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Objective CD8 +T cells increased in the airway of patients with chronic obstructive pulmonary disease and exis -ted constantly .The aim was to investigate the role of CD 8 +T-cells in rats with chronic bronchitis ( CB) which was induced by cigarette smoking and intratracheal injection with lipopolysaccharide ( LPS) . Methods 18 health Wistar rats were radomly divided into sham smoking group(group A), CB group(group B) and N-acetylcysteine prevention group (group C).The rats in group B and group C re-ceived intratracheal injection with LPS twice and exposed to cigarette smoking for 4 weeks to induce CB model .The rats in Group C re-ceiving intragastric administration with N-acetylcysteine (NAC)(200mg/kg) before received LPS and smoking.Group A was the sham smoking group.The lung tissue of all rats were stained by HE then evaluated about pathological scores .The expression of nuclear fac-tor-κB (NF-κB), major histocompatibility complex class I (MHCI), CD8 +T cell and Vascular endothelial growth factor (VEGF) in airway were detected by immunohistochemisty which was stained by labeled streptavidin biotin method . Results The pathological scores of airway ( 10 .83 ±3 .31 ) in group B were higher than (1.17 ±2.40) in group A(P <0.05).The pathological scores of airway(4.66 ±2.25) in group C were less than (10.83 ±3.31) in group B(P <0.05).The expression of NF-κB(4.84), MHC I (2.48),CD8 +T cell(5.35)and VEGF(5.02) in airway increased in group B when compared with (1.18, 1.25, 1.33) and (1.18) in group A respectively(P <0.05).The expression of NF-κB (2.18), MHC I(1.46),CD8 +(2.35)and VEGF(2.02) in airway decreased in group C when compared with (4.84), MHC I(2.48),CD8 +T cell(5.35)and VEGF(5.02) in group B respectively (P<0.05 ). There were positive correlations between the expression of NF-κB, MHC I and CD8 +T cells in airways(r=0.670, r=0.701, respec-tively, all P<0.01).There were positive correlations between the expression of CD 8 +T cells and VEGF the pathological scores of air-ways(r=0.689, r=0.782, respectively, all P<0.01). Conclusion NAC can inhibit airway inflammation which is regulated by CD8 +T-cells and VEGF through suppressing the expression of NF -κB and MHC I.
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Objective:To study the effect of erythromycin(EM) on cigarette smoke-induced histone deacetylase-3(HDAC3) protein expression in human macrophages in vitro .Methods:The Aqueous cigarette smoke extract ( CSE) was always prepared fresh on the day of the experiment .The U937 monocytic cells were differentiated into macrophages by using phorbol 12-myristate 13-acetate (PMA) according to standard procedures .The U937 differentiated cells were treated with either CSE (1%) or EM (1 μg/ml) pre-treatment, and HDAC inhibitor trichostatin A (TSA;100 ng/ml) for 24 h.HDAC activity was measured with a colorimetric assay kit and Western blot was used for HDAC3 and factor nuclear-kappaB (NF-κB) protein assays.The levels of tumor necrosis factor-α(TNF-α) release in the supernatant were determined by enzyme linked immunosorbent assay (ELISA).Results:CSE(1%) significantly de-creased HDAC activity and HDAC 3 protein levels at 24 h.Preincubation with EM (1μg/ml ) for 24 h significantly inhibit CSE (1%) induced decrease of HDAC3 protein expression.Furthermore, Preincubation with EM(1 μg/ml) for 24 h significantly inhibit NF-κB activity and TNF-αrelease in human macrophages .Conclusion:EM is able to restore HDAC3 levels decreased by cigarette smoke and inhibit NF-κB activity resulting in decreasing CSE-mediated TNF-αrelease, which has shown an important explanation that EM possess the anti-inflammatory effect induced by cigarette smoke .
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Objective To study the expression and significance of Th17 and Tc17 cells in the peripheral blood,skin and lung in a murine model of bleomycin (BLM)-induced systemic sclerosis (SSc).Methods Thirty female BALB/c mouse were randomly divided into 3 groups,including a control group ( A group),a injected with BLM 4 week without pulmonary fibrosis(PF) group( B group) and with obviously PF group(C group).Pathological changes of skin and lung were detected.The proportion of CD4+,CD8+,CD4+IL-17+(Th17),CD8+IL-17+(Tc17) cells in the peripheral blood,skin and lung of mouse was determined by flow cytometry.The mRNA expressions of RORγt,IL-17A in skin and lung of mouse were evaluated by real-time PCR.Enzyme linked immunosorbent assay(ELISA) was used to measure the levels of IL-17 in serum.Results Dermal hydroxyproline(HYP) contents and the score of PF were significantly increased in C group [ (3.07±1.26) μg/mg,4.0±1.41 ]and B group [ (2.43±0.61) μμg/mg,1.50±0.76]as compared with A group [ (1.45±0.40) μg/mg,0.60±0.70 ],and pulmonary HYP contents was obviously increased in C group than in A and B groups,all P＜0.05.Compared with the A group,the percentage of CD4+ and Th17 cells in the peripheral blood,skin and lung of B and C groups,Tc17 cells of C group was significantly increased,and CD8+ cells was significantly decreased(all P＜0.05).The ratio of Th17/CD4+CD8+ in the peripheral blood,skin and lung of B and C groups [ ( 1.41 ±0.36)％,( 1.79±0.77)％ ],[ (2.58±1.07)％,(5.23±2.34)％ ]and [ (3.50±1.20)％,(4.02±1.32) ％ ]was significantly increased compared with A group (0.71±0.25)％,(1.15±0.59)％,(0.99±0.46)％.The ratio of Tc17/CD4+CD8+ in the lung of C groups( 1.62±0.53) ％ and in the skin of B and C groups [ (1.70±0.70) ％,( 1.63±0.63 ) ％ ]was significantly increased compared with A group [ ( 1.00±0.47 ) ％,( 1.1 1 ±0.34 ) ％ ],all P＜0.05.Compared with the A group,the mRNA levels of IL-17A,RORγt in skin of B and C groups,and in lung of C group were higher and the levels of IL-17 in serum was significantly increased,all P＜0.05.Th17 cells and the levels of IL-17 in blood were positive correlation with dermal and pulmonary inflammation,fibrosis and H YP contents,all P＜0.01.The frequency of Th17 and Tc17 cells in skin and lung respectively had a positive correlation with dermal and pulmonary inflammation,the score of fibrosis,and HYP contents of skin and lung,all P＜0.01.Conclusion Th17 and Tc17 cells were significantly increased in the peripheral blood,skin and lung of a murine model of SSc,and Th17 cells is dominated.They correlated with the inflammation and fibrosis of skin and lung,and may participate in the pathogenesis of SSc through secrete IL-17.
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ObjectiveThe expression and significance of interleukin(IL)-17 in a murine model of experimental systemic sclerosis(SSc) was studied and its correlation with transforming growth factor-beta 1 (TGF-β1) was explored.Methods Thirty female BALB/c mice were randomly divided into 3 groups,including a control group, bleomycin(BLM) injection for 4 weeks group(model 1 group) and a termination injection of BLM 4 weeks group(model 2 group).The pathological changes of skin and lung were detected.The mRNA expressions of IL-17A,RORγt,TGF-β1 mRNA were evaluated by real-time PCR.Enzyme linked immunosorbent assay was used to measure the levels of IL-17 and TGF-β1 in the serum and bronchoalveolar lavage fluid(BALF).Comparisons among groups were performed by variance analysis.ResultsSkin and lung of the model groups showed evident inflammatory cell infiltration and increased deposition of collagen fibers.The score of dermal inflammation and lung fibrosis was significantly higher in the model 1 and model 2 groups (2.5±0.8,3.0±1.8), (2.4±0.8,3.1±1.2) as compared to that of the control group (0.9±0.7,0.9±1.0),(F=12.19,8.367,25.11,4.641; all P＜0.05).The amount of hydroxyproline was markedly increased in the model groups than in the control group.Compared with those of the control group,the mRNA levels of IL-17A,RORγt,TGF- 31 in the skin and lung of the model 1 group were higher.The levels of IL-17 in serum and BALF of the model 1 group was significantly increased and the levels of TGF- β1 were increased in BALF and decreased in the serum (all P＜0.05).The mRNA levels of IL-17A in skin and lung had a positive correlation with the mRNA levels of TGF- β1,score of dermal inflammation and lung fibrosis.The levels of IL-17 in serum had a positive correlation with hydroxyproline of the skin and lung.ConclusionIL-17 may participate in systemic immune-mediated inflammation and changes of skin and lung in SSc and when combined with TGF-β1 togetter will cause damage to skin and lung in SSc.
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Objective To evaluate the expression of Tc17 in a cigarette smoke-induced mice model of emphysema.To explore the probable mechanisms about how Tc17 cells to elevate in lungs of mice.Methods Forty male Balb/c mice were randomly divided into four groups,including control group ( 12 weeks,C12),control group (24 weeks,C24),smoke-exposure group (12 weeks,S12) and smoke-exposure group (24 weeks,S24 ),10 mice each group,Emphysema of mice was observed by HE pigmentation.Morphological changes were evaluated by mean linear intercepts (Lm) and destructive index (DI).The proportion of CD8+ IL-17 + Tc17,CD8+ IL-17 + CC chemokine receptor type 6 ( CCR6 ) + and 6CCR6 + Tc17 cells in lungs of mice was determined by flow cytometry.The mRNA expressions of retinoidrelated orphan nuclear receptor(RORγt) and IL-17 were evaluated by real-time PCR.The levels of IL-1 β,IL-6,IL-23,transforming growth factor β (TGFβ) and CC chemokine ligand 20 (CCL20) were tested by ELISA.Correlations among these indexes were analyzed.Results Lm and DI were significantly higher in S12 and S24 than in C12 and C24,S24 in particular (t value 4.378-15.188,all P ＜ 0.05).The percentages of Tc17 in S12 and S24[(9.28 ± 1.12)%,( 13.13 ±3.56)%]was significantly increased as compared with that in C12 and C24[(2.40 ±0.60 )%,(2.64 ±0.96 )%],S24 in particular.The mRNA levels of RORγt and IL-17 in S12 and S24 were higher than in C12 and C24,S12 and S24 in particular.There was significant difference (all P ＜0.05 ).The frequency of Tc17 cells had a positive correlation with Lm and DI ( r value were 0.734 and 0.884 respectively,P ＜ 0.01 ).The percentages of CD8+ IL-17 + CCR6 +T cells and CCR6 + Tc17 were significantly elevated in S12 and S24 compared to C12 and C24,S24 in particular (all P ＜ 0.05 ).There was positive correlation between Tc17 cell ratio and CCL20 levels( r =0.899,P ＜0.01 ).The levels of IL-1 β,IL-6,IL-23 and TGFβ in S12 and S24 were significantly increased as compared with that in C12 and C24.There was significant difference (all P ＜0.05).Meanwhile,the frequency of Tc17 cells had a positive correlation with IL-1β,IL-6,IL-23,and TGFβ.Conclusions An up-regulation of proportions Tc17 in lungs of cigarette smoke-induced emphysema mice were detected.The CCR6/CCL20 axis and the increased IL-1β,IL-6,IL-23 and TGFβ probably contributed to this up-regulation.
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This study was aimed to evaluate the application of64-slice spiral CT in imaging anatomy of the normal optic canal. The optic canals of 100 healthy subjects were examined by 64-slice spiral CT,and the imaging measurement of the anatomy structures were performed by the multi-planar reconstruction. The longest and the shorzest walls of the optic canal were the medial wall and the inferior wall, respectively.Results indicate that the imaging anatomic measurement of the optic canal can be accurately and easily performed by means of multi-planar reconstruction of 64-slice spiral CT.
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Objective To investigate the effect of cigarette smoke exposure on the interleukin-17-producing CD4+T helper lymphocyte( Th17 ) in peripheral blood and lungs of cigarette smoke-induced emphysema mice. MethodsForty male BALB/c mice were randomly divided into 4 groups, including a control group C12, a control group C24, a smoke-exposure group S12 and a smoke-exposure group S24, 10 mice each group. Morphological changes were evaluated by mean linear intercepts (Lm) and destructive index (DI). The concentration of IL-17, IFN-γ and TNF-α in bronchoalveolar lavage fluid(BALF) and the concentration of IFN-γ and TNF-α in lung homogenates were measured by enzyme-linked immunosorbent assay (ELISA). The proportion of CD4+IL-17+ Th17 cells in peripheral blood and lungs of mice was determined by flow cytometry. The mRNA expressions of RORγt and IL-17 in peripheral blood and lungs were evaluated by real-time PCR. ResultsLm and DI were significantly higher in S12 and S24 groups [(39.19±3.51)μm vs (46.87±7.16) μm, 39.13±1.57 vs 45.16±3.13]than that in C12 and C24 groups [(32.60± 3.21 ) μm vs (32.38±3.73) μm, 28.23± 1.62 vs 28.86±2.07], all P＜0.05. IL-17, IFN-γand TNF-α in BALF of S12 and S24 groups [(119.72±10.72) ng/L vs (296.40±14.00) ng/L,(129.7±22.2) ng/L vs(251. 1±62.4) ng/L, (17.35±1.60) ng/L, (36.35±1.43) ng/L]were higher than those in C12 and C24 groups [(52.06±4.70) ng/L vs (51.89 ±6.82) ng/L, ( 85.8 ±26.8) ng/L vs ( 88.9 ± 11.5 ) ng/L,(6.41 ±0.90) ng/L vs (5.85±0.92) ng/L], IFN-γ and TNF-α in lungs of S12 and S24 groups [( 1124.3±174.4) ng/L vs (1342.7±206.1) ng/L, (77.2±13.7) ng/L vs (101.7±19.0) ng/L, (129.7±22.2)ng/L vs (251.1 ±62.4) ng/L]were higher than those in C12 and C24 groups[(946.2±81.9) ng/L vs (1027.2±188.3) ng/L, (62.1±16.1) ng/L vs(64.4±15. 1) ng/L], all P＜0.05. The percentage of Th17 cells in lungs of S12 and S24 groups [(3.27±1.12)％ vs (7.19±2.24)％, ( 1.96±0.61 )％ vs (3.82±1.26)％]was significantly increased as compared with that of C12 and C24 groups [(1.80± 0.75)％ vs (1.99±0.59)％], all P＜0.05. And the percentage of Th17 cells in peripheral blood of S12 and S24 groups [(1.96±0.61)％ vs ( 3.82± 1.26)％]was also significantly higher than those in C12 and C24 groups [(0.90±0.37)％ vs (0.97±0.32)％], all P＜0.05. In peripheral blood and lungs,the mRNA levels of RORγt and IL-17 in S12 and S24 groups were higher than in C12 and C24 groups, all P＜0.05.Moreover, the frequency of Th17 cells in peripheral blood and lungs had a positive correlation with Lm and DI( r=0.706-0.772 ,all P＜0.05 ). ConclusionAn up-regulation of proportions Th17 in peripheral blood and lungs of cigarette smoke-inducsed emphysema mice were detected. It may be involved in the amplified and persistent inflammation.
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ObjectiveTo study the pathological characteristics of intra-acinar pulmonary artery inflammation and its correlation with smoking index and disease progression in smokers with normal lung function and smokers with chronic obstructive pulmonary disease (COPD).MethodsPatients requiting lung resection for peripheral lung cancer were divided into group A (nonsmokers with normal lung function,n = 10), group B (smokers with normal lung function, n = 13), and group C (smokers with stable COPD,n = 10).The lung tissue far away from rumor were resected to compare the pathological changes of intraacinar pulmonary arteries and infiltration level of inflammatory cell in pulmonary non-muscularized arteries (NMA), pulmonary partially muscularized arteries (PMA) and muscularized arteries (MA) among the three groups.The correlation analysis was made among infiltration level, smoking index, percentage of predicted value of forced expiratory volume in one second (FEV,％ Pred), six-minute-walk distance (6MWD) and BODE index.Results (1) Both group B and group C showed the intima and media thickness of MA was significantly higher, the lumen area of MA was narrower and the proportion of MA was higher, and collagenous fiber of MA adventitial proliferated and area increased in group C(P ＜0.05 or P ＜0.01).(2) In group B and group C, the percentage of the intra-acinar pulmonary arteries that contained leukocytes, T lymphocytes, CD8+ T lymphocytes and the number of these positive cells infiltrating the intraacinar pulmonary arteries were increased, especially an increased number of CD8+ T lymphocytes infiltrating in the arterial adventitia as compared with group A, moreover there were significant difference between group C and group B (P ＜ 0.05 or P ＜ 0.01).In group B and group C, the degree of these positive cellsinfiltrating NMA, PMA and MA presented a decreasing sequence (P ＜ 0.05 or P ＜ 0.01).Among the intima, media and adventitia of MA, the infiltration of these positive cells was the highest in the adventitia.Among group A, group B and group C, infiltration degree of CD4+ T lymphocyte, B lymphocyte, macrophage and neutrophil demonstrated no significant difference, also among NMA, PMA and MA (P ＞ 0.05).(3)The number of leukocytes, T lymphocytes, CD8+T lymphocytes infiltrating MA showed a positive correlation with the thickness of MA (r =0.563,0.627,0.589 ,P ＜0.01 ,respectively) and smoking index (r =0.551,0.665, 0.600, P ＜ 0.01, respectively), moreover the degree of these cells infiltrating MA demonstrated negative correlation with FEV1 ％ Pred (r = - 0.763, - 0.703, - 0.767, P ＜ 0.01, respectively).Also infiltrating degree of T lymphocytes and CD8+ T lymphocytes was positively correlated with BODE(r = 0.390,0.476,P ＜ 0.05, respectively). Furthermore the infiltrating degree of CD8+ T lymphocytes had negative correlation with 6MWD (r = - 0.356, P ＜ 0.05).Conclusions(1) Pulmonary arterial inflammation appears in smokers with normal lung function and smokers with COPD patients.It involves in all types of intra-acinar pulmonary arteries especially NMA and infiltrates whole layer of MA with a characteristic of CDs+T lymphocytes infiltrating in the adventitia of intra-acinar pulmonary arteries. (2)Pulmonary inflammation is closely correlated to cigarette smoking and clinical parameters such as BODE index, FEV1％pred and 6MWD.It is one of the key factors affecting the progression of COPD.
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Objective To explore the clinical,laboratory,and pathologic manifestations of the interstitial lung disease(ILD)associated with primary Sj(o)gren's syndrome(pSS,pSS-ILD).Methods Clinical data of 15 patients with pSS-ILD admitted to our hospital from 2006 to 2008 were collected and the different features were compared with 18 patients with pSS without ILD.Eight patients with pSS-ILD were followed up and observed the changes of high-resolution computed tomography (HRCT).Results The age at onset was later in pSS-ILD[(57±11)years]than in pSS without ILD[(43±11)years](P<0.01).The initial symptoms in six of patients with pSS-ILD were cough,expectoration,chest distress or dyspnea upon exertion.The respiratory clinical manifestations,circulationsystem involvement and pulmonary artery hypertension (PAH) were more common in pSS-ILD than in pSS without ILD(P<0.01).Compared with patients with pSS without ILD,patients with pSS-ILD had significantly higher serum IgG level(P<0.01).The common findings of HRCT included reticular changes,irregular linear hyper-attenuating areas,and nodules.Pleural involvement was found in 8 patients,honeycomb change in 5 patients and PAH in 3 patients.After treated for 6 months of 8 patients,radiological findings improved in 4 patients,stable in 2 patients,and worse in 2 patients.The comlnon histological findings included focal fibrosis in alveolar wall and alveolus with and alveolar space inflammatory cell infiltration,interstitial inflammation with mulifocal lymphocyte infiltration.One patient had the pathological changes of nonspecific interstitial pneumonia(NSIP).Conclusion The age at onset of pSS-ILD is late and tends to produce respiratory symptoms and prone to have circulationsystem involvement such as PAH and elevated serum IgG level.Honeycomb change in HRCT can be seen in one third of patients and most patients can improve after treatment,however.NSIP can be observed in histopathologieal
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Objective To study the pathological characteristics of interleukin-16 (IL-16) and CXC chemokine receptor 3 (CXCR3) in pulmonary artery of smokers with normal lung function and smokers with chronic obstructive pulmonary disease (COPD). Methods We examined surgical specimens from three groups of subjects undergoing lung resection for localized pulmonary lesions: group NS(nonsmokers with normal lung function, n=10); group S (smokers with normal lung function, n=13); group COPD (smokers with stable COPD, n=10). The clinical datas including blood gas analysis, pulmonary function,BMI, smoking index, BODE index, six-minute-walk distance (6MWD), Medical Research Council dyspened scale (MRC), St. George Respiratory Questionnaire (SGRQ) were recorded in all subjects before the operation. We applied technique of hematoxylin-eosin staining to observe pathomorphological changes of the pulmonary arteries. The concentration of IL-16 in lung tissues were measured by ELISA. Muscularized arteries were examined with immunohistochemical methods to identify T-lymphocytes (CD_3), CD_4 T-lymphocytes, CD_8 T-lymphocytes, IL-16, CXCR3. The correlation of IL-16 and CXCR3 in muscnlarized arteries in smokers with stable COPD were analysed. Results (1) The group COPD showed the highest concentration of IL-16 in lung tissue (P <0. 01) . The concentration of IL-16 in group S was higher than group NS (P<0.05). (2) Both in group S and group COPD, the percentage of the muscularized arteries that contained CXCR3 and IL-16 were increased as compared with group NS (P < 0. 01). Moreover there were statistical significance have been observed between group COPD and group S(P < 0.01). (3) The intensity of IL-16 infiltrating the muscularized arteries in group COPD showed a positive correlation with CD_3~+ T-lymphocytes, CD_8~+ T-lymphocytes, CXCR3 (r=0.639,0. 803,0. 696; P < 0. 05 or P < 0. 01), smoking index, BODE index (r= 0.737,0. 704; P < 0. 05). There was inverse relationship between the content of IL-16 in the muscularized arteries in group COPD and forced expiratory volume in one second% predicted (FEV_1 % Pred) and 6MWD (r=-0.803,-0.787; P<0.01). We also found the intensity of CXCR3 infiltrating the muscularized arteries in group COPD showed a positive correlation with CD_3~+ T-lymphocytes,CD_8~+ T-lymphocytes(r=0.650,0.767; P<0.05), smoking index, BODE index (r=0.650,0.767; P< 0.05). There was inverse relationship between the content of CXCR3 in the muscularized arteries in group COPD and FEV_1 % Pred and 6MWD (r=-0.778,-0.774;P<0.01). Conclusions (1) Both in group S and group COPD, IL-16 and CXCR3 were mainly expressed in lymphocytes which were correlated with CD_8~+ T-lymphocytes infiltrating the muscularized arteries. There were some suggestion that IL-16 prohaly recruited CD_8~+ T-lymphocytes into muscularized arteries by enhancing the expression of CXCR3. (2) The intensity of IL-16 and CXCR3 were correlated with the index of clinical and pulmonary function that suggested pulmonary arterial inflammation might be one of the key factors associated with the progression of COPD, and inhibiting the pulmonary artery inflammation played an important role in prevention and cure of COPD.
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Objective To study the characteristics of patients with low body mass index (BMI) chronic obstructive pulmonary disease(COPD). Methods A total of 38 clinically stable patients with moderate-to-severe COPD were enrolled. They were divided into two groups: underweight (UW) group (n=16,BMI<20);normal weight(NW) group(n=22, 20≤BMI<26). Body height and weight, smoking indexs, and six minutes walk distance (6MWD) were assayed. The British Medical Research Council (MRC) dyspnea scale was used to assess the degree of dyspnea. St. George's Respiratory Questionnaire (SGRQ) and Short Form 36 item Questionnaire (SF-36) were used for health-related quality of life (HRQoL) evaluation. The serum concentrations of leptin and ghrelin were detected by enzyme-linked immunosorbent assay (ELISA). Results Compared with the NW group, the inspiratory eapacity(IC), forced expiratory volume in one second (FEV), vital capacity (VC) ,most ventilate volume (MVV) and peak expiratory flow(PEF) were lower(P<0. 05) in the UW group. Residual volume-to-total lung capacity ratio (RV/TLC), smoking indexs and MRC score were higher (all P<0. 05) and 6MWD was significantly lower (P<0. 05) in the UW group than in NW group. Activity scores,impact scores and total scores of SGRQ showed significant deterioration in the UW group (P<0. 05). SF-36 also showed significantly worse scores for the parameters of the emotional and social functioning (P < 0. 05 ). Serum leptin was significantly lower ( P< 0.01 ) and ghrelin was higher in UW group than in NW group (P<0. 05). Stepwise multiple regression analyse showed that lC,mental health(MH) and physical function (PF) of SF-36, leptin,6MWD and smoking indexs were independently correlated with BMI. Conchtsions The pulmonary function, nutritional status, PF and life quality of COPD patients with low BMI were more deteriorative. The most significant influencing factor for BMI in COPD patients was IC. M H,exercise capacity,leptin level and smoking indexs were independently correlated with BMI in COPD patients. It is important to retrieve low BMI in the management of COPD patients.
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Objective To analyze the clinical data of patients with penicilliosis marneffei(PSM),summarize clinical characteristics of serosal involvement and provide experience to diagnose and treat serous effusion.Methods We retrospectively analyzed 61 patients with estabolished PSM infection in our hospital from March,2001 to March,2008.Patients were divided into positive groups while presented one or more abnormal serous effusion such as pleural effusion,ascites,pericardial effusion or cerebrospinal fluid.There were ten patients in positive groups finally,including nine male and one female whose ages ranging from 36yr to 67yr[mean(54.2?8.3)yr].Results(1)There were ten cases with pleural effusion,including two cases with pericardial effusion,five cases with ascites and two cases with abnormal cerebrospinal fluid.Ten cases were misdiagnosed as tuberculous pleurisy and accepted anti-tuberculosis treatment,two cases as tuberculous meningitis,two cases as tuberculous pericarditis,five cases as tuberculous peritonitis and five cases as malignant pleural effusion.(2)All patients manifested with fever,anemia,hypodynamia or emaciation,nine cases with cough,eight cases with chest pain,six cases with dyspnea,two cases with alvi profluvium,three cases with bellyache,five cases with necrotic papula,eight cases with subcutaneous abscess,nine cases with lymphadenectasis,nine cases with splenohepatomegalia and seven cases with moist rales.(3)Total white blood cells count increase in nine cases which mainly presented with significantly increase in neutrophil count[(17.6?5.3)?109/L]and ratio(0.841?0.048).Lymphocyte ratio was relatively low(0.976?0.035),but count was normal[(1.59?0.7)?109/L].(4)Human Immunodeficiency Viruses was negative in all patients and the CD4/CD8 ratio was 1.19?0.38.(5)Ratio of A/G was inversion in ten cases.Bilirubin,erythrocyte sedimentation rate and C-reactive protein increase in six cases,ten cases and ten cases respectively.Abnormal renal function appeared in five cases.(6)All cases were defined according to etiology including hemoculture(5 cases),medulloculture(2 cases),sputum culture(1 case),abscess secretion culture(4 cases) and histopathology(4 cases).(7)Imaging check demonstrated parenchymatous abnormality in lung(10 cases),splenohepatomegalia or abdominal para-aortic lymphadenectasis(9 cases)and osteolytic damage(6 cases).(8)The property of serous effusion which appeared cloudy yellow or uprightness was exudate.The cell count especially neutrophil count and protein content increased in it.(9)Anti-eumycete medicine were administered to four cases and achieved improvement.Three cases died of respiratory failure,cardiac failure,hepatic and renal failure.Two patient's condition aggravated and one patient voluntarily leaved hospital without treatment.Conclusion Penicilliosis marneffei often occurs in serous cavity of normal immune function crowd.Clinical characteristics manifest with chronic pyogenic and infected diseases which appear significant increase in neutrophil count.It invades lung,abdominal organ and might be complicated with pleural effusion,ascites and abnomal cerebrospinal fluid.The property of effusion is consistent with inflammatory efflusion which can be totally absorbed under effective anti-fungal treatment.Clinical prognosis relates with general body state.
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Chronic obstructive pulmonary disease(COPD) is a chronic inflammatory disease characterized by infiltration of T-lymphocytes,which plays a key role in the immune response of human.Exploration on the characters of immune response in the pathologic process related to COPD may be useful to explore the mechenism of immunity response in COPD patients,thus,contrubute to improve the knowledge of COPD and investigating new avenues of treatment.