[Association between Severity of Scrub Typhus and Serum Procalcitonin Level].

Objective To explore the association between the severity of scrub typhus (ST) and the serum procalcitonin (PCT) level. Methods The clinical data of 58 ST patients who were treated in the First Affiliated Hospital of Xiamen University and confirmed by Xiamen Municipal Center for Disease Prevention and Control (CDC) from January 2016 to October 2017,were retrospectively analyzed. According to clinical manifestations and related laboratory tests,these patients were divided into four grades:Ⅰ,Ⅱ,Ⅲ,and Ⅳ. These four grade groups were compared in terms of age,interval from symptom onset to hospital presentation,hospitalization days,and serum PCT level. Results These 58 patients were divided into four grade groups:grade Ⅰ group (n=17),grade Ⅱ group (n=17),grade Ⅲ group (n=11),and grade Ⅳ group (n=13). No significant difference was found among these four groups in terms of age (F=0.618,P=0.606),interval from symptom onset to hospital presentation (F=1.744,P=0.169),and hospitalization days (F=0.398,P=0.755).However,the median serum PCT level in the grade Ⅳ patients[2.60(1.33,61.08)ng/ml] was significantly higher than those in grade I[0.24(0.10,0.33)ng/ml;Z=-4.63,P=0.000], grade Ⅱ[0.29(0.21,0.51)ng/ml;Z=-4.63,P=0.000], and grade Ⅲ[1.33(0.89,2.41)ng/ml;Z=-2.09,P=0.040].The median serum PCT level in the grade Ⅲ patients was also significantly higher than grade Ⅰ (Z=-4.16,P=0.000)and grade Ⅱ(Z=-3.83,P=0.000).There was no significant difference between the grade Ⅰ patients and grade Ⅱ patients(Z=-1.37,P=0.170).There was significantly positive correlation between PCT level and the severity of ST (r=0.804,P=0.000).Conclusion There is positive correlation between serum PCT level and the severity of ST,and serum PCT level may be a biomarker in assessing the severity of ST.

Interleukin-22 exacerbates airway inflammation induced by short-term exposure to cigarette smoke in mice.

AIM: Interleukin-22 (IL-22) exhibits both proinflammatory and anti-inflammatory properties in various biological processes. In this study we explored the effects of exogenous recombinant IL-22 (rIL-22) on cigarette smoke (CS)-induced airway inflammation in mice. METHODS: Male C57BL/6 mice were divided into groups: (1) CS group exposed to tobacco smoke for 3 consecutive days, (2) rIL-22 group received rIL-22 (100 mg/kg, ip), and (3) CS plus rIL-22 group, received rIL-22 (100 mg/kg, ip) before the CS exposure. The airway resistance (Rn), lung morphology, inflammatory cells in the airways, and inflammatory cytokines and CXCR3 ligands in both bronchoalveolar lavage (BAL) fluids and lung tissues were analyzed. RESULTS: CS alone significantly elevated IL-22 level in the BAL fluid. Both CS and rIL-22 significantly augmented airway resistance, an influx of inflammatory cells into the airways and lung parenchyma, and significantly elevated levels of pro-inflammatory cytokines (TGFß1 and IL-17A) and CXCR3 chemokines (particularly CXCL10) at the mRNA and/or protein levels. Furthermore, the effects of rIL-22 on airway resistance and inflammation were synergistic with those of CS, as demonstrated by a further increased Rn value, infiltration of greater numbers of inflammatory cells into the lung, higher levels of inflammatory cytokines and chemokines, and more severe pathological changes in CS plus rIL-22 group as compared to those in CS group. CONCLUSION: Exogenous rIL-22 exacerbates the airway inflammatory responses to CS exposure in part by inducing expression of several proinflammatory cytokines and CXCR3 ligands.

Differential expression of the inflammation-associated chemokines/cytokines in mouse lung after exposure to cigarette smoke and smoking cessation.

OBJECTIVE: To determine the changes in the airway inflammation-related cytokine/chemokine profiles after exposure to cigarette smoke (CS) and smoking cessation (SC). METHODS: A total of 18 male C57BL/6 mice were equally divided into three groups: CS group, SC group, and normal control group. The airway resistance, lung morphology, and collagen deposition around airways were determined. HE staining and Masson trichrome staining were used for histopathological analysis. The inflammatory cells in bronchoalveolar lavage fluid (BALF) were assessed. The inflammation-associated cytokines were determined using real-time PCR and immunohistochemistry. Expressions of CXCR3 ligands including the CXCL9, CXCL10, CXCL11 and other cytokines in lung tissue and BALF were also analyzed. RESULTS: The airway resistance significantly increased in both CS group and SC group when compared with the normal control group. Lung pathological scores in both CS group and SC group were also higher than that in the normal control group, while there was no significant difference between the CS group and SC group. Inflammatory cells including the neutrophils, macrophages, and lymphocytes also increased in both the CS group and SC group at both mRNA and protein levels. The mRNA levels of CXCL9, CXCL10, MMP9, and MMP12 were significantly higher in CS group and SC group than those in the normal control group (all P<0.05). The protein expression levels of CXCL9, CXCL10, CXCL11, MMP2, MMP9, MMP12, and TGF-Β1 were significantly higher in CS group and SC group than those in the normal control group (all P<0.05). Compared with the normal control group,the concentrations of CXCL9, CXCL10, CXCL11, IL-8, and TGF-Β1 in the BALF supernatants of the CS group and SC group significantly increased (P<0.05); in addition, the IL-6 and TNF-Α concentrations also increased in the CS group (both P<0.05). CONCLUSIONS: CS exposure triggers inflammatory cell flux and accumulation in the lung parenchyma and BALF. As a consequence, the inflammatory cytokines increase dramatically. After CS, the cytokines/chemokines can decrease, but is still higher than in non-smokers.

[Clinical evaluation of 136 inpatients with bronchiectasis in Peking Union Medical College Hospital].

OBJECTIVE: To summarize the clinical features of bronchiectasis. METHODS: We retrospectively analyzed the clinical data of 136 patients who had been admitted to Peking Union Medical College Hospital from January 2010 to December 2012 due to bronchiectasis, which was confirmed by high-resolution computed tomography. RESULTS: The average age of these 136 patients (61 men and 75 women) was (57.7±16.3) years. The average clinical history was (17.2±15.8) years. The exact etiology was unidentified in 77.2% (105/136) of the patients. The most commonly identified cause was previous infections (14.7%, 20/136), particularly tuberculosis. The main symptoms of bronchiectasis were cough and sputum production. The types of bronchiectasis were cylindrical in 37.7% (37/98), varicose in 40.8% (40/98), cystic in 21.4% (21/98) of these patients. Multilober involvement was most common (77.2%, 105/136). The most commonly involved lobes were left lower lobe (76.5%, 104/136). Of 77 patients who had undergone pulmonary function test, 47 (61.0%) showed obstructive. For each bronchiectasis type, the values (percentages of predicted) of forced expiratory volume in one second (FEV1) (P=0.918), forced vital capacity (FVC) (P=0.982), and FEV1/FVC (P=0.211) showed no statistical significance. The most commonly identified pathogen in sputum culture was Pseudomonas aeruginosa, which was sensitive to most broad-spectrum antibiotics. Current infections were most common in patients with cystic bronchiectasis, among whom rales were frequently heard. CONCLUSIONS: Most bronchiectasis patients are old women. The main etiology is previous infection, especially tuberculosis. The main symptom of bronchiectasis is productive cough. Many patients can have obstructive pulmonary function. The distribution of lesions is diffuse, and the lesions are often seen in both lungs, particularly in the left lower lobe. Cystic bronchiectasis may be a more severe type, and should be carefully managed once identified by radiology.