Objective To investigate the role of inflammatory cytokines in the pathogenesis of chronic non-bacterial prostatitis/chronic pelvic pain syndrome (CAP/CPPS) patients. Methods The 38 cases with CAP/CPPS patients (18 cases of CAP and 20 cases of CPPS) and 20 cases of healthy controls were selected. The differential expressions of 40 kinds of inflammatory cytokines were detec-ted by antibody arrays in prostate fluid. Results The inflammatory cytokines which increased more than 1.5 times expression have been found. There were seven kinds in CAP including monocyte che-moattractant protein (MCP)-1, solution tumor necrosis factor receptor Ⅱ(s TNF R Ⅱ), platelet-de-rived growth faetor-BB (PDGF-BB), interleukin (IL)-β, IL-11、IL-6、MCP-2 and five kinds in CPPS groups including MCP-1、PDGF-BB、MCP-2、s TNF R Ⅱ、It-11 respectively, compared with healthy control group. The cluster analysis results showed that protein expression of Monocyte chemoattrac-tant protein 1 (MCP-1)and platelet-derived growth factor BB (PDGF-BB) were significantly increased in CAP (3.47 and 2.07 times) and CPPS (2.25 and 2.19 times) compared with healthy control group and were the final polymerization of inflammatory cytokines. The protein expression of interleukin 1 β (IL-1 β), MCP-1 and soluble tumor necrosis factor Ⅱ (s TNF R Ⅱ) in CAP group was increased more than 1.85,1.55,1.67 times compared with CPPS group. Conclusions Elevated expression of inflammatory cytokines may play an important role in the course of CAP/CPPS disease. The extent of the inflammatory response of CAP was higher than CPPS. The inflammatory factors of MCP-1 and PDGF-BB could serve as a novel diagnostic marker.

BACKGROUNDAirway hyperresponsiveness (AHR) is one of the most important characteristics of asthma. This study investigated the parameters, by which assess the airway responsiveness under tidal ventilation.

METHODSFemale BALB/c mice were sensitized and challenged with ovalbumin (OVA) (group A), and part of them were treated with budesonide aerosol (group B). All the mice were anaesthetized and mechanically ventilated. The values of tidal volume (Vt), airway pressure (PA), airway flow (F), expiratory lung resistance (RL) and dynamic compliance of the thorax and lung (CT-L) were recorded by the AniRes2003 animal lung function system. In addition, the expiratory volume in the first 0.1 second after the start of expiration (EV0.1) was obtained according to the flow-volume (F-V) curve. The maximal or minimal values of EV0.1, RL and CT-L were documented after each dose of methacholine (MCH) and compared with values from negative control group (group C).

RESULTS(1) When the dose of MCH reached 100 ng/g or 200 ng/g, the decrease of Vt in group A was much more significant than group C (P = 0.001, < 0.001 respectively), but not so between groups B and group C (P = 0.974, 0.362 respectively). (2) With the dose of 25, 50, 100 or 200 ng/g MCH, the decrease in percentage of EV0.1 in group A was much higher than group C (P = 0.012, 0.025, 0.001, 0.003 respectively), while that in group B showed no significant difference as compared with group C (P = 0.507, 0.896, 0.972, 0.785). (3) RL and CT-L: with the dose of 200 ng/g MCH, there was a statistically significant increase of RL in group A compared to group B or group C (P < 0.001, < 0.001 respectively), but no significant difference between groups B and C (P = 0.266). With doses of 100 ng/g and 200 ng/g MCH, there was a statistically significant decrease of CT-L in group A compared to group B (P = 0.001, = 0.001) and group C (P < 0.001, < 0.001 respectively), but no significant difference between groups B and C (P = 0.775, 0.310). (4) Histopathology: there were eosinophilic predominant peribronchial and perivascular inflammatory influx in murine lungs after OVA sensitizing and challenging, which could be counteracted by inhalation of budesonide in group B.

CONCLUSIONSThe decline in EV0.1 in response to MCH challenge correlated with simultaneous changes in Vt, RL and CT-L, but more sensitively than all the other parameters. The decline in EV0.1 and inflammation in murine lung could be significantly alleviated by inhalation of nebulized budesonide solution, which indicated that EV0.1 to MCH is a valid measure of AHR in mice.

Airway Resistance ; drug effects ; Animals ; Bronchial Hyperreactivity ; drug therapy ; Budesonide ; therapeutic use ; Female ; Lung Compliance ; drug effects ; Methacholine Chloride ; pharmacology ; Mice ; Mice, Inbred BALB C ; Ovalbumin ; immunology

Background Airway hyperresponsiveness (AHR) is one of the most important characteristics of asthma. This study investigated the parameters, by which assess the airway responsiveness under tidal ventilation.Methods Female BALB/c mice were sensitized and challenged with ovalbumin (OVA) (group A), and part of them were treated with budesonide aerosol (group B). All the mice were anaesthetized and mechanically ventilated. The values of tidal volume (Vt), airway pressure (PA), airway flow (F), expiratory lung resistance (RL) and dynamic compliance of the thorax and lung (CT-L) were recorded by the AniRes2003 animal lung function system. In addition, the expiratory volume in the first 0.1 second after the start of expiration (EV0.1) was obtained according to the flow-volume (F-V) curve. The maximal or minimal values of EV0.1, RL and CT-L were documented after each dose of methacholine (MCH) and compared with values from negative control group (group C).Results (1) When the dose of MCH reached 100 ng/g or 200 ng/g, the decrease of Vt in group A was much more significant than group C (P=0.001, <0.001 respectively), but not so between groups B and group C (P=0.974, 0.362 respectively). (2) With the dose of 25, 50, 100 or 200 ng/g MCH, the decrease in percentage of EV0.1 in group A was much higher than group C (P=0.012, 0.025, 0.001, 0.003 respectively), while that in group B showed no significant difference as compared with group C (P=0.507,0.896,0.972,0.785). (3) RL and CT-L: with the dose of 200 ng/g MCH, there was a statistically significant increase of RL in group A compared to group B or group C (P<0.001, < 0.001 respectively), but no significant difference between groups B and C (P=0.266). With doses of 100 ng/g and 200 ng/g MCH, there was a statistically significant decrease of CT-L in group A compared to group B (P=0.001,= 0.001) and group C (P<0.001,< 0.001 respectively), but no significant difference between groups B and C (P=0.775, 0.310). (4) Histopathology: there were eosinophilic predominant peribronchial and perivascular inflammatory influx in murine lungs after OVA sensitizing and challenging, which could be counteracted by inhalation of budesonide in group B.Conclusions The decline in EV0.1 in response to MCH challenge correlated with simultaneous changes in Vt, RL and CT-L, but more sensitively than all the other parameters. The decline in EV0.1 and inflammation in murine lung could be significantly alleviated by inhalation of nebulized budesonide solution, which indicated that EV0.1 to MCH is a valid measure of AHR in mice.

Bone Neoplasms/complications* ; Humans ; Osteosarcoma/complications* ; Pulmonary Embolism/etiology*