokines, hyperplasia of type II cells, and increased expression of matrix metalloproteinase-7, were also present in chronically infected IFN-gammaR-/- mice. There also was altered synthesis of surfactant proteins, which is seen in some patients with familial IPF. MHV68 viral protein was found in type II alveolar epithelial cells, especially in lung areas with extensive alveolar remodeling. In summary, chronic herpesvirus pulmonary infection in IFN-gammaR-/- mice causes progressive pulmonary fibrosis and many of the pathological features seen in IPF.

Animals↗
PubMed2005

stx2vha is the dominant genotype of Shiga toxin-producing Escherichia coli O157:H7 isolated from patients and domestic animals in three regions of China.

Shiga toxin-producing Escherichia coli(STEC) O157: H7 strains were isolated from domestic animals and patients from Xuzhou City, Jiangsu Province, China and the bordering Anhui and Henan Provinces and were examined for the stx genotype. Of 390 strains, 277 were identified as genotype stx2vha ; 41, stx2 ; 51, stx2-stx1 ; 1, stx2-stx2vha-stx1 ; 5, stx2-stx2vha ; and 15 were un-typeable. Of the 277 stx2vha-bearing isolates, 116 were isolated from goats; 42, cattle; 38, hens, and 35 from pigs. The study shows stx2vha is the dominant genotype and goats are an important reservoir.

Animals↗
PubMed2005

Structural and genetic characterization of enterohemorrhagic Escherichia coli O145 O antigen and development of an O145 serogroup-specific PCR assay.

Enterohemorrhagic Escherichia coli O145 strains are emerging as causes of hemorrhagic colitis and hemolytic uremic syndrome. In this study, we present the structure of the E. coli O145 O antigen and the sequence of its gene cluster. The O145 antigen has repeat units containing three monosaccharide residues: 2-acetamido-2-deoxy-D-glucose (GlcNAc), 2-acetamidoylamino-2,6-dideoxy-L-galactose, and N-acetylneuraminic acid. It is very closely related to Salmonella enterica serovar Touera and S. enterica subsp. arizonae O21 antigen. The E. coli O145 gene cluster is located between the JUMPStart sequence and the gnd gene and consists of 15 open reading frames. Putative genes for the synthesis of the O-antigen constituents, for sugar transferase, and for O-antigen processing were annotated based on sequence similarities and the presence of conserved regions. The putative genes located in the E. coli O145 O-antigen gene cluster accounted for all functions expected for synthesis of the structure. An E. coli O145 serogroup-specific PCR assay based on the genes wzx and wzy was also developed by screening E. coli and Shigella isolates of different serotypes.

Amino Sugars↗
PubMed2005

Distribution of tccP in clinical enterohemorrhagic and enteropathogenic Escherichia coli isolates.

Enterohemorrhagic Escherichia coli (EHEC) and enteropathogenic E. coli (EPEC) are diarrheagenic pathogens that colonize the gut through the formation of attaching and effacing lesions, which depend on the translocation of effector proteins via a locus of enterocyte effacement-encoded type III secretion system. Recently, two effector proteins, EspJ and TccP, which are encoded by adjacent genes on prophage CP-933U in EHEC O157:H7, have been identified. TccP consists of a unique N-terminus region and several proline-rich domains. In this project we determined the distribution of tccP in O157:H7, in non-O157 EHEC, and in typical and atypical EPEC isolates. All the EHEC O157:H7 strains tested were tccP(+). Unexpectedly, tccP was also found in non-O157 EHEC, and in typical and atypical EPEC isolates, particularly in strains belonging to serogroups O26 (EHEC), O119 (typical EPEC), and O55 (atypical EPEC). We recorded some variation in the length of tccP, which reflects diversity in the number of the proline-rich repeats. These results show the existence of a class of "attaching and effacing" pathogens which express a combination of EPEC and EHEC virulence determinants.

Animals↗
PubMed2005

Molecular evolution analysis and geographic investigation of severe acute respiratory syndrome coronavirus-like virus in palm civets at an animal market and on farms.

Massive numbers of palm civets were culled to remove sources for the reemergence of severe acute respiratory syndrome (SARS) in Guangdong Province, China, in January 2004, following SARS coronavirus detection in market animals. The virus was identified in all 91 palm civets and 15 raccoon dogs of animal market origin sampled prior to culling, but not in 1,107 palm civets later sampled at 25 farms, spread over 12 provinces, which were claimed to be the source of traded animals. Twenty-seven novel signature variation residues (SNVs) were identified on the spike gene and were analyzed for their phylogenetic relationships, based on 17 sequences obtained from animals in our study and from other published studies. Analysis indicated that the virus in palm civets at the live-animal market had evolved to infect humans. The evolutionary starting point was a prototype group consisting of three viral sequences of animal origin. Initially, seven SNV sites caused six amino acid changes, at positions 147, 228, 240, 479, 821, and 1080 of the spike protein, to generate low-pathogenicity viruses. One of these was linked to the first SARS patient in the 2003-2004 period. A further 14 SNVs caused 11 amino acid residue changes, at positions 360, 462, 472, 480, 487, 609, 613, 665, 743, 765, and 1163. The resulting high-pathogenicity groups were responsible for infections during the so-called early-phase epidemic of 2003. Finally, the remaining six SNVs caused four amino acid changes, at positions 227, 244, 344, and 778, which resulted in the group of viruses responsible for the global epidemic.

Amino Acid Sequence↗
PubMed2005

SARS-CoV infection in a restaurant from palm civet.

Epidemiologic investigations showed that 2 of 4 patients with severe acute respiratory syndrome (SARS) identified in the winter of 2003-2004 were a waitresss at a restaurant in Guangzhou, China, that served palm civets as food and a customer who ate in the restaurant ashort distance from animal cages. All 6 palm civets at the restaurant were positive for SARS-associated coronavirus (SARS-CoV). Partial spike (S) gene sequences of SARS-CoV from the 2 patients were identical to 4 of 5 Sgene viral sequences from palm civets. Phylogenetic analysis showed that SARS-CoV from palm civets in the restaurant was most closely related to animal isolates. SARS cases at the restaurant were the result of recent interspecies transfer from the putative palm civet reservoir, and not the result of continued circulation of SARS-CoV in the human population.

Adult↗
PubMed2005

Mechanism of the effect of hydroxyethyl starch on reducing pulmonary capillary permeability in a rat model of sepsis.

Hydroxyethyl starch (HES) is one of the most frequently used plasma substitutes. Recent studies have indicated that HES may reduce capillary leakage. The present in vivo study was performed to investigate the effects of HES on pulmonary capillary permeability, inflammatory mediators, and transcription factors in sepsis. Septic rats induced by cecal ligation and puncture (CLP) were treated with different doses of HES (7.5, 15, or 30 ml/kg, iv). At 5 or 12 hr after CLPq the rat lung tissues were collected. Pulmonary microvascular permeability, various cytokine levels (tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6), mRNA expressions (cytokine-induced neutrophil chemoattractant (CINC), P-selectin, CD 11b/CD18 (Mac-1), and intercellular adhesion molecule-1 (ICAM-1)), and activities of nuclear factor (NF)-kappaB and activator protein (AP)-1 were determined in each group. HES, in a dose-related manner, significantly reduced pulmonary capillary permeability in the CLP model of sepsis. HES also down-regulated pulmonary proinflammatory cytokines (TNF-alpha, IL-1beta, and IL-6) and mRNA expressions (CINC and P-selectin), and inhibited pulmonary activities of NF-kappaB and AP-1. The results suggest that during sepsis HES reduces pulmonary capillary permeability and this beneficial effect of HES may act through down-regulation of inflammatory mediators and suppression of NF-kappaB and AP-1 activation.

Animals↗
PubMed2004

Ovariotomy and persistent pain affect long-term Fos expression in spinal cord.

Sex differences in pain have been confirmed both in clinical and experimental studies. Estrogen has a great role in this process and can affect response to noxious stimuli. In this study, we used Fos as a marker to investigate the mechanism underlying the phenomenon. Sprague-Dawley rats were randomly assigned to ovariotomy (OVX) or sham surgery (OVX-sham) group (n=20 rats/condition). All the rats received CCI surgery three weeks after ovariotomy. We used hot-plate test as a sign of neuropathic pain. On PO days 3, 7, 14, and 21, paw withdrawal latency was determined and 2 h later, the L4-L5 segments of the spinal cord were removed and immunostained for Fos protein. Number of Fos-like immunoreactive (Fos-LI) neurons of each section was counted bilaterally. We find that ovariotomy can regulate the sensitivity to thermal stimuli and Fos protein level will change in the spinal dorsal horn. However, the alternation of Fos expression does not extremely account for the behavior.

Animals↗
PubMed2004

Endotoxin-induced lung injury in mice: structural, functional, and biochemical responses.

Acute lung injury is usually a complication of sepsis, and endotoxin treatment of mice is a frequently used experimental model. To define this model and to clarify pathogenesis of the lung injury, we injected with 1 mg/kg endotoxin ip and measured pulmonary function, pulmonary edema, serum concentrations of cytokines and growth factors, and lung histology over 48 h. During the first 6 h, tidal volume and minute volume increased and respiratory frequency decreased. Serum concentrations of cytokines showed three patterns: 10 cytokines peaked at 2 h and declined rapidly, two peaked at 6 h and declined, and two had biphasic peaks at 2 and 24 h. Growth factors increased later and remained elevated longer. Both collagen and fibronectin were deposited in the lungs beginning within hours of endotoxin and resolving over 48 h. Histologically, lungs showed increased cellularity at 6 h with minimal persistent inflammation at 48 h. Lung water peaked at 6 h and gradually decreased over 48 h. We conclude that intraperitoneal administration of endotoxin to mice causes a transient systemic inflammatory response and transient lung injury and dysfunction. The response is characterized by successive waves of cytokine release into the circulation, early evidence of lung fibrogenesis, and prolonged increases in growth factors that may participate in lung repair.

Animals↗
PubMed2004

Interaction with cystic fibrosis transmembrane conductance regulator-associated ligand (CAL) inhibits beta1-adrenergic receptor surface expression.

G protein-coupled receptors such as the beta1-adrenergic receptor (beta1AR) must be trafficked to the plasma membrane in order to bind with their extracellular ligands and regulate cellular physiology. By using glutathione S-transferase pull-down techniques, we found that the beta1AR carboxyl terminus directly interacts with the cystic fibrosis transmembrane conductance regulator-associated ligand (CAL; also known as PIST, GOPC, and FIG), a protein known to be primarily localized to the Golgi apparatus. CAL contains two predicted coiled-coil domains and one PSD-95/Discs-large/ZO-1 homology (PDZ) domain. The beta1AR carboxyl terminus (CT) binds to the PDZ domain of CAL, with the last few amino acids (ESKV) of the beta1AR-CT being the key determinants for the interaction. Mutation of the terminal valine residue resulted in markedly reduced association of the beta1AR-CT with CAL. Numerous other mutations to the ESKV motif also impaired the beta1AR-CT/CAL interaction, suggesting that this motif is close to optimal for association with the CAL PDZ domain. In cells, full-length beta1AR robustly associates with CAL, and this interaction is abolished by mutation of the terminal valine to alanine of the receptor (V477A), as determined by co-immunoprecipitation experiments and immunofluorescence co-localization studies. Consistent with observations that CAL is a Golgi-associated protein, overexpression of CAL reduces surface expression of beta1AR. Interaction with CAL promotes retention of beta1AR within the cell, whereas PSD-95, another beta1AR-associated PDZ domain-containing protein, competitively blocks beta1AR association with CAL and promotes receptor trafficking to the cell surface. These data reveal that CAL, a novel beta1AR-binding partner, modulates beta1AR intracellular trafficking, thereby revealing a new mechanism of regulation for beta1AR anterograde trafficking through the endoplasmic reticulum-Golgi complex to the plasma membrane.

Adaptor Proteins, Signal Transducing↗
PubMed2004

Structure of the Shigella dysenteriae 7 O antigen gene cluster and identification of its antigen specific genes.

Shigella strains are human pathogens. The O antigen gene cluster of Shigella dysenteriae O7 was sequenced and analyzed. It contains genes for synthesis of nucleotide sugars including UDP-2-acetamido-2-deoxy-D-galacturonamide, UDP-2-acetamido-2-deoxy-D-galacturonic acid and dTDP-4-amino-4,6-dideoxy-D-glucose. Also found in the gene cluster are genes encoding O unit flippase, O antigen polymerase and sugar transferases. The Escherichia coli O121 O antigen, which is present in an important Shiga toxin-producing strain, has the same structure as that of S. dysenteriae O7, and we found that the gene clusters also had the same genes and organization. Four genes specific to S. dysenteriae O7 and E. coli O121 were identified by PCR screening against representatives of 186 E. coli (including Shigella) O serotypes. E. coli O121 and S. dysenteriae O7 isolates can be distinguished by PCR of the H antigen fliC gene.

Carrier Proteins↗
PubMed2004

Laboratory diagnosis of four recent sporadic cases of community-acquired SARS, Guangdong Province, China.

Four cases of severe acute respiratory syndrome (SARS) that occurred from December 16, 2003, to January 8, 2004, in the city of Guangzhou, Guangdong Province, China, were investigated. Clinical specimens collected from these patients were tested by provincial and national laboratories in China as well as members of the World Health Organization SARS Reference and Verification Laboratory Network in a collaborative effort to identify and confirm SARS-associated coronavirus (SARS-CoV) infection. Although SARS-CoV was not isolated from any patient, specimens from three patients were positive for viral RNA by reverse transcription-polymerase chain reaction assay, and all patients had detectable rises in SARS-CoV-specific antibodies. This study shows the effectiveness of a collaborative, multilaboratory response to diagnose SARS.

Adult↗
PubMed2004

Effect of ketamine on NF-kappa B activity and TNF-alpha production in endotoxin-treated rats.

The effects of ketamine on endotoxin-induced NF-kappaB activation and TNF-alpha expression were studied in vivo. A sepsis model was created by bolus injection of endotoxin (5 mg/kg) into the tail vein of adult Wistar rats. The rats were immediately treated with various doses of ketamine (0.5, 5, or 50 mg/kg) or 0.9% NaCl (10 ml/kg) i.p. At 1, 4, or 6 hr post-treatment, NF-kappaB and TNF-alpha were assayed in the intestine, liver, and lung by electrophoretic mobility shift assay (EMSA) and reverse-transcription polymerase chain reaction (RT-PCR), respectively. Serum TNF-alpha was analyzed by ELISA. Endotoxin enhanced NF-kappaB activity and TNF-alpha expression in the intestine, liver, and lung and it increased TNF-alpha concentration in serum. Ketamine dosages 0.5 mg/kg suppressed the endotoxin-induced NF-kappaB activation and TNF-alpha expression in the intestine. The lowest dose to inhibit NF-kappaB activity and TNF-alpha expression in the lung was 5 mg/kg. Ketamine did not inhibit endotoxin-induced NF-kappaB activity or TNF-alpha expression in the liver; ketamine itself at a dose of 50 mg/kg enhanced NF-kappaB activity and TNF-alpha expression in the liver. Ketamine dosage 0.5 mg/kg inhibited endotoxin-induced TNF-alpha elevation in the serum. In conclusion, ketamine can suppress the induction of NF-kappaB and TNF-alpha by endotoxin in vivo. Subanesthetic dosages of ketamine have an anti-inflammatory effect, but large dosages may be harmful.

Animals↗
PubMed2004

Pentoxifylline inhibits endotoxin-induced NF-kappa B activation and associated production of proinflammatory cytokines.

The effects of graded doses of pentoxifylline (PTX) on endotoxin-induced production of inflammatory cytokines and activation of nuclear factor kappa B (NF-kappaB) were studied in vivo in rat intestine. Sepsis was induced in rats by ip injection of lipopolysaccharide (LPS, 5 mg/kg). PTX was injected via the tail vein at dosages of 6.25, 12.5, 25, 50, or 100 mg/kg at 1 min after LPS challenge. NF-kappaB activation in intestine was investigated by electrophoretic mobility shift assay (EMSA). Tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and interleukin-10 (IL-10) levels were measured in intestine by enzyme-linked immunosorbance assays (ELISA). Intestinal TNF-alpha, IL-6, and IL-10 mRNA expression were studied by the reverse-transcription polymerase chain reaction (RT-PCR). The measurements of NF-kappaB, TNF-alpha, IL-6, and IL-10 were performed, respectively, at 1, 4, 4, and 1 hr after endotoxin injection. The results showed that LPS elevated the production of TNF-alpha, IL-6, and IL-10 and enhanced NF-kappaB activation in rat intestine. At all dosages, PTX reduced the activation of NF-kappaB and the production of TNF-alpha and IL-6, but enhanced the release of IL-10. These effects were greatest at dosages of 50 mg/kg for TNF-alpha and IL-6, and 25 mg/kg for IL-10. In conclusion, PTX suppressed the production of proinflammatory cytokines such as TNF-alpha and IL-6 in rat intestine, and enhanced the endotoxin-induced production of IL-10. The suppressive effect of proinflammatory cytokines may act by inhibiting NF-kappaB activation, but not by induction of IL-10.

Animals↗
PubMed2003

Estrogen affects BDNF expression following chronic constriction nerve injury.

To investigate the effect of estrogen on BDNF expression in neuropathic pain. Using chronic constriction injury model, we detected BDNF mRNA and protein level by reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. A hot-plate test was used as a sign of neuropathic pain. The rats with higher estrogen level exhibited more sensitive to thermal stimuli and had a higher level of BDNF mRNA and protein expression. The results suggest that BDNF level can be elevated by estrogen and estrogen may potentiate the sensitivity to thermal stimuli by its effect on BDNF expression. Thus, this study improves our understanding of the role of estrogen in the nociceptive processing.

Animals↗