Updated guidelines on cough launched.
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Cough↗
Biomedical subjects
Zeng-li Wang
Publications and source records attributed to Zeng-li Wang.
Increasing awareness of recognition of chronic obstructive pulmonary disease.
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Humans↗
[STAT1 antisense oligonucleotides inhibit secretion of TNF-alpha, IL-8 and NO in alveolar macrophages of rats suffering from interstitial pulmonary fibrosis].
AIM: To investigate the effect of signal transducer and activator of transcription 1 (STAT1) antisense oligonucleotides (ASON) on secretion of TNF-alpha, IL-8 and NO by alveolar macrophages (AMs) of rats with bleomycin (BLM)-induced pulmonary fibrosis. METHODS: Five adult female Wistar rats were intratracheally instilled with BLM. After 7 days, the rats were sacrificed under ketamine anaesthesia and bronchoalveolar lavage (BAL) was performed to obtain AMs. AMs were divided into four groups: STAT1 ASON, STAT1 sense oligonucleotides (SON), dexamethasone (DEX) and control groups. Culture medium was collected at 36 hours after adding STAT1 ASON, STAT1 SON and DEX, respectively. The concentrations of TNF-alpha, IL-8 and NO in the culture medium were detected. RESULTS: The concentrations of TNF-alpha, IL-8 and NO in STAT1 ASON group were lower than those in STAT1 SON, DEX and control groups (P<0.05). Moreover, the concentrations of TNF-alpha, IL-8 and NO in DEX group were also lower than those in control and STAT1 SON groups (P<0.05). But compared with control group, the concentrations of TNF-alpha, IL-8 and NO in STAT1 SON group was not significantly different (P<0.05). CONCLUSION: STAT1 ASON can inhibit the secretion of TNF-alpha, IL-8 and NO in AMs. STAT1 may become a target for treating pulmonary fibrosis.
Animals↗
Research on airway inflammation: present status in Mainland China.
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Animals↗
[Effect of tyrosine kinase inhibitors on airway remodeling in bronchial asthma].
OBJECTIVE: To investigate the effect of tyrosine kinase inhibitors (TKIs) on asthmatic rat airway remodeling. METHODS: The inhibitive effects of three TKIs (Genistein, jin-zhuan-ting and Tyrphostin AG1478) on proliferation of primary cultures of rat tracheal epithelial cells were assessed by MTT assay. Then, jin-zhuan-ting was adopted in the asthmatic rat model; immunohistofluorescene method was used to stain phosphorylated tyrosine (P-tyr) for disclosing the activation of EGFR; Sirius Red staining of submucosal collagen I and III was performed, and an analysis was made on the correlation between EGFR activation and collagen I and III deposition. RESULTS: All the three TKIs inhibited the growth of tracheal epithelial cells in a time and dose depending manner, and the inhibition rates among them showed no statistical differences; airway subepithelial collagen I and III deposition degrees were markedly elevated in asthmatic groups and jin-zhuan-ting reduced the deposition in a certain degree; EGFR activation (P-tyr) in airways epithelium of asthmatic groups was greatly increased in comparison with that of control groups, and it was evidently decreased in jin-zhuan-ting groups. Correlation analysis demonstrated that the amount of airway subepithelial collagen I and III was positively correlated to EGFR activation. CONCLUSION: TKIs may have preventive implications for asthmatic airway remodeling.
Animals↗
[Simvastatin induces eosinophil apoptosis in vitro].
OBJECTIVE: To investigate the effect of simvastatin, a 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR) inhibitor, on eosinophils (EOSs) apoptosis in asthma patients. METHODS: Peripheral blood EOSs from 10 asthma patients were cultured in the presence or absence of simvastatin (1, 5, 10, 20 micromol/L), together with or without mevalonate (100 micromol/L) for 6, 12, 24, and 48 h. Apoptosis was monitored by annexin V/PI staining and flow cytometry. Caspase-3 was measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: EOSs were particularly susceptible to apoptosis after incubated with 5 micromol/L simvastatin for 6, 12, 24, and 48 h [the rates of EOSs undergoing apoptosis were: (23 +/- 3)%, (24 +/- 3)%, (41 +/- 6)%, (70 +/- 12)% in control and (32 +/- 4)%, (47 +/- 7)%, (62 +/- 9)%, (86 +/- 14)% in simvastatin; compared with control at the same time point: P = 0.000]. EOS apoptosis occurred at doses of 1 micromol/L and was already maximal at 5 micromol/L after incubated with simvastatin for 12 h [the rates of EOSs undergoing apoptosis were: (24 +/- 3)% in control, (37 +/- 3)%, (51 +/- 3)%, (53 +/- 4)%, (52 +/- 4)% in 1, 5, 10, 20 micromol/L simvastatin, respectively; compared with control: P = 0.000]. The level of caspase-3 in EOSs was consistent with the rate of cell apoptosis [(8 +/- 3) microg/L in control, (14 +/- 4), (22 +/- 4), (24 +/- 4), (23 +/- 5) microg/L in 1, 5, 10, 20 micromol/L simvastatin, respectively; compared with control: P = 0.000 - 0.003]. However, Co-incubation of simvastatin with mevalonate (the production of HMGR) completely reversed the activity of simvastatin on EOS apoptosis even when the highest simvastatin (20 micromol/L) dose was used; the rates of EOSs undergoing apoptosis in the control, mevalonate plus simvastatin and simvastatin alone were (24 +/- 3)%, (52 +/- 4)% and (25 +/- 3)%, respectively; while the caspase-3 levels were (8 +/- 3) microg/L, (23 +/- 5) microg/L and (9 +/- 3) microg/L, respectively. CONCLUSION: Simvastatin induces apoptosis of EOSs in asthma patients via its ability to block the synthesis of the important isoprenoid intermediates, which leads to the inhibition of small GTP-binding protein activity.
Adult↗
[The effect of STAT1 antisense oligonucleotides on lung fibroblast proliferation and hydroxyproline secretion].
OBJECTIVE: To investigate the effect of signal transducer and activator of transcription 1 (STAT1) antisense oligonucleotides on lung fibroblast proliferation and hydroxyproline secretion. METHODS: Ten adult female Wistar rats were randomly divided into two groups: one group was intratracheally instilled with bleomycin (BLM), while another group with 0.9% NaCl solution (NS). After 7 days, the rats were killed by right ventricle of heart exsanguinations under ketamine anaesthesia, and bronchoalveolar lavage (BAL) was performed to obtain alveolar macrophage (AM). AMs from the BLM group were divided into four groups, treated with STAT1 antisense oligonucleotides, STAT1 sense oligonucleotides, dexamethasone and medium alone (control), respectively. AMs and media were collected after culture for 36 h. The mRNA and protein expression of STAT1 and ICAM-1 in AMs were detected by RT-PCR and Cell-ELISA, respectively. The conditioned media were co-cultured with lung fibroblasts for 30 h, and then the cell proliferation and the concentration of hydroxyproline were examined. RESULTS: (1) The STAT1 mRNA expression by AMs in the STAT1 antisense oligonucleotides group (31.8 +/- 3.5) was lower than those of AMs in the STAT1 sense oligonucleotides group (64.2 +/- 4.3), the dexamethasone group (44.1 +/- 4.6) and the control group (65.5 +/- 4.6) (P < 0.05). Moreover, the STAT1 mRNA expression by AMs in the dexamethasone group was also lower than those of AMs in the STAT1 sense oligonucleotides group and the control group (P < 0.05), but the STAT1 mRNA expression by AMs in the STAT1 sense oligonucleotides group was not different from that of the control group (P > 0.05). The STAT1 mRNA expression by AMs in the NS group (14.9 +/- 3.1) was lower than those of AMs in the STAT1 antisense oligonucleotides group, the STAT1 sense oligonucleotides group, the dexamethasone group and the control group (P < 0.05). (2) The mRNA expression of ICAM-1 showed similar changes to the STAT1 mRNA expression by AMs. (3) The STAT1 protein expression by AMs in the STAT1 antisense oligonucleotides group (4.4 +/- 0.6) or in the NS group (3.7 +/- 0.4) was lower than those of AMs in the STAT1 sense oligonucleotides group (7.7 +/- 0.7), the dexamethasone group (5.9 +/- 0.4) and the control group (7.6 +/- 0.6) (P < 0.05); and the STAT1 protein expression by AMs in the dexamethasone group was also lower than those of AMs in the STAT1 sense oligonucleotides group and the control group (P < 0.05), but the STAT1 protein expression by AMs in the STAT1 sense oligonucleotides group was not different from that of the control group (P > 0.05). (4) The changes of ICAM-1 protein expression, lung fibroblast proliferation and hydroxyproline concentration were consistent with the changes of STAT1 protein expression by AMs. CONCLUSIONS: STAT1 antisense oligonucleotides could inhibit the mRNA and the protein expression of STAT1 and ICAM-1 in AMs. STAT1 antisense oligonucleotides also inhibited lung fibroblast proliferation and hydroxyproline secretion.
Animals↗
Relationship between bone marrow-derived CD34 + cells expressing interleukin-5 receptor messenger RNA and asthmatic airway inflammation.
BACKGROUND: Asthma is clinically related with the degree of eosinophilic inflammation. How asthmatic airway inflammation is affected is still poorly understood. So the effects of bone marrow-derived hematopoietic cells expressing CD(34) (CD(34)(+)) and interleukin-5 (IL-5) receptor messenger RNA (IL-5R mRNA+) on asthmatic airway inflammation were investigated. METHODS: Balb/c mice were sensitized and challenged by ovalbumin (OVA) to establish an asthmatic model while control mice were sensitized and exposed to sterile saline. The mice were killed at different time points after being challenged by OVA and sterile saline. Then, bronchoalveolar lavage fluid (BALF), peripheral blood (PB) and bone marrow (BM) were prepared. Eosinophils in PB (PBEOS) and BALF (BALFEOS), nuclear cells in BALF, PB and BM were counted. By flow cytometry, the percentage of CD(34)(+) cells to nucleated cells in PB, BM and the relative number of CD(34)(+) cells in PB (PBCD(34)(+)) and BM (BMCD(34)(+)) were calculated. Immunocytochemistry and in situ hybridization were used to investigate the hematopoietic cells with co-localized expression of CD(34) and IL-5R mRNA in BM (BMCD34+IL-5R mRNA+). The percentage of BMCD34+IL-5R mRNA+ to BMCD(34)(+) was calculated. RESULTS: Twelve hours after challenge by OVA, BALFEOS and PBEOS in the experimental group were significantly higher than those in the control group (P < 0.01). Twenty-four hours after OVA challenge, BALFEOS, PBEOS and BMCD34+IL-5R mRNA+ were elevated maximally, significantly different from those in the control group (P < 0.01). Forty-eight hours after OVA challenge, BALFEOS and BMCD34+IL-5R mRNA+ were still significantly higher than those of the controls (P < 0.01). The other markers reverted to normal. In 60 mice, BMCD34+IL-5R mRNA+ was closely correlated with the BALEOS, PBEOS, BMCD(34)(+) and BMCD(34)(+) (%) (P < 0.05). CONCLUSIONS: The amount of CD(34)(+) cells expressing IL-5R mRNA increased in the BM of asthmatic model mice, which favors eosinophilopoiesis and eosinophilic airway inflammation. A signal pathway exists between the lungs and the bone marrow, which is involved in the initiation and maintenance of asthmatic airway inflammation.
Animals↗
[Relationship between the locus 16 geontype of beta 2 adrenergic receptor and the nocturnal asthma phenotype].
OBJECTIVE: To investigate the relationship between the polymorphism of beta 2 adrenergic receptor (beta 2 AR) at loci 16, 27 and the nocturnal asthma phenotype. METHODS: Forty-nine asthmatic patients were divided into nocturnal asthmatic group (n = 25) and non-nocturnal asthmatic group(n = 24) by their peak expiratory flow rates (PEFR). The genotypes at loci 16, 27 of beta 2 AR were delineated by PCR product sequencing. Then the relationships of beta 2 AR genotypes with the PEFR, FEV1 and the situation of drug use in the two groups were analyzed. RESULTS: By the criteria of overnight decrements in PEFR, the nocturnal asthma group had a mean overnight decrement in PEFR of 33.6%, compared to 7.0% for the non-nocturnal asthma group (P < 0.001). The mean values of daytime baseline percent predicted forced expiratory volume in 1 s (FEV1) were 73.7% and 85.8% for the nocturnal and non-nocturnal cohorts, respectively (P < 0.001). The frequency of the Gly16 allele was 56.0% in the nocturnal group, compared to 22.9% in the non-nocturnal group (P < 0.05). The results from comparison of the two cohorts as to homozygosity for Gly16, homozygosity for Arg16, or heterozygosity were also consistent with the segregation of Gly16 with nocturnal asthma. There was no significant difference in the frequency of polymorphisms at locus 27 (Gln27 or Glu27). CONCLUSION: The Gly16 polymorphism of beta 2 AR appears to be associated with nocturnal asthma.
Alleles↗
[The effects of anti-inflammatory and anti-asthmatic agents on CD34+ hematopoietic cells in bone marrow of asthmatic mice].
OBJECTIVE: To observe the effects of glucocorticoids and cysteinyl leukotrienes 1 receptor antagonist on CD(34)(+) hematopoietic cells, and to study the rationality of a bone marrow-targeting anti-inflammatory strategy. METHODS: Twenty-four BALB/c mice were sensitized and challenged by 1% ovalbumin (OVA) to establish the asthmatic model. Asthmatic mice were challenged by 1% OVA and divided into 4 groups: fed by sterile saline (group A), prednisone (group B), montelukast (group C) and prednisone plus montelukast (group D) respectively for two consecutive weeks. The mice were killed at 24 h after the last challenge, then bronchoalveolar lavage fluid (BALF), peripheral blood and bone marrow were prepared. Eosinophils in peripheral blood and BALF, nucleate cells in BALF, peripheral blood and bone marrow were counted. The percentage of CD(34)(+) cells, CD(4)(+), CD(8)(+) T lymphocyte to nucleate cells in peripheral blood and bone marrow were counted by flow cytometry. Immunocytochemistry and in situ hybridization were employed to detect the hematopoietic cells expression of CD(34)(+) and IL-5Ralpha mRNA in bone marrow (CD(34)(+) IL-5Ralpha mRNA(+) cells). RESULTS: The number of EOS in BALF and peripheral blood and the number of CD(34)(+) cells in peripheral blood and bone marrow in group A were [(18.3 +/- 1.3) x 10(5)/L], [(2.5 +/- 0.4) x 10(8)/L], [(9.6 +/- 5.1) x 10(7)/L] and [(7.7 +/- 3.2) x 10(7)/femur] respectively, compared with the corresponding indices in group B [(4.6 +/- 1.7) x 10(5)/L, (1.5 +/- 0.3) x 10(8)/L, (3.9 +/- 2.1) x 10(7)/L, (3.3 +/- 1.8) x 10(7)/femur] and group D [(3.7 +/- 1.4) x 10(5)/L, (1.7 +/- 0.3) x 10(8)/L, (4.1 +/- 1.8) x 10(7)/L, (2.2 +/- 0.7) x 10(7)/femur]; the differences all were significant (all P < 0.01). The number of bone marrow CD(34)(+) IL-5Ralpha mRNA(+) in group B and D were (23 +/- 7)% and (21 +/- 4)%, as compared with the corresponding index in group A [(37 +/- 4)%], the differences were significant (P < 0.01); the number of eosinophils in BALF in group C was (12.2 +/- 1.1) x 10(5)/L, as compared with the corresponding index in group A [(18.3 +/- 1.3) x 10(5)/L], the difference was significant (P < 0.05). CONCLUSIONS: Prednisone probably inhibits the proliferation, differentiation and emigration of CD(34)(+) cells in the bone marrow of asthmatic mice, and inhibits eosinophilopoiesis in bone marrow, eosinophil migration into peripheral blood and recruitment to the airways. Montelukast may suppress eosinophil infiltrating into lungs of asthmatic mice, but it does not inhibit the proliferation and emigration of CD(34)(+) cells and does not show apparent synergistic effect with prednisone.
Acetates↗
[Regulative effect of STAT1 on inflammation of lung tissue in bleomycin-induced rat interstitial pulmonary fibrosis].
OBJECTIVE: To investigate the role of signal transducer and activator of transcription 1 (STAT1) in alveolar macrophage (AM) in bleomycin-induced rat pulmonary fibrosis. METHODS: Fifty adult female Wistar rats were randomly divided into two groups. The rats of BLM group were intratracheally instilled with bleomycin (BLM), and those of the control group with normal saline(NS). The kinetic change of STAT1 activation and the intercellular adhesion molecule-1 (ICAM-1) expression in AM were examined. RESULTS: STAT1 was slightly activated in AM of NS group. After bleomycin treatment, the STAT1 activation of AM significantly increased on day 1, reached the peak value on day 7, and then gradually decreased, yet it remained significantly above the value of the NS group on day 28 (P < 0.05). There were a few positive staining cells for ICAM-1 expression in AM of NS group. After intratracheal instillation of bleomycin, the number of positive staining cells for ICAM-1 expression significantly increased on day 1, reached the peak value on day 7, gradually decreased from then on, but still it was higher than that of the NS group on day 28 (P < 0.05). There was a significant correlation between STAT1 activation and ICAM-1 expression in AM (r = 0.913, P < 0.01); moreover, ICAM-1 expression in AM was significantly correlated with the degree of inflammation in lung tissue (r = 0.947, P < 0.01). CONCLUSION: STAT1 was found abnormally activated in AM in bleomycin-induced rat interstitial pulmonary fibrosis (IPF). The abnormal STAT1 activation may play a role in the pathogenesis of acute alveolitis and pulmonary fibrosis.
Animals↗
[Inflammatory memory of pulmonary local lymphocytes in asthmatic mice].
OBJECTIVE: To investigate if long-lived inflammatory memory exists in the airway of asthmatic mice, and whether pulmonary local lymphocytes could transfer the inflammatory memory. METHODS: 97 mice were divided into six groups by random number meter: asthma group (group A, n = 50), long term group (group B, n = 20), control group of long term (group C, n = 6), adoptive transfer group (group D, n = 12, subgroups D1, D2 and D3 divided based on the transferred cells counts), adoptive transfer control group (group E, n = 6), and naive group( group F, n = 3). There were subgroups using BSA (bovine serum album) substituting OVA (ovalbumin) for the second challenge, named subgroup B-BSA in group B and subgroup D-BSA in group D. Pathologic changes, alveolar eosinophil infiltration, total cell counts (TCC) in bronchoalveolar lavage fluid (BALF), leukocyte differentials, and BALF IL-5 level were assayed in every group. Comparisons of inflammation responses between group B and group A, also between group D and group A were made. From asthmatic mice 34 d post aerosol, bronchoalveolar lavage (BAL) cells and splenocytes free of red blood cells (NR-splenocyte in brief) were cultured in vitro and stimulated with allergens, to detect cell proliferations and IL-5 levels in the supernatant. RESULTS: (1) Vasculitis, alveolitis and bronchiolitis were observed in group A. TCC, BALF eosinophil and IL-5 reached peak on 240 h and 8 h, 24 h post aerosol respectively [ (22 +/- 5 ) x 10(4)/ml, (1.43 +/- 0.09) x 10(4)/ml and (75.1 +/- 52. 9) pg/ml, respectively]. There were scattered vasculitis and al)veolitis in group B before second OVA challenge; and more severe vasculitis and 3-fold higher alveolitis (ratio of alveolar eosinophil inflammation indexes is 21.23/7.14) were observed after second challenge. TCC and BALF eosinophils reached peak 24 h post aerosol [(121.5 +/- 19.1) x 10(4)/ml and (12.960 +/- 2.040) x 10(4)/ml respectively], BALF IL-5 reached to its highest level [(50.8 +/- 18.5) pg/ml] 48 h post aerosol. There were mild vasculitis in group B-BSA, while TCC [(5.3 +/- 2. 1) x 10(4)/ml] and eosinophil [(0.060 +/- 0. 050) x 10(4)/ml] were both significantly lower than those of group B 24 h post aerosol [(121.5 +/- 19. 1 ) x 10(4)/ml and (12.960 +/- 2.040) x 10(4)/ml respectively, P < 0.05]. BAL cells stimulated with OVA in vitro proliferated stronger [(166.8 +/- 4.81) Bq] than those with BSA stimulation [(61.0 +/- 24.1) Bq] (P < 0.05). Supernatant IL-5 levels in cell cultures with OVA or BSA stimulation were similar [(49 +/- 4) pg/ml and (46 +/- 21) pg/ml respectively] (P > 0.05). (2) There were vasculitis in group D2, with TCC [(5.0 +/- 1.0) x 10(4)/ml] and BALF IL-5 [(24.4 +/- 2.1) pg/ml] 24 h post aerosol. There were bronchiolitis in group D3, with TCC [(7.3 +/- 5.8) x 10(4)/ml] and BALF IL-5 [(45 +/- 6.2) pg/ml] 24 h post aerosol. There was significant difference between group D2 and D3 on BALF IL-5 (P < 0. 05), but not on TCC (P > 0. 05). No vasculitis was observed in group D-BSA, with TCC [(3.3 +/- 4.2) x 10(4)/ml] not statistically different from group D [(5.0 +/- 1.0) x 10(4)/ml] (P > 0. 05). CONCLUSION: It is illustrated that long-lived inflammatory memory may exist in asthmatic mice lung, and pulmonary local lymphocytes may sufficient to transfer the memory.
Adoptive Transfer↗
[Bone marrow-derived CD+34 cells expressing interleukin-5 receptor messenger RNA and asthmatic airway inflammation].
OBJECTIVE: To study the possible role of bone marrow-derived hematopoietic cells expressing CD(34)(+) and IL-5 receptor messenger RNA (IL-5R mRNA(+)) in asthmatic airway inflammation. METHODS: Balb/c mice were sensitized and challenged by ovalbumin (OVA) to establish the asthmatic model. The control mice were sensitized and exposed to sterile saline. The mice were killed at different time points after challenged by OVA and sterile saline, and bronchoalveolar lavage (BALF), peripheral blood (PB) and bone marrow (BM) were prepared. Eosinophils (EOS) in PB and BALF, and nuclear cells in PB and BM were counted. The percentage of CD(34)(+) cells to nuclear cells (CD(34)(+)%) in PB and BM, and the relative number of CD(34)(+) cells (CD(34)(+)) in PB and BM were calculated by flow cytometry. Immunocytochemistry and in situ hybridization were used to observe the hematopoietic cells with co-localized expression of CD34 and IL-5R mRNA (CD(34)(+)/IL-5R mRNA(+)) in BM. The percentage of BM CD(34)(+)/IL-5R mRNA(+) to BM CD(34)(+) was calculated. RESULTS: (1) At 6 h after OVA challenge, the number of BALF EOS [(2.67 +/- 1.00) x 105/L] was significantly increased as compared to the number in controls [(0.46 +/- 0.06) x 105/L] (P < 0.01). At 12 h after OVA-challenge, the numbers of BALF EOS [(7.74 +/- 1.98) x 105/L] and PB EOS [(2.91 +/- 0.64) x 108/L] were significantly higher than those in the controls (P < 0.01). At 24 h after OVA-challenge, the numbers of BALF EOS[(19.43 +/- 3.69) x 105/L], PB EOS[(3.93 +/- 0.51) x 108/L] and BM CD(34)(+)/IL-5R mRNA(+) [(300.50 +/- 90.02) per thousand] were increased to the highest levels. The differences were significant as compared to the corresponding parameters in the controls (P < 0.01). At 48 h after OVA-challenge, the numbers of BALF EOS [(12.05 +/- 5.31) x 105/L] and BM CD(34)(+)/IL-5R mRNA(+) [(220.80 +/- 53.41) per thousand] were decreased, but were still significantly different compared to the numbers in the controls (P < 0.01), while other markers returned to the normal levels. (2) The number of BM CD(34)(+)/IL-5R mRNA(+) in the 60 mice was closely correlated with BALF EOS, PB EOS, BM CD(34)(+) and BM CD(34)(+) (P < 0.05). CONCLUSION: CD(34)(+) cells expressing IL-5R mRNA, which may favor eosinophilopoiesis and eosinophilic airway inflammation, were increased in the BM of this mouse asthmatic model. A feedback mechanism between the lungs and the bone marrow likely exists, which may be involved in the development and persistence of asthmatic airway inflammation.
Animals↗
[Expression of Clara cell secretory protein in airways of rat asthma remodel].
OBJECTIVE: To investigate the mRNA expression of Clara cell secretory protein (CCSP) and the Clara cell number in airways of rat asthma remodel. METHODS: A rat asthma model was established by sensitization and challenge with ovalbumin (OA). The mRNA expression of CCSP in the lung tissue, the CCSP level in bronchial alveolar lavage fluid (BALF), the thickness of the airways and the number of Clara cells in bronchioles were determined by RT-PCR, image analysis system, dot immunoblotting and immunohistochemistry methods. RESULTS: There was a progressive decline in CCSP mRNA expression in the lung tissue of rat asthma model group (0.53 +/- 0.07 and 0.49 +/- 0.03, respectively, after 1 week and 2 weeks of challenge) as compared to that of control group (0.67 +/- 0.04). The CCSP levels in BALF of asthma model group (47.00 +/- 6.58 and 45.95 +/- 3.20, respectively, after 1 week and 2 weeks of challenge) were significantly decreased than that of control group (63.08 +/- 2.84, P < 0.01). The ratio(%) of Clara cells was also reduced after challenge. The WAt/Pbm, WAi/Pbm, and WAm/Pbm were significantly increased 2 weeks after OA challenge and were negatively correlated with the level of CCSP and its mRNA expression. CONCLUSION: The Clara cells and CCSP may participate in the pathogenesis of asthma in the rat asthma remodel.
Animals↗
[Individualized treatment of respiratory infection should be emphasized].
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Anti-Bacterial Agents↗
[A study on the heterogeneous apoptosis of lymphocytes, eosinophils, and neutrophils from peripheral blood of asthmatic patients].
OBJECTIVES: To observe different responsiveness of lymphocytes, eosinophils, and neutrophils from peripheral blood of asthmatic patients to dexamethasone and montelukast-induced apoptosis and to explore the roles of Fas antigen and caspase-3 in the heterogeneity of cell apoptosis. METHODS: Lymphocytes, eosinophils, and neutrophils were isolated from peripheral blood of 18 asthmatic patients. Cells were incubated in vitro and treated with dexamethasone and leukotriene receptor antagonist montelukast respectively. Cell apoptosis rates and Fas expression rates were examined by flowcytometry whereas caspase-3 levels in these cells were detected by enzyme linked immunosorbent assay (ELISA). RESULTS: (1) Apoptosis rates: in vitro lymphocytes, eosinophils and neutrophils were compromised of spontaneous apoptosis at lower rates [(6.9 +/- 0.7)%, (31 +/- 11)% and (32 +/- 30)%, respectively]. With induction of dexamethasone, the apoptosis rates were (17.1 +/- 10.8)%, (44 +/- 22)% and (35 +/- 24)%. Montelukast markedly elevated the apoptosis rates of these three cells [(22.5 +/- 17.6)%, (50 +/- 27)% and (55 +/- 22)%, respectively] (compared to control, P < 0.01, < 0.05, > 0.05, respectively). (2) Fas expression: lymphocytes, eosinophils and neutrophils expressed low levels of Fas antigen at baseline [(1.50 +/- 0.07)%, (2.20 +/- 0.10)% and (1.21 +/- 0.09)%, respectively]. Dexamethasone induced Fas antigen expression levels of these cells of (6.58 +/- 2.10)%, (7.52 +/- 3.20)% and (3.24 +/- 2.34)%, and montelukast induced the expression levels of (5.06 +/- 1.66, 7.45 +/- 2.63, 3.03 +/- 2.47, P < 0.01, < 0.01, > 0.05, respectively). (3) caspase-3 levels: lymphocytes, eosinophils and neutrophils expressed constitutive caspase-3 levels of [(3.3 +/- 2.9) ng/L, (5 +/- 4) ng/L and (4.3 +/- 2.6) ng/L, respectively]. The dexamethasone induced caspase-3 levels were (6.7 +/- 3.1) ng/L, (6 +/- 3) ng/L and (3.1 +/- 1.8) ng/L. The montelukast induced levels were (5.2 +/- 3.7) ng/L, (8 +/- 4) ng/L, and (3.1 +/- 2.0) ng/L (compared to control, P < 0.01, < 0.01, > 0.05, respectively). It was demonstrated that dexamethasone and montelukast significantly induced apoptosis of lymphocytes and eosinophils which were assocreased with increased expression of Fas antigen and caspase-3. Dexamethasone was incapable of inducing neutrophils to apoptosis and had no significant effects on Fas expression and caspase-3 activity. Neutrophils underwent significant apoptosis after montelukast treatment, however, the induction was unlikely to be regulated by Fas and caspase-3 pathway. CONCLUSIONS: In asthmatic inflammatory modulating and effective cells, neutrophils is distinct from lymphocytes and eosinophils in profile of apoptosis induced by glucocorticoids and leukotriene receptor antagonist. The signal pathway contributing neutrophil apoptosis heterogeneity may involve deficient caspase cascade or Fas/FasL.
Acetates↗
[IgE regulation in asthma pathogenesis and development of a monoclonal anti-IgE antibody for the treatment of allergic asthma].
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Antibodies, Anti-Idiotypic↗
STAT1 activation and STAT1-dependent immune-response gene ICAM-1 expression in alveolar macrophages of rats suffered from interstitial pulmonary fibrosis.
AIM: To investigate the role of signal transducer and activator of transcription 1(STAT(1)) in alveolar macrophages (AMs) from rats with bleomycin-induced pulmonary fibrosis. METHODS: Fifty adult female Wistar rats were randomly divided into two groups: One group was intratracheally instilled with bleomycin (BLM), while another group with 9 g/L NaCl solution (NS). The kinetic change of STAT(1) activation and intercellular adhesion molecule-1(ICAM-1) expression in AMs was examined by Western blot and immunohistochemical staining, respectively. RESULTS: (1)STAT(1) was rarely activated in AMs of NS group. After bleomycin treatment, the STAT(1) activation of AMs was significantly increased on day 1, climaxed on day 7, and then gradually decreased, but remaining significantly higher than that of NS group on day 28 (P<0.05). (2)There was only a few cells ICAM-1 higher than that positively stained in AMs of NS group. After intratracheal instillation of bleomycin, the number of ICAM-1 positive stained cells was significantly increased on day 1, reached its peak values on day 7, and then gradually decreased, and still higher than that of NS group on day 28 (P<0.05).(3)There was a significant correlationship between STAT(1) activation and ICAM-1 expression in AMs (r =0.913, P<0.01). Further more, the ICAM-1 expression in AMs was significantly correlated with the severity of inflammation in lung tissues (r =0.947, P<0.01). CONCLUSION: STAT(1) was abnormally activated in AMs of rats with bleomycin-induced interstitial pulmonary fibrosis (IPF). The abnormal STAT(1) activation may play a role in the pathogenesis of acute alveolitis and pulmonary fibrosis.
Animals↗