病毒性肺炎常为吸入性感染,主要传染源是病人,通过飞沫和密切接触传染,可由上呼吸道病毒感染向下蔓延引起,也可继发于出疹性病毒感染,常伴气管-支气管感染.流行性感冒病毒是成年人和老人病毒性肺炎最为常见的病原,婴幼儿病毒性肺炎则常由呼吸道合胞病毒感染所致.其他如副流感病毒、巨细胞病毒、冠状病毒、腺病毒、鼻病毒和某些肠道病毒,如柯萨奇、埃可病毒等也可引起病毒性肺炎.在非细菌性肺炎中,病毒性肺炎占25%～50%,多发生于冬春季节,可散发或流行,多见于婴幼儿、老年人和原有慢性心肺疾病的病人.近年来由于免疫抑制药物广泛应用于器官移植病人,以及爱滋病发病人数的增多,病毒性肺炎的发病率逐渐增多,而SARS的流行使得病毒性肺炎显得尤为重要.一般的病毒性肺炎临床表现大多轻微,与支原体肺炎症状相似,病程1～2周.但重症肺炎可有持续高热、心悸、气急、呼吸困难、发绀,还可伴有休克和呼吸衰竭。

Viral pneumonia

Summary
Background: Respiratory syncytial virus (RSV) is a major public health burden worldwide. We aimed to review the current literature on the incidence and mortality of severe RSV in children globally. Methods: Systematic literature review and meta-analysis of published data from 2000 onwards, reporting on burden of acute respiratory infection (ARI) due to RSV in children. Main outcomes were hospitalization for severe RSV-ARI and death. Results: Five thousand two hundred and seventy-four references were identified. Fifty-five studies were included from 32 countries. The global RSV-ARI hospitalization estimates, reported per 1,000 children per year (95% Credible Interval (CrI), were 4.37 (2.98, 6.42) among children <5 years, 19.19 (15.04, 24.48) among children <1 year, 20.01 (9.65, 41.31) among children <6 months and 63.85 (37.52, 109.70) among premature children <1 year. The RSV-ARI global case-fatality estimates, reported per 1,000 children, (95% Crl) were 6.21 (2.64, 13.73) among children <5 years, 6.60 (1.85, 16.93) for children <1 year, and 1.04 (0.17, 12.06) among preterm children <1 year. Conclusions: A substantial proportion of RSV-associated morbidity occurs in the first year of life, especially in children born prematurely. These data affirm the importance of RSV disease in the causation of hospitalization and as a significant contributor to pediatric mortality and further demonstrate gestational age as a critical determinant of disease severity. An important limitation of case-fatality ratios is the absence of individual patient characteristics of non-surviving patients. Moreover, case-fatality ratios cannot be translated to population-based mortality. Pediatr Pulmonol. © 2016 The Authors. Pediatric Pulmonology Published by Wiley Periodicals, Inc.

https://onlinelibrary.wiley.com/doi/pdf/10.1002/ppul.23570

Respiratory syncytial virus hospitalization and mortality: Systematic review and meta-analysis

Background The ongoing COVID-19 pandemic is a global threat. Identification of markers for symptom onset and disease progression is a pressing issue. We described the clinical features of people infected on board the Diamond Princess cruise ship who were diagnosed with asymptomatic severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection or mild or severe COVID-19, on admission to the Self-Defense Forces Central Hospital (Tokyo, Japan) and at the end of observation. Methods This retrospective, single-centre study included participants with laboratory-detected SARS-CoV-2 infection who were admitted to the Self-Defense Forces Central Hospital from Feb 11 to Feb 25, 2020. Clinical records, laboratory data, and radiological findings were analysed. Clinical outcomes were followed up until discharge or Feb 26, 2020, whichever came first. We defined asymptomatic infection as SARS-CoV-2 infection with no history of clinical signs and symptoms, severe COVID-19 as clinical symptoms of pneumonia (dyspnoea, tachypnoea, peripheral capillary oxygen saturation Findings Among the 104 participants included in the final analysis, the median age was 68 years (IQR 47-75) and 54 (52%) were male. On admission, 43 (41%) participants were classified as asymptomatic, 41 (39%) as having mild COVID-10, and 20 (19%) as having severe COVID-19. At the end of observation, 33 (32%) participants were confirmed as being asymptomatic, 43 (41%) as having mild COVID-19, and 28 (27%) as having severe COVID-19. Serum lactate hydrogenase concentrations were significantly higher in the ten participants who were asymptomatic on admission but developed symptomatic COVID-19 compared with the 33 participants who remained asymptomatic throughout the observation period (five [50%] vs four [12%] participants; odds ratio 7·25, 95% CI 1·43-36·70; p=0·020). Compared with patients with mild disease at the end of observation, patients with severe COVID-19 were older (median age 73 years [IQR 55-77] vs 60 years [40-71]; p=0·028) and had more frequent consolidation on chest CT (13 [46%] of 28 vs nine [21%] of 43; p=0·035) and lymphopenia (16 [57%] vs ten [23%]; p=0·0055) on admission. Interpretation Older age, consolidation on chest CT images, and lymphopenia might be risk factors for disease progression of COVID-19 and contribute to improved clinical management. Funding None.

Clinical characteristics of COVID-19 in 104 people with SARS-CoV-2 infection on the Diamond Princess cruise ship: a retrospective analysis.

Macrophages are dynamic cells that play critical roles in the induction and resolution of sterile inflammation. In this review, we will compile and interpret recent findings on the plasticity of macrophages and how these cells contribute to the development of non-infectious inflammatory diseases, with a particular focus on allergic and autoimmune disorders. The critical roles of macrophages in the resolution of inflammation will then be examined, emphasizing the ability of macrophages to clear apoptotic immune cells. Rheumatoid arthritis (RA) is a chronic autoimmune-driven spectrum of diseases where persistent inflammation results in synovial hyperplasia and excessive immune cell accumulation, leading to remodeling and reduced function in affected joints. Macrophages are central to the pathophysiology of RA, driving episodic cycles of chronic inflammation and tissue destruction. RA patients have increased numbers of active M1 polarized pro-inflammatory macrophages and few or inactive M2 type cells. This imbalance in macrophage homeostasis is a main contributor to pro-inflammatory mediators in RA, resulting in continual activation of immune and stromal populations and accelerated tissue remodeling. Modulation of macrophage phenotype and function remains a key therapeutic goal for the treatment of this disease. Intriguingly, therapeutic intervention with glucocorticoids or other DMARDs promotes the re-polarization of M1 macrophages to an anti-inflammatory M2 phenotype; this reprogramming is dependent on metabolic changes to promote phenotypic switching. Allergic asthma is associated with Th2-polarised airway inflammation, structural remodeling of the large airways, and airway hyperresponsiveness. Macrophage polarization has a profound impact on asthma pathogenesis, as the response to allergen exposure is regulated by an intricate interplay between local immune factors including cytokines, chemokines and danger signals from neighboring cells. In the Th2-polarized environment characteristic of allergic asthma, high levels of IL-4 produced by locally infiltrating innate lymphoid cells and helper T cells promote the acquisition of an alternatively activated M2a phenotype in macrophages, with myriad effects on the local immune response and airway structure. Targeting regulators of macrophage plasticity is currently being pursued in the treatment of allergic asthma and other allergic diseases. Macrophages promote the re-balancing of pro-inflammatory responses towards pro-resolution responses and are thus central to the success of an inflammatory response. It has long been established that apoptosis supports monocyte and macrophage recruitment to sites of inflammation, facilitating subsequent corpse clearance. This drives resolution responses and mediates a phenotypic switch in the polarity of macrophages. However, the role of apoptotic cell-derived extracellular vesicles (ACdEV) in the recruitment and control of macrophage phenotype has received remarkably little attention. ACdEV are powerful mediators of intercellular communication, carrying a wealth of lipid and protein mediators that may modulate macrophage phenotype, including a cargo of active immune-modulating enzymes. The impact of such interactions may result in repair or disease in different contexts. In this review, we will discuss the origin, characterization, and activity of macrophages in sterile inflammatory diseases and the underlying mechanisms of macrophage polarization via ACdEV and apoptotic cell clearance, in order to provide new insights into therapeutic strategies that could exploit the capabilities of these agile and responsive cells.

/pdf/macrophages-the-good-the-bad-and-the-gluttony-16dga3zobo.pdf

Macrophages: the Good, the Bad, and the Gluttony

Community-acquired pneumonia (CAP) is the leading cause of mortality in children under 5 years of age globally. To improve the management of CAP, we must distinguish CAP from other common pediatric conditions and develop better diagnostic methods to detect the causative organism, so as to best direct appropriate resources in both industrialized and developing countries. Here, we review the diagnostic modalities available for identifying viruses and bacteria in the upper and lower respiratory tract of children, with a discussion of their utility and limitations in diagnosing CAP in children.

Community-Acquired Pneumonia in Children: the Challenges of Microbiological Diagnosis.

BACKGROUND: Corticosteroids have been used for refractory Mycoplasma pneumoniae pneumonia and have beneficial effects. The aim of this study was to identify the biomarkers for predicting refractory M. pneumoniae pneumonia in a timely fashion to initiate steroid therapy. METHODS: This was a prospective cohort study of children with M. pneumoniae pneumonia admitted to the Children9s Hospital of Fudan University from September 2012 to August 2013. Lactate dehydrogenase (LDH) and other laboratory tests, including complete blood counts, C-reactive protein, erythrocyte sedimentation rate (ESR), alanine aminotransferase, aspartate aminotransferase, α-hydroxybutyrate dehydrogenase (HBDH), creatine kinase, and creatine kinase MB, were performed on admission. Based on the definition of refractory M. pneumoniae pneumonia, subjects were divided into 2 groups: refractory M. pneumoniae pneumonia and usual M. pneumoniae pneumonia. The diagnostic values of laboratory findings were analyzed. RESULTS: In total, 653 subjects were enrolled, including 300 in the refractory pneumonia group and 353 in the usual pneumonia group. There was no significant difference in sex distribution between the 2 groups. The average age in the refractory M. pneumoniae pneumonia group was greater than that in the usual M. pneumoniae pneumonia group. Compared with the usual pneumonia group, the refractory pneumonia group showed significantly higher levels of C-reactive protein, serum LDH, serum HBDH, serum alanine aminotransferase, serum aspartate aminotransferase, and neutrophils and higher ESRs. Logistic regression showed that age, LDH, and ESR were the significant factors in predicting refractory M. pneumoniae pneumonia. In addition, LDH and HBDH were strongly correlated, and receiver operating characteristic curve analysis showed that the area under the curve of LDH was 0.718 with a cutoff of 379 IU/L, that of ESR was 0.683 with a cutoff of 32.5 IU/L, and that of HBDH was 0.691 with a cutoff of 259.5 IU/L. CONCLUSIONS: Serum LDH can be used as a biomarker to predict refractory M. pneumoniae pneumonia at the early stage of hospitalization.

http://rc.rcjournal.com/content/respcare/60/10/1469.full.pdf

Lactate Dehydrogenase as a Biomarker for Prediction of Refractory Mycoplasma pneumoniae Pneumonia in Children

Associations of short-term exposure to air pollution and emergency department visits for pediatric asthma in Shanghai, China

The role of eNOS in the migration and proliferation of bone-marrow derived endothelial progenitor cells and in vitro angiogenesis

Background Dysregulation of long noncoding RNAs (lncRNAs) is associated with a variety of human diseases; however, whether they have a role in childhood asthma is unknown. Objective We sought to determine the differential expression profiles of lncRNAs in PBMCs of children with asthma and the mechanisms underlying the effects of lncRNAs on the pathogenesis of asthma. Methods The differential expression profiles of lncRNAs were analyzed by transcriptome microarray. The effects and mechanisms by which lncRNAs influence macrophage activation were detected by real-time quantitative PCR, Western blot, RNase protection assay, and chromatin immunoprecipitation assay. The roles played by lncRNAs in asthma were tested in a cockroach allergen extract (CRE)-induced mouse model. Results We identified 719 lncRNAs that were differentially expressed in PBMCs of children with asthma, 502 of which were upregulated and 217 were downregulated. An lncRNA of unknown function, lnc-BAZ2B, was dominantly expressed in monocytes and significantly upregulated in children with asthma. lnc-BAZ2B promotes M2 macrophage activation by enhancing BAZ2B expression and exacerbated lung inflammation in an M2 macrophage–associated CRE-induced asthma model. Mechanistically, lnc-BAZ2B promoted the expression of its cis target gene BAZ2B by stabilizing its pre-mRNA. BAZ2B, a reader of H3K14ac modification, enhanced the transcription of IRF4 and promoted M2 macrophage activation. lnc-BAZ2B expression was correlated with that of BAZ2B in PBMCs from children with asthma. Baz2b knockdown could alleviate asthma severity in a CRE-induced asthma model. Conclusion lnc-BAZ2B promotes M2 macrophage activation and inflammation in children with asthma and may serve as a potential therapeutic and diagnostic target in children with asthma.

Liling Qian

Papers

Lactate Dehydrogenase as a Biomarker for Prediction of Refractory Mycoplasma pneumoniae Pneumonia in Children

Associations of short-term exposure to air pollution and emergency department visits for pediatric asthma in Shanghai, China

The role of eNOS in the migration and proliferation of bone-marrow derived endothelial progenitor cells and in vitro angiogenesis

lnc-BAZ2B promotes M2 macrophage activation and inflammation in children with asthma through stabilizing BAZ2B pre-mRNA

Clinical and Genetic Spectrum of Children with Primary Ciliary Dyskinesia in China.