A rare case of acute eosinophilic pneumonia induced by vaping-associated lung injury: a case report.

BACKGROUND: Acute eosinophilic pneumonia (AEP) is well-known as one of the primary eosinophilic pulmonary diseases of unknown etiology. It's defined as a febrile illness along with acute onset respiratory failure that is commonly misdiagnosed at the initial presentation as infectious pneumonia. Despite the fact that AEP sometimes classified as idiopathic as no exact cause can be identified in most cases, it has been suggested recently to be linked with electronic cigarette or vaping products and associated with electronic cigarette or vaping associated lung injury (EVALI). Therefore, history of recent tobacco smoking or vaping exposure along with peripheral eosinophilia are crucial clinical findings suggestive of AEP. CASE PRESENTATION: A previously healthy 17-year-old female presented to the Emergency Room with one day history of progressively worsening shortness of breath accompanied by left sided pleuritic chest pain and fever. She wasn't taking any medications, denied traditional cigarette smoking, exposure to pulmonary irritants, recent travel and had no history of close contact with sick patient. She recently started vaping 20 days prior to the presentation. Initially, she was admitted with a presumptive diagnosis of atypical pneumonia but was found to have AEP due to a recent vaping exposure. CONCLUSION: Vaping is a well-known health hazard that has become a growing trend among adolescents and have been promoted as a safe and effective alternative to traditional cigarettes. The etiology of AEP remains unclear, but many studies suggest a possible link with recent tobacco smoking or vaping. A key challenge for this clinical entity is to reach the diagnosis after excluding all other pulmonary eosinophilia causes, and it has an excellent prognosis if diagnosed early and treated appropriately.

Acute Eosinophilic Pneumonia after Combined Use of Conventional and Heat-Not-Burn Cigarettes: A Case Report.

Background: Acute eosinophilic pneumonia (AEP) is a rare acute respiratory disease accompanied by fever, shortness of breath, and cough. Although the pathogenesis of the disease is not yet established, the patient's condition improves with a rapid therapeutic response to systemic corticosteroids. Conventional cigarettes or heat-not-burn cigarettes are the most common cause of AEP among young people. Case Presentation: A 22-year-old woman with dyspnea, cough, and fever did not improve after visiting the local medical center and was admitted to the emergency room. The patient denied having any recent travel history or insect bites. She was treated with appropriate antibiotics according to the community acquired pneumonia, but there was no improvement. Chest radiography showed bilateral patches of pulmonary infiltration, and chest computed tomography revealed bilateral multifocal patchy consolidations with multiple small nodular ground-glass opacities and interlobular septal thickening. The bronchoalveolar lavage result was dominantly eosinophilic. The patient's condition improved rapidly after the use of intravenous methylprednisolone and then a change to oral methylprednisolone. Finally, the patient was hospitalized for 9 days, and the duration of use of methylprednisolone including outpatient visits was 14 days. Results: The early treatment of AEP yields a good prognosis, but since the symptoms of AEP are similar to those of infectious diseases such as community-acquired pneumonia, physicians should be meticulous in differentiating AEP from other diseases. Conclusions: Since AEP shows a good response to steroids, early detection using an appropriate diagnostic method is recommended. In addition, there should be strong education against smoking in any form.

Lung natural helper cells are a critical source of Th2 cell-type cytokines in protease allergen-induced airway inflammation.

Overproduction of cytokines by T helper 2 (Th2) cells in the lung is thought to be a cause of asthma. Here we report that innate lymphocytes termed lung natural helper (LNH) cells are a T cell-independent source of Th2 cell-type cytokines in protease allergen-treated lungs. LNH (Lin(-)Sca-1(+)c-kit(+/lo)CD25(+)CD127(+)) cells, when stimulated by IL-33 plus IL-2, IL-7, or thymic stroma lymphopoietin (TSLP), produced large amounts of IL-5 and IL-13. Intranasal administration of protease allergen papain induced eosinophil infiltration and mucus hyperproduction in the lung of wild-type and Rag1(-/-) mice, but not in Rag2(-/-)Il2rg(-/-) mice that lack LNH cells. LNH cell depletion inhibited papain-induced airway inflammation in Rag1(-/-) mice whereas adoptive transfer of LNH cells enabled Rag2(-/-)Il2rg(-/-) mice to respond to papain. Treatment of lung explants with papain induced IL-33 and TSLP production by stroma cells and IL-5 and IL-13 production by LNH cells. Thus, LNH cells are critical for protease allergen-induced airway inflammation.

Identification of Complex Pneumonia during the Outbreak of COVID-19: Bacterial Pneumonia Combined with Acute Eosinophilic Pneumonia in Patients with Maintenance Hemodialysis.

It is of crucial importance to diagnose patients in a timely and clear manner during the outbreak of COVID-19. Different causes of pneumonia makes it difficult to differentiate COVID-19 from others. Hemodialysis patients are a special group of people in this outbreak. We present a successfully treated case of a patient with maintenance hemodialysis from acute eosinophilic pneumonia for using meropenem when treating bacterial pneumonia, avoiding possible panic and waste of quarantine materials in dialysis centers.

Immune-Associated Proteins Are Enriched in Lung Tissue-Derived Extracellular Vesicles during Allergen-Induced Eosinophilic Airway Inflammation.

Studying the proteomes of tissue-derived extracellular vesicles (EVs) can lead to the identification of biomarkers of disease and can provide a better understanding of cell-to-cell communication in both healthy and diseased tissue. The aim of this study was to apply our previously established tissue-derived EV isolation protocol to mouse lungs in order to determine the changes in the proteomes of lung tissue-derived EVs during allergen-induced eosinophilic airway inflammation. A mouse model for allergic airway inflammation was used by sensitizing the mice intraperitoneal with ovalbumin (OVA), and one week after the final sensitization, the mice were challenged intranasal with OVA or PBS. The animals were sacrificed 24 h after the final challenge, and their lungs were removed and sliced into smaller pieces that were incubated in culture media with DNase I and Collagenase D for 30 min at 37 °C. Vesicles were isolated from the medium by ultracentrifugation and bottom-loaded iodixanol density cushions, and the proteomes were determined using quantitative mass spectrometry. More EVs were present in the lungs of the OVA-challenged mice compared to the PBS-challenged control mice. In total, 4510 proteins were quantified in all samples. Among them, over 1000 proteins were significantly altered (fold change >2), with 614 proteins being increased and 425 proteins being decreased in the EVs from OVA-challenged mice compared to EVs from PBS-challenged animals. The associated cellular components and biological processes were analyzed for the altered EV proteins, and the proteins enriched during allergen-induced airway inflammation were mainly associated with gene ontology (GO) terms related to immune responses. In conclusion, EVs can be isolated from mouse lung tissue, and the EVs' proteomes undergo changes in response to allergen-induced airway inflammation. This suggests that the composition of lung-derived EVs is altered in diseases associated with inflammation of the lung, which may have implications in type-2 driven eosinophilic asthma pathogenesis.

Eosinophils, basophils and type 2 immune microenvironments in COPD-affected lung tissue.

Although elevated blood or sputum eosinophils are present in many patients with COPD, uncertainties remain regarding the anatomical distribution pattern of lung-infiltrating eosinophils. Basophils have remained virtually unexplored in COPD. This study mapped tissue-infiltrating eosinophils, basophils and eosinophil-promoting immune mechanisms in COPD-affected lungs.Surgical lung tissue and biopsies from major anatomical compartments were obtained from COPD patients with severity grades Global Initiative for Chronic Obstructive Lung Disease stages I-IV; never-smokers/smokers served as controls. Automated immunohistochemistry and in situ hybridisation identified immune cells, the type 2 immunity marker GATA3 and eotaxins (CCL11, CCL24).Eosinophils and basophils were present in all anatomical compartments of COPD-affected lungs and increased significantly in very severe COPD. The eosinophilia was strikingly patchy, and focal eosinophil-rich microenvironments were spatially linked with GATA3+ cells, including type 2 helper T-cell lymphocytes and type 2 innate lymphoid cells. A similarly localised and interleukin-33/ST2-dependent eosinophilia was demonstrated in influenza-infected mice. Both mice and patients displayed spatially confined eotaxin signatures with CCL11+ fibroblasts and CCL24+ macrophages.In addition to identifying tissue basophilia as a novel feature of advanced COPD, the identification of spatially confined eosinophil-rich type 2 microenvironments represents a novel type of heterogeneity in the immunopathology of COPD that is likely to have implications for personalised treatment.

[Acute Eosinophilic Pneumonia (AEP) after Hookah Smoking]. / Akute eosinophile Pneumonie (AEP) nach Shisha-Rauchen.

A 27-year-old, previously physically healthy man presented to an emergency department with an acute onset of thoracic pain, dyspnea, non-productive cough and fever. Hours before the onset of symptoms, the patient has smoked tobacco using a waterpipe (spearmint taste, not commercially available in Germany). Due to a progressive respiratory failure the patient required invasive mechanical ventilation. The computertomography scan of the chest showed bilateral diffuse, infiltrative changes. The diagnosis of hookah smoking associated Acute Eosinophilic Pneumonia (AEP) was based on the patient's history, the eosinophilic count in broncho-alveolar lavage and the computertomographic findings. After treatment with corticosteroids, the patient could be extubated after 9 days. The outpatient follow-up revealed a normal lung function testing and X-ray of the chest without any physical sequelae. CONCLUSION: In cases of acute onset of thoracic pain, dyspnea, non-productive cough and fever, acute eosinophilic pneumonia should be considered for differential diagnosis in association with shisha smoking. Severe respiratory lung failure can be successfully treated with corticosteroid therapy and ventilation resulting in full recovery.

The Innate Immune Protein S100A9 Protects from T-Helper Cell Type 2-mediated Allergic Airway Inflammation.

Calprotectin is a heterodimer of the proteins S100A8 and S100A9, and it is an abundant innate immune protein associated with inflammation. In humans, calprotectin transcription and protein abundance are associated with asthma and disease severity. However, mechanistic studies in experimental asthma models have been inconclusive, identifying both protective and pathogenic effects of calprotectin. To clarify the role of calprotectin in asthma, calprotectin-deficient S100A9-/- and wild-type (WT) C57BL/6 mice were compared in a murine model of allergic airway inflammation. Mice were intranasally challenged with extracts of the clinically relevant allergen, Alternaria alternata (Alt Ext), or PBS every third day over 9 days. On Day 10, BAL fluid and lung tissue homogenates were harvested and allergic airway inflammation was assessed. Alt Ext challenge induced release of S100A8/S100A9 to the alveolar space and increased protein expression in the alveolar epithelium of WT mice. Compared with WT mice, S100A9-/- mice displayed significantly enhanced allergic airway inflammation, including production of IL-13, CCL11, CCL24, serum IgE, eosinophil recruitment, and airway resistance and elastance. In response to Alt Ext, S100A9-/- mice accumulated significantly more IL-13+IL-5+CD4+ T-helper type 2 cells. S100A9-/- mice also accumulated a significantly lower proportion of CD4+ T regulatory (Treg) cells in the lung that had significantly lower expression of CD25. Calprotectin enhanced WT Treg cell suppressive activity in vitro. Therefore, this study identifies a role for the innate immune protein, S100A9, in protection from CD4+ T-helper type 2 cell hyperinflammation in response to Alt Ext. This protection is mediated, at least in part, by CD4+ Treg cell function.

Elevated Periostin Concentrations in the Bronchoalveolar Lavage Fluid of Patients with Eosinophilic Pneumonia.

BACKGROUND: Eosinophilic pneumonia (EP) is characterized by massive pulmonary infiltration by eosinophils. Although serum periostin is a novel marker for eosinophil-dominant asthma, the upregulation of periostin in the airway of asthmatics is controversial. In this study, we examined whether periostin concentrations are elevated in the bronchoalveolar lavage fluid (BALF) of patients with EP. METHODS: BAL was performed in healthy volunteers and in patients with acute eosinophilic pneumonia (AEP), chronic eosinophilic pneumonia (CEP), and sarcoidosis. The periostin concentrations in the BALF were measured. RESULTS: The periostin concentration in the BALF increased significantly with pulmonary eosinophil ia and was higher in AEP and CEP patients than in healthy volunteers and sarcoidosis patients, even after adjusting the albumin concentration. In pulmonary eosinophilia, the periostin concentration correlated with the eosinophil and lymphocyte counts, the concentration of albumin, and the concentration of cytokines such as IL-5, IL-13, and transforming growth factor ß1. CONCLUSIONS: Although some blood leakage may be involved in the elevation of periostin in the BALF of EP, periostin can be induced locally, at least in part. Therefore, periostin may play a role in the development of EP.

Lung-Infiltrating Foxp3+ Regulatory T Cells Are Quantitatively and Qualitatively Different during Eosinophilic and Neutrophilic Allergic Airway Inflammation but Essential To Control the Inflammation.

Understanding functions of Foxp3+ regulatory T cells (Tregs) during allergic airway inflammation remains incomplete. In this study, we report that, during cockroach Ag-induced allergic airway inflammation, Foxp3+ Tregs are rapidly mobilized into the inflamed lung tissues. However, the level of Treg accumulation in the lung was different depending on the type of inflammation. During eosinophilic airway inflammation, ∼30% of lung-infiltrating CD4 T cells express Foxp3, indicative of Tregs. On the contrary, only ∼10% of infiltrating CD4 T cells express Foxp3 during neutrophilic airway inflammation. Despite the different accumulation, the lung inflammation and inflammatory T cell responses were aggravated following Treg depletion, regardless of the type of inflammation, suggesting regulatory roles for Tregs. Interestingly, however, the extent to which inflammatory responses are aggravated by Treg depletion was significantly greater during eosinophilic airway inflammation. Indeed, lung-infiltrating Tregs exhibit phenotypic and functional features associated with potent suppression. Our results demonstrate that Tregs are essential regulators of inflammation, regardless of the type of inflammation, although the mechanisms used by Tregs to control inflammation may be shaped by environmental cues available to them.

A tricky and rare cause of pulmonary eosinophilia: myeloid/lymphoid neoplasm with eosinophilia and rearrangement of PDGFRA.

BACKGROUND: Eosinophilic lung diseases represent a heterogeneous group of disorders with prominent infiltrate of eosinophils in lung interstitium and alveolar spaces. Peripheral blood eosinophilia is often present. Infections, drugs, allergens, toxic agents have to be evaluated as possible causes of eosinophilic lung infiltrates. The category of myeloid/lymphoid neoplasms with eosinophilia and rearrangement of PDGFRA, PDGFRB, FGFR1 and PCM1-JAK2 represents an uncommon cause of eosinophilic lung infiltrate. CASE PRESENTATION: We report the case of a 70-year old man complaining of dry cough and dyspnea. Ground glass-opacities were seen on imaging studies and peripheral blood eosinophilia was present. A thorough step-wise patient's evaluation led to identify the clonal nature of eosinophilia and the diagnosis of myeloid/lymphoid neoplasm with eosinophilia and rearrangement of PDGFRA was made. CONCLUSIONS: Correlation with clinical history, laboratory tests and imaging studies is essential to achieve the correct diagnosis when facing with eosinophilic lung infiltrates. A prolonged eosinophilia can cause life-threatening organ damage. Identification of PDGFRA rearrangement, as in the present case, is particularly critical given the sensitivity and excellent response to imatinib, which has completely changed the natural history of this neoplasm.

Acute eosinophilic pneumonia triggered by secondhand cigarette smoke exposure in an elderly man.

The spectrum of eosinophilic lung diseases comprises a diverse group of pulmonary disorders associated with tissue or peripheral eosinophilia. [Acute eosinophilic pneumonia (AEP)] is an uncommon eosinophilic lung disease that can be idiopathic, but identifiable causes include medications, inhalational exposures and infections. Most cases in the literature are associated with first-time cigarette smoking or resuming smoking. Herein, we present a case of AEP in an elderly man triggered by exposure to secondhand tobacco smoke, in whom a transbronchial biopsy was diagnostic. The patient recovered fully with glucocorticoid therapy without recurrence after avoiding further secondhand smoke.

Eosinophilic pneumonia: A review of the previous literature, causes, diagnosis, and management.

Eosinophilic pneumonia (EP) is a rare disorder, comprising several heterogeneous diseases. Two major types of EP are acute eosinophilic pneumonia (AEP) and chronic eosinophilic pneumonia (CEP), both of which are characterized by marked accumulation of eosinophils in lung tissues and/or BAL fluid. AEP and CEP share some similarities in terms of pathophysiology, radiological findings, and treatment response to corticosteroids. However, they distinctly differ in etiology, clinical manifestations, and the nature of disease course. Especially, although AEP and CEP respond well to corticosteroids, relapse frequently occurs in patients with CEP, but rarely in those with AEP. Although CEP occasionally persists and becomes corticosteroid dependent, most patients with AEP completely recover. This article reviews previous studies and discusses the etiology, clinical manifestations, and treatment of AEP and CEP.

Lung eosinophilia induced by house dust mites or ovalbumin is modulated by nicotinic receptor α7 and inhibited by cigarette smoke.

Eosinophilia (EOS) is an important component of airway inflammation and hyperresponsiveness in allergic reactions including those leading to asthma. Although cigarette smoking (CS) is a significant contributor to long-term adverse outcomes in these lung disorders, there are also the curious reports of its ability to produce acute suppression of inflammatory responses including EOS through poorly understood mechanisms. One possibility is that proinflammatory processes are suppressed by nicotine in CS acting through nicotinic receptor α7 (α7). Here we addressed the role of α7 in modulating EOS with two mouse models of an allergic response: house dust mites (HDM; Dermatophagoides sp.) and ovalbumin (OVA). The influence of α7 on EOS was experimentally resolved in wild-type mice or in mice in which a point mutation of the α7 receptor (α7E260A:G) selectively restricts normal signaling of cellular responses. RNA analysis of alveolar macrophages and the distal lung epithelium indicates that normal α7 function robustly impacts gene expression in the epithelium to HDM and OVA but to different degrees. Notable was allergen-specific α7 modulation of Ccl11 and Ccl24 (eotaxins) expression, which was enhanced in HDM but suppressed in OVA EOS. CS suppressed EOS induced by both OVA and HDM, as well as the inflammatory genes involved, regardless of α7 genotype. These results suggest that EOS in response to HDM or OVA is through signaling pathways that are modulated in a cell-specific manner by α7 and are distinct from CS suppression.

IL-37 inhibits IL-4/IL-13-induced CCL11 production and lung eosinophilia in murine allergic asthma.

BACKGROUND: IL-37 is emerging as an anti-inflammatory cytokine, particularly in innate inflammation. However, the role of IL-37 in Th2-mediated allergic lung inflammation remains uncertain. We sought to determine the role and the underlying mechanisms of IL-37 in the development of house dust mites (HDM)-induced murine asthma model. METHODS: We examined the effect of IL-37 administration during the sensitization or challenge phase on Th2-mediated allergic asthma induced by inhaled HDM. Cellular source of CCL11 and distribution of IL-37 receptors, IL-18Rα and IL-1R8, were determined in HDM-exposed lungs. Finally, we examined the effect of IL-37 on CCL11 production and STAT6 activation in different primary lung structural cell types upon IL-4/IL-13 stimulation. RESULTS: IL-37 had no effect on HDM sensitization, but when administrated during the challenge phase, significantly attenuated pulmonary eosinophilia, CCL11 production, and airway hyper-reactivity (AHR). Interestingly, IL-37 treatment had no significant effects on lung infiltrating T cells and Th2 cytokine production. Intranasal co-administration of CCL11 reversed the inhibiting effect of IL-37 on HDM-induced pulmonary eosinophilia and AHR. Furthermore, we demonstrated that CCL11 was primarily expressed by fibroblasts and airway smooth muscle cells (AMSC), while IL-37 receptors by tracheobronchial epithelial cells (TEC). In vitro study showed that IL-37 inhibited IL-4/IL-13-induced STAT6 activation and CCL11 production by fibroblasts and AMSC, which was dependent on its direct action on TEC. Moreover, cell contact was required for the inhibitory effect of IL-37-treated TEC. CONCLUSIONS: IL-37 attenuates HDM-induced asthma, possibly by inhibiting IL-4/IL-13-induced CCL11 production by fibroblasts and AMSC via its direct act on TEC.

The Rare Complication and Diagnostic Challenges of Pulmonary Eosinophilia in Graft versus Host Disease Patients after Hematopoietic Stem Cell Transplantation.

PURPOSE: Chronic graft versus host disease (cGvHD) is a common complication of hematopoietic stem cell transplantation (HSCT). Eosinophilic lung disease is a rare poorly understood complication in HSCT patients with cGvHD. These patients present similarly to those with Acute Eosinophilic Pneumonia (AEP). The purpose of this study is to better elucidate the presentation and potential treatment of this phenomenon. METHODS: We reviewed over 170 bronchoscopies in post-HSCT patients with respiratory symptoms. Of these, four patients, whose course was complicated by cGvHD, presented with respiratory symptoms, diffuse ground-glass opacities (GGO) on chest computerized tomography (CT), bronchoalveolar lavage (BAL) eosinophilia, and no evidence of infection. The clinical course of these patients was reviewed. RESULTS: Despite clinical presentation similar to AEP, not all patients had > 25% eosinophils on BAL, one criterion for AEP, however all improved with steroids. Steroid initiation was often delayed in favor of empiric antibiotics despite negative infectious workup. Several patients had recurrent episodes. Regarding possible associations, we examined but found no link between particular demographics, reason for HSCT, chemotherapy, immunosuppressants, or peripheral eosinophil count and pulmonary eosinophilia in these patients. GGO present on initial CT imaging became chronic in several of these patients. CONCLUSION: We propose that in post-HSCT patients with GvHD presenting with respiratory symptoms, GGO on CT, BAL eosinophilia of > 10%, and negative respiratory cultures, an autoimmune eosinophilic process may be occurring. Earlier recognition and initiation of corticosteroids in these patients may improve their outcomes as an autoimmune diagnosis was often delayed in favor of antibiotics.

How to manage lung infiltrates in adults suffering from haematological malignancies outside allogeneic haematopoietic stem cell transplantation.

Pulmonary complications affect up to 40% of patients with severe neutropenia lasting for more than 10 d. As they are frequently associated with fever and elevation of C-reactive protein or other signs of inflammation, they are mostly handled as pneumonia. However, the differential diagnosis is broad, and a causative microbial agent remains undetected in the majority of cases. Pulmonary side effects from cytotoxic treatment or pulmonary involvement by the underlying malignancy must always be taken into account and may provide grounds for invasive diagnostic procedures in selected patients. Pneumocystis jirovecii (in patients not receiving co-trimoxazole as prophylaxis), multi-resistant gram-negative bacilli, mycobacteria or respiratory viruses may be involved. High-risk patients may be infected by filamentous fungi, such as Aspergillus spp., but these infections are seldom proven when treatment is initiated. Microorganisms isolated from cultures of blood, bronchoalveolar lavage or respiratory secretions need careful interpretation as they may be irrelevant for determining the aetiology of pulmonary infiltrates, particularly when cultures yield coagulase-negative staphylococci, enterococci or Candida species. Non-culture based diagnostics for detecting Aspergillus galactomannan, beta-D-glucan or DNA from blood, bronchoalveolar lavage or tissue samples can facilitate the diagnosis, but must always be interpreted in the context of clinical and imaging findings. Systemic antifungal treatment with mould-active agents, given in combination with broad-spectrum antibiotics, improves clinical outcome when given pre-emptively. Co-trimoxazole remains the first-line treatment for Pneumocystis pneumonia, while cytomegalovirus pneumonia will respond to ganciclovir or foscarnet in most cases. The clinical outcome of acute respiratory failure can also be successful with proper intensive care, when indicated.

Early diagnosis based on clinical history and BALF for successful management of smoking-induced acute eosinophilic pneumonia without unnecessary antibiotic usage: a case report.

INTRODUCTION: Acute eosinophilic pneumonia (AEP) is a rapid onset and severe respiratory illness characterized by acute febrile respiratory insufficiency, eosinophilic infiltration in the lungs and unique findings on chest imaging. Difficulty in differentiating from other respiratory distress caused by community-acquired pneumonia may result in a delayed diagnosis or treatment with empirical antibiotics. CASE STUDY: Sixteen-year-old boy who developed AEP with marked eosinophilia in bronchoalveolar lavage fluid (BALF, 36.6%), decreased diffusion capacity of the lung for carbon monoxide (62%) and unique radiological findings. Although he initially denied tobacco use, on repeated thorough clinical history questioning, he eventually admitted beginning smoking 19 days before the onset of symptoms with gradually increasing frequency. RESULTS: His symptoms resolved quickly without use of antibiotics after cessation of tobacco and treatment with corticosteroids. CONCLUSION: Careful clinical history taking regarding tobacco use combined with early examination of BALF and recognition of unique radiological findings are critical for proper management of AEP.

Differences in allergic inflammatory responses in murine lungs: comparison of PM2.5 and coarse PM collected during the hazy events in a Chinese city.

Urban particulate matter (PM) is associated with an increase in asthma. PM2.5 (

Periostin levels and eosinophilic inflammation in poorly-controlled asthma.

BACKGROUND: Periostin levels are associated with airway eosinophilia and are suppressed by corticosteroid treatment in asthma. This study sought to determine the relationship between serum and sputum periostin, airway inflammatory phenotype and asthma control. METHODS: Adults with poorly-controlled asthma (n = 83) underwent a clinical assessment, sputum induction and blood sampling. Dispersed sputum was used for a differential cell count and periostin assessment (ELISA). Serum periostin was determined by the Elecsys® immunoassay. RESULTS: Periostin levels were significantly higher in serum (median (IQR) of 51.6 (41.8, 62.6) ng/mL) than in sputum (1.1 (0.5, 2.0) ng/mL) (p < 0.001). Serum and sputum periostin were significantly higher in patients with eosinophilic asthma (n = 37) compared with non-eosinophilic asthma. Both serum and sputum periostin levels were significantly associated with proportion of sputum eosinophils (r = 0.422, p < 0.001 and r = 0.364, p = 0.005 respectively) but were not associated with asthma control. In receiver operator characteristic curve analysis, the area under the curve (AUC) for serum periostin (n = 83) was 0.679, p = 0.007. Peripheral blood eosinophils assessed in 67 matched samples, had a numerically greater AUC of 0.820 compared with serum periostin, p = 0.086 for the detection of eosinophilic asthma. CONCLUSION: In poorly-controlled asthma, sputum and serum periostin levels are significantly related to sputum eosinophil proportions while their ability to predict the presence of eosinophilic asthma is modest.