Chronic hypersensitivity pneumonitis caused by Aspergillus complicated with pulmonary aspergilloma

A 57-year-old man consulted our hospital with a history of the gradual onset of dyspnea and a productive cough. Chest computed tomographic (CT) scans showed a nodular shadow in a cavity lesion, and reticulonodular, cystic, and ground-grass opacities in the bilateral lung fields with honeycombing. He was diagnosed as having pulmonary aspergilloma and idiopathic pulmonary fibrosis (IPF). As an outpatient, he suffered from dyspnea upon physical exertion with exacerbation of the high-resolution CT (HRCT) opacities. An inhalation provocation test for Aspergillosis fumigatus was positive and chronic hypersensitivity pneumonitis (CHP) caused by Aspergillus was finally diagnosed. Insidious CHP is sometimes misdiagnosed as IPF. The diagnosis of insidious CHP should be made on the basis of a detailed history, specific HRCT findings, and lymphocyte-dominant bronchoalveolar lavage fluid cell findings.     

Polymorphonuclear Leukocytes Released from the Bone Marrow Preferentially Sequester in Lung Microvessels

Objective : A hallmark of the systemic response to an inflammatory stimulus is the release of polymorphonuclear leukocytes (PMNs) from the bone marrow. This study was designed to measure the release of PMNs from the bone marrow and to determine their sequestration in the lung after an intravenous injection of either endotoxin (n = 5) or saline (n = 5). Methods and Results : The thymidine analogue 5′-bromo-2-deoxyuridine (BrdU) was used to pulse label dividing PMNs in the bone marrow of rabbits (n = 13), and immunohistochemistry and morphometry were used to detect the release of BrdU-labeled PMNs into the circulation and to determine their sequestration in the lung. Endotoxin treatment caused a drop in the circulating PMN counts (3.3 ± 0.08 at baseline to 0.12 ± 0.02 × 10⁹/L at 1 hour after endotoxin), which was followed by a neutrophilia at 8 hours (6.3 ± 1.1 × 10⁹/L, p < 0.01), an increase in circulating band cells (0.12 ± 0.01 at baseline to 2.18 ± 0.4 × 1⁹/L at 8 hours, p < 0.001), and an increase in the percentage of BrdU-labeled PMNs (0.01% ± 0.004% at baseline to 26.1% ± 3.2% at 8 hours, p < 0.001). Endotoxemia caused an arteriovenous difference in BrdU-labeled PMNs across the lung (35.9% ± 2.9% versus 26.1% ± 3.1%, mixed venous versus arterial, p < 0.02). Morphometric studies showed that endotoxin caused sequestration of PMNs in the lung (2.2 ± 0.4 versus 1.0 ± 0.2 × 10¹⁰, endotoxin versus saline, p < 0.03) with preferential retention of BrdU-labeled PMNs (0.79 ± 0.21 versus 0.039 ± 0.016 × 10¹⁰, endotoxin versus saline, p < 0.05). The percentage of BrdU-labeled PMNs in the alveolocapillary walls was higher than in circulating blood (64.01% ± 4.3% versus 26.1% ± 3.2%, p < 0.01) in the endotoxin group. In vitro filtration of cells through 5-mm pore size filters showed that circulating BrdU-labeled PMNs, 8 hours after endotoxin, were preferentially retained in the filters (p < 0.01). Conclusions : We conclude that endotoxemia stimulates the bone marrow to release mature and immature PMNs. Compared to PMNs released from the bone marrow during normal turnover, these PMNs are less deformable and preferentially sequester in the lung microvessels.     

Systemic lupus erythematosus associated with recurrent lupus enteritis and peritonitis

We describe the case of a 41-year-old woman with systemic lupus erythematosus (SLE) who suffered from repeated reversible lupus enteritis characterized by marked edematous thickening of the small intestine. Ultrasonography (US) and computed tomography (CT) manifested as an accordion-like appearance and a target-like appearance, respectively. Resolution of gastrointestinal tract wall thickening was observed on follow-up US performed a week after the increase in predinosolone (PSL). We conclude that careful evaluation of sonographic and radiographic findings helps to establish the diagnosis of lupus enteritis.Abbreviations CT Computed tomography - FANA Fluorescent antinuclear antibody - GI Gastrointestinal - SLE Systemic lupus erythematosus - US Ultrasound     

Systemic inflammation in chronic obstructive pulmonary disease and asthma: Similarities and differences

Background and objective:   While recent studies have shown that patients with COPD and patients with asthma exhibit evidence of airway and systemic inflammation, markers of systemic inflammation have not been compared between the two diseases.
Methods:   To evaluate circulating inflammatory markers, blood was sampled from 111 patients with COPD, 75 control subjects and 46 asthmatic patients (some of whom were smokers). Measurements of WCC, serum levels of fibrinogen, high-sensitivity (hs)-CRP, IL-8, IL-6, tumour necrosis factor-α (TNF-α), transforming growth factor (TGF)-β1, tissue inhibitors of metalloproteinase (TIMP)-1, neutrophil elastase and alpha1-antitrypsin (α1-AT) were performed.
Results:   Serum TNF-α, IL-6 and TIMP-1 concentrations were significantly higher in patients with stable COPD and patients with asthma than in control patients. Serum α1-AT levels were significantly higher in COPD patients than in asthmatic patients and control subjects, and serum TGF-β1 levels were higher in asthma patients than in COPD patients. Smoking status had no effect on markers in COPD and asthmatic patients.
Conclusions:   Although COPD and asthma share common markers of systemic inflammation, serum levels of TGF-β1 and α1-AT may reflect differences between the diseases.     

Immune regulation by phospholipase C-β isoforms

Rapid progress has recently been made regarding how phospholipase C (PLC)-β functions downstream of G protein-coupled receptors and how PLC-β functions in the nucleus. PLC-β has also been shown to interplay with tyrosine kinase-based signaling pathways, specifically to inhibit Stat5 activation by recruiting the protein-tyrosine phosphatase SHP-1. In this regard, a new multimolecular signaling platform, named SPS complex, has been identified. The SPS complex has important regulatory roles in tumorigenesis and immune cell activation. Furthermore, a growing body of work suggests that PLC-β also participates in the differentiation and activation of immune cells that control both the innate and adaptive immune systems.     

Effects of spatial frequency on visual evoked magnetic fields

Psychophysical and visual evoked potential (VEP) studies have shown that spatial frequency of a visual stimulus affects contrast sensitivity and VEPs in humans. However, it is not clear whether and how the effect of spatial frequency varies among cortical areas. Considering that all visual inputs to the retina could be expressed as a sum of sinusoidal gratings of different spatial frequencies, the effect of spatial frequency must be clarified to separate the brain activity specific to each visual stimulus. In order to examine the effect of spatial frequency on different cortical areas, the present study compared cortical responses to sinusoidal gratings of seven different spatial frequencies using magnetoencephalography (MEG). MEG waveforms of twelve healthy adults in response to sinusoidal gratings of 0.3–18.1 cycles per degree were subjected to a multi-dipole analysis. As a result, the effect of spatial frequency was significant on the first peak latency and amplitude of the source activity around V1 and V2 but not on the source activity around V3 and V6, indicating that the effect of spatial frequency varies across different visual areas in the human brain. Our results also suggest that the responses in V1 and V2 that have a peak around 90 ms and that of V6 peaking around 120 ms should be separated to investigate the stimulus-specific cortical response, particularly when examining effects of spatial frequency on the response latency.