Pathogenesis Of Severe Pneumonia Research Articles

LncRNA RP11-773H22.4 is upregulated in severe pneumonia and may be a diagnostic and prognostic marker for severe pneumonia.

The incidence of pneumonia has become increasingly prevalent, and its severity has been continuously escalating, bringing significant damage and stress to people's lives. The regulatory role of RP11-773H22.4 in the onset and development of severe pneumonia is emerging as an important factor, however, the exact mechanisms controlling its effects have not been fully elucidated. ROC curve and Kaplan-Meier curve were employed to assess the diagnostic and prognostic significance of RP11-773H22.4 in severe pneumonia. qRT-PCR was employed to assess the RP11-773H22.4 and miR-1287-5p expression. The CCK-8 was employed to assess cell viability. The rate of apoptosis was measured utilizing flow cytometric. The concentration of inflammatory factors was detected by ELISA kit. The interaction between RP11-773H22.4 and miR-1287-5p was verified by dual luciferase reporter gene assay. In individuals afflicted with severe pneumonia, there was an observed up-regulation in RP11-773H22.4 expression and a corresponding decline in miR-1287-5p expression. RP11-773H22.4 demonstrated diagnostic and prognostic significance for severe pneumonia. RP11-773H22.4 augmented the viability of MRC-5 cells with LPS treatment by modulating miR-1287-5p, leading to a reduction in apoptosis and lower levels of inflammatory cytokines. RP11-773H22.4 was highly expressed in severe pneumonia and may serve as a diagnostic and prognostic marker for severe pneumonia. miR-1287-5p was downregulated in severe pneumonia, and RP11-773H22.4 participated in the pathogenesis of severe pneumonia by regulating the expression of miR-1287-5p.

维生素D调控T细胞在儿童重症肺炎发病中的作用研究进展

维生素D调控T细胞在儿童重症肺炎发病中的作用研究进展

Potential use of Citrus essential oils against acute respiratory syndrome caused by coronavirus

ABSTRACT The treatments being investigated for the pandemic associated with a severe acute respiratory syndrome caused by the new coronavirus (SARS-CoV2) aim to inhibit viral replication or inhibit enzymatic elastase in the lung, responsible for the SARS-CoV cell entry mechanism and the pathogenesis of severe pneumonia caused by infection. There is also a need to improve alveolar surfactant capacity and inhibition of the exacerbated inflammatory response. Current knowledge allows us to infer that Citrus essential oils could be considered an individual or a complementary highly valuable alternative for the viral infection caused by SARS-CoV due to its antiviral activity, particularly against coronavirus, anti-elastase, anti-inflammatory, antibacterial and antibiofilm properties. Furthermore, its proven capacity of biosurfactants, antioxidants, and pain inhibitors would help to treat acute respiratory syndrome. This review aims to encourage the development of more detailed studies on Citrus essential oils as a new multi-objective strategy to treat SARS-CoV2 infection. Abbreviations: SARS-CoV: Severe Acute Respiratory Syndrome Coronavirus; GRAS: Generally Recognized as Safe; TRP: Transient Receptor Proteins; HeLa-CEACAM1a: HeLa-epithelial carcinoembryonic antigen-related cell adhesion molecule 1a; HSV: Herpes Simplex Virus; FDA: Food and Drug Administration; ANMAT: National Administration of Medicines, Food and Medical Technology, Argentina; AFSSAPS: Agence Française de Sécurité Sanitaire des Produits de Santé, France; ACE2:Angiotensin-converting enzyme-2

Pathogenesis of severe pneumonia: advances and knowledge gaps.

Pneumonia is a common disease that becomes severe in a subset of patients, dependent on host biology including mechanisms of immune resistance and tissue resilience. This review emphasizes discoveries in pneumonia biology from 2016, highlighting questions and directions that are especially pressing or newly emerging. Novel cell-cell interactions mediating innate immune responses against microbes in the lung have been elucidated, between distinct leukocyte subtypes as well as between leukocytes and the structural cells of the lung. Adaptive immunity has received growing attention for determining the outcome of pneumonia, particularly the lung resident memory cells that arise from repeated prior respiratory infections and direct heterotypic recall responses. New tissue resilience components have been identified that contribute to anti-inflammatory, proresolution, tissue-protective, and reparative regeneration pathways in the infected lung. Recent findings will direct research into fundamental mechanisms of lung protection. Over the longer term, manipulating these pathways has implications for clinical practice, as strategies to bolster resistance and resilience have potential to ameliorate severe pneumonia.

CD4+ T cells promote the pathogenesis of Staphylococcus aureus pneumonia.

We postulated that the activation of proinflammatory signaling by methicillin-resistant Staphylococcus aureus (MRSA) strain USA300 is a major factor in the pathogenesis of severe pneumonia and a target for immunomodulation. Local activation of T cells in the lung was a conserved feature of multiple strains of S. aureus, in addition to USA300. The pattern of Vβ chain activation was consistent with known superantigens, but deletion of SelX or SEK and SEQ was not sufficient to prevent T-cell activation, indicating the participation of multiple genes. Using Rag2(-/-), Cd4(-/-), and Cd28(-/-) mice, we observed significantly improved clearance of MRSA from the airways and decreased lung pathology, compared with findings for wild-type controls. The improved outcome correlated with decreased production of proinflammatory cytokines (tumor necrosis factor, KC, interleukin 6, and interleukin 1β). Our data suggest that T-cell-mediated hypercytokinemia induced by infection with MRSA strain USA300 contributes to pathogenesis and may be a therapeutic target for improving outcomes of this common infection in a clinical setting.

Increased levels of cytokines and high-mobility group box 1 are associated with the development of severe pneumonia, but not acute encephalopathy, in 2009 H1N1 influenza-infected children

BackgroundThe 2009 A(H1N1) influenza virus has caused a large outbreak, and resulted in major complications of severe pneumonia and acute encephalopathy in the pediatric population in Japan. MethodsThis study examined six patients with acute encephalopathy, 34 patients with severe pneumonia, five patients with both pneumonia and encephalopathy, and 46 patients without severe complications. The concentrations of 27 cytokines were examined in the cerebrospinal fluid of patients with encephalopathy, and the levels of these cytokines, Cytochrome c, high-mobility group box 1 (HMGB1) were measured in the serum of all patients. ResultsPatients with severe pneumonia had higher serum concentrations of 16 cytokines, including Th1 cytokines, Th2 cytokines, chemokines, and growth factors, than patients with uncomplicated influenza. The distribution of 27 cytokines in the CSF did not parallel the serum levels in 11 patients with acute encephalopathy. HMGB1 concentrations in the serum were significantly higher in pneumonia patients with or without encephalopathy than in uncomplicated influenza patients, and were significantly associated with the upregulation of 10 cytokines. ConclusionsElevated levels of Th2 cytokines appear to be unique to influenza caused by 2009 H1N1 influenza virus and HMGB1 could play an important role in the pathogenesis of severe pneumonia. There appear to be different pathologic processes for encephalopathy and pneumonia.

Inflammatory profiles in severe pneumonia associated with the pandemic influenza A/H1N1 virus isolated in Mexico City

The immune mechanisms underlying the pathogenesis of severe pneumonia associated with the A/H1N1 virus are not well known. The objective of this study was to determine whether severe A/H1N1-associated pneumonia can be explained by the emergence of particular T-cell subsets and the cytokines/chemokines they produced, as well as distinct responses to infection. T-cell subset distribution and cytokine/chemokine levels in peripheral blood and bronchoalveolar lavage (BAL) were determined in patients with severe A/H1N1 infection, asymptomatic household contacts, and healthy controls. Cytokine and chemokine production was also evaluated after in vitro infection with seasonal H1N1 and pandemic A/H1N1 strains. We found an increase in the frequency of peripheral Th2 and Tc2 cells in A/H1N1 patients. A trend toward increased Tc1 cells was observed in household contacts. Elevated serum levels of IL-6, CXCL8, and CCL2 were found in patients and a similar cytokine/chemokine profile was observed in BAL, in which CCL5 was also increased. Infection assays revealed that both strains induce the production of several cytokines/chemokines at 24 and 72 h, however, IL-6, CCL3, and CXCL8 were strongly up-regulated in 72-h cultures in presence of the A/H1N1 virus. Several inflammatory mediators are up-regulated in peripheral and lung samples from A/H1N1-infected patients who developed severe pneumonia. In addition, the A/H1N1 strain induces higher levels of pro-inflammatory cytokines and chemokines than the seasonal H1N1 strain. These findings suggest that it is possible to identify biomarkers of severe pneumonia and also suggest the therapeutic use of immunomodulatory drugs in patients with severe pneumonia associated with A/H1N1 infection.

Plasma neutrophil elastase correlates with pulmonary vascular permeability: A prospective observational study in patients with pneumonia

Little is known about plasma neutrophil elastase (PNE) levels in patients with community-acquired pneumonia (CAP) requiring treatment in the intensive care unit (ICU) or high care unit (HCU). In addition, the influence of PNE on pulmonary vascular permeability in a clinical setting has not been investigated. The aims of this study were (i) to investigate PNE levels in patients with CAP and (ii) to explore the relationship between PNE and pulmonary vascular permeability. Fourteen consecutive CAP patients who were admitted to the HCU (n = 8) or ICU (n = 6) were prospectively investigated over a 6-month period. A group of eight patients with hydrostatic pulmonary oedema without CAP served as a control group (CG). PNE levels were measured at regular intervals. The pulmonary vascular permeability index (PVPI) was monitored in all ICU and CG patients, using the PiCCO system. PNE levels were higher in the CAP patients (132 (84-261) ng/mL) than in the CG patients (77 (64-107) ng/mL) (P = 0.04), and were highest in the ICU patients (186 (75-466) ng/mL). The PVPI was higher in the ICU patients (2.85 (1.90-4.00)) than in the CG patients (1.15 (0.75-2.35)) (P = 0.02). PNE levels correlated with PVPI in the ICU patients (r = 0.81, P < 0.001) but there was no correlation among the CG patients (r = 0.14, P = 0.73). Patients with severe CAP had high levels of PNE, which was closely correlated with PVPI. PNE may be involved in the pathogenesis of severe pneumonia.