H the number of leukocytes in the NE and MC was greater than that in the EO and PA groups. InClinical characteristics in different groups of AECOPD patientsThe results of clinical assessments in these four groups of AECOPD patients are summarised in Table 2. There were no significant difference in age and FEV1/FVC ( ) among these groups of patients (Age: F = 0.54, P = 0.657; FEV1/FVC ( ): F = 0.303, P = 0.823). The MC, NE, and EO groups of patients had significantly lower predicted FEV1 than PA (P,0.05), and the MC group of patients had significantly lower values of the post-FEV1 than those in the NE and PA groups (P,0.05). There was significant difference in the values of BODE scores and GOLD stages among these groups of patients. The EO, NE, and MC groups of patients had significantly higher BODE scores than that of the PA group of patients. The MC group of patients had the highest GOLD stages, followed by the EO, NE, and PA groups of patients. The NE and MC groups of patients produced more amounts of sputum than those in the EO and PA groups. Consistently, microbiological analysis indicated that 19 and 43 of AECOPD patients had evidence of virus and bacterial infection,Sputum Cellular Phenotypes in AECOPDcontrast, the number of eosinophils in the EO and MC groups was greater than that in the NE and PA groups of patients and there was no significant difference in the number of blood neutrophils among the different groups of patients. Similarly, the NE and MC groups of patients had significantly greater numbers of inflammatory infiltrates and neutrophils in the sputum samples, while the EO and MC groups of patients had significantly greater numbers of eosinophils in the sputum samples. Finally, significantly higher concentrations of sputum CRP, MMP-9, and IL-6 and serum CRP, IL-6, and SAA were detected in the NE and MC groups of patients, as FD&C Yellow 5 custom synthesis compared with that in the EO and PA groups of patients (Table 5). Apparently, the NE and MC groups of patients with stable COPD still had higher degrees of inflammation.DiscussionIn this study, we found that 61 of AECOPD patients not only had impairment of lung function, but also had varying levels of airway inflammation, accompanied by various types of inflammatory infiltrates in their lungs. These data are consistent with CB5083 web previous 23148522 observations [2,3] and support the notion that any reason-mediated local inflammation can trigger the development of AECOPD in COPD patients [1]. Interestingly, 39 of AECOPD patients (termed a paucigranulocytic pattern) had their airway inflammatory infiltrates similar to that in the healthy controls, but they had significantly higher levels of sputum IL-6 and MMP-9 and serum CPR and SAA. These observations suggest that inflammation in the non-lung organs may cause airway responses that promote higher levels of inflammatory mediators in the lungs, leading to the development of AECOPD. Indeed, these patients had shorter recovery time and hospital stay, implicating that these patients responded well to the standard therapies. Although the precise factors that trigger the development of AECOPD remain to be investigated, these patients may only require standard therapies. Characterisation of sputum 1676428 inflammatory cells in majority of AECOPD patients revealed that sputum inflammatory cells were comprised predominantly of neutrophils, eosinophils, and macrophages in the lungs. Further stratification of patients, according to the predominant types of inflammatory infiltrate.H the number of leukocytes in the NE and MC was greater than that in the EO and PA groups. InClinical characteristics in different groups of AECOPD patientsThe results of clinical assessments in these four groups of AECOPD patients are summarised in Table 2. There were no significant difference in age and FEV1/FVC ( ) among these groups of patients (Age: F = 0.54, P = 0.657; FEV1/FVC ( ): F = 0.303, P = 0.823). The MC, NE, and EO groups of patients had significantly lower predicted FEV1 than PA (P,0.05), and the MC group of patients had significantly lower values of the post-FEV1 than those in the NE and PA groups (P,0.05). There was significant difference in the values of BODE scores and GOLD stages among these groups of patients. The EO, NE, and MC groups of patients had significantly higher BODE scores than that of the PA group of patients. The MC group of patients had the highest GOLD stages, followed by the EO, NE, and PA groups of patients. The NE and MC groups of patients produced more amounts of sputum than those in the EO and PA groups. Consistently, microbiological analysis indicated that 19 and 43 of AECOPD patients had evidence of virus and bacterial infection,Sputum Cellular Phenotypes in AECOPDcontrast, the number of eosinophils in the EO and MC groups was greater than that in the NE and PA groups of patients and there was no significant difference in the number of blood neutrophils among the different groups of patients. Similarly, the NE and MC groups of patients had significantly greater numbers of inflammatory infiltrates and neutrophils in the sputum samples, while the EO and MC groups of patients had significantly greater numbers of eosinophils in the sputum samples. Finally, significantly higher concentrations of sputum CRP, MMP-9, and IL-6 and serum CRP, IL-6, and SAA were detected in the NE and MC groups of patients, as compared with that in the EO and PA groups of patients (Table 5). Apparently, the NE and MC groups of patients with stable COPD still had higher degrees of inflammation.DiscussionIn this study, we found that 61 of AECOPD patients not only had impairment of lung function, but also had varying levels of airway inflammation, accompanied by various types of inflammatory infiltrates in their lungs. These data are consistent with previous 23148522 observations [2,3] and support the notion that any reason-mediated local inflammation can trigger the development of AECOPD in COPD patients [1]. Interestingly, 39 of AECOPD patients (termed a paucigranulocytic pattern) had their airway inflammatory infiltrates similar to that in the healthy controls, but they had significantly higher levels of sputum IL-6 and MMP-9 and serum CPR and SAA. These observations suggest that inflammation in the non-lung organs may cause airway responses that promote higher levels of inflammatory mediators in the lungs, leading to the development of AECOPD. Indeed, these patients had shorter recovery time and hospital stay, implicating that these patients responded well to the standard therapies. Although the precise factors that trigger the development of AECOPD remain to be investigated, these patients may only require standard therapies. Characterisation of sputum 1676428 inflammatory cells in majority of AECOPD patients revealed that sputum inflammatory cells were comprised predominantly of neutrophils, eosinophils, and macrophages in the lungs. Further stratification of patients, according to the predominant types of inflammatory infiltrate.
