Levels of Transferrin in Bronchoalveolar Lavage Fluid in Sarcoidosis

There has been only one report showing high levels of transferrin (Tf) in bronchoalveolar lavage fluid (BALF) in patients with sarcoidosis. This study was designed to assess the levels of Tf in both BALF and serum and to examine the relationship between the levels of Tf and other disease markers in sarcoidosis. Subjects were 64 sarcoidosis and 10 healthy controls. Tf in BALF and serum was measured by nephelometric assay. Median Tf levels in BALF from sarcoidosis was 0.70 (range, 0.00–3.97) mg/dl, which was significantly higher compared with controls (0.36 (range, 0.00–1.02) mg/dl; p = 0.005). In contrast, median Tf levels in serum from sarcoidosis was 258 (range, 171–383) mg/dl, which was significantly lower compared with controls (322 (range, 234–356) mg/dl; p = 0.003). Tf levels in BALF were significantly correlated with both the percentage of lymphocytes (r = 0.617, p = 0.001) and serum angiotensin-converting enzyme activity (r = 0.363, p = 0.003) and serum soluble interleukin-2 receptor (r = 0.450, p = 0.001) in sarcoidosis. Levels of Tf in BALF from patients with sarcoidosis were not influenced by smoking status. The levels of Tf in sarcoidosis are high in BALF, but low in serum. Increased levels of Tf in BALF may reflect the disease activity.     

Clinical differentiation of atypical pneumonia using Japanese guidelines

BACKGROUND AND OBJECTIVE: Atypical pneumonia occupies an important position in community-acquired pneumonia. The aim of this study was to examine whether making a diagnosis of atypical pneumonia is possible based upon the Japanese Respiratory Society guidelines. METHODS: The data from three prospective studies were reviewed. A total of 285 patients with mycoplasmal pneumonia or chlamydial pneumonia and 515 patients with pneumococcal pneumonia or Haemophilus influenzae pneumonia were assessed to determine whether these pneumonias met the diagnostic criteria for atypical pneumonia used in the Japanese Respiratory Society guidelines. The criteria were: (i) age less than 60 years; (ii) no or only minor underlying diseases; (iii) persistent cough; (iv) limited chest auscultatory findings; (v) no sputum, or no identified aetiological agent by rapid diagnosis; and (vi) a peripheral white blood cell count below 10,000/microL. RESULTS: All items of the criteria proved to be valid except for 'age' in patients with Chlamydophila pneumoniae pneumonia using multiple regression analysis. The sensitivity and specificity for atypical pneumonia were 77.0% and 93.0% based on four or more of the criteria respectively. CONCLUSION: Pure atypical pneumonia can be differentiated to some degree by clinical symptoms and laboratory findings. It is important to differentiate and treat bacterial pneumonia and atypical pneumonia in regions such as Japan, where Streptococcus pneumoniae resistance to macrolides is high. Treatment covering the two types of pneumonia should be considered in elderly patients and those with underlying respiratory disease.     

Elsberg syndrome with eosinophilic meningoencephalitis caused by Angiostrongylus cantonensis

A 42-year-old man was admitted to our hospital with a history of fever, headache and disorientation. His cerebrospinal fluid revealed eosinophilia and his serum had an antibody against Angiostrongylus cantonensis (A. cantonensis). Then, he was diagnosed as eosinophilic meningoencephalitis caused by A. cantonensis. He was treated with repeated lumbar punctures and oral prednisolone. Although a symptom he had been suffering from at the time of his admission was urinary retention, this symptom disappeared as his general condition improved. Therefore his case was considered to be Elsberg syndrome with eosinophilic meningoencephalitis caused by A. cantonensis.     

Luminal space enlargement by carbachol in rat parotid intralobular ducts

Carbachol (CCh) enlarges the luminal space in rat parotid intralobular ducts, but the mechanism of their enlargement remains obscure. We investigated the involvement of intracellular calcium ions in the enlargement of luminal space by monitoring the luminal space under optical sectioning in a confocal laser scanning microscope using sulforhodamine B. Carbachol increased the intracellular concentration of calcium ions ([Ca2+]i) and the inside diameter without any change in the outside diameter. Removal of extracellular calcium ions modulated CCh-induced changes in [Ca2+]i to transient, but did not markedly inhibit the CCh-induced increase in the inside diameter. Additional loading of BAPTA (1,2-bis (o-aminophenoxy-ethane-n,n,n',n'-tetraacetic acid) in the duct cells suppressed CCh-induced changes. Diphenylamine-2-carboxylate (DPC), but not cytochalasin D, calmodulin inhibitor or nitric oxide synthase inhibitor profoundly suppressed CCh-induced changes. These results suggest that CCh induces enlargement of the luminal space through the activation of DPC-sensitive channels by the release of calcium ions from the intracellular pool.     

Role of macrophage inflammatory protein 2 in acute lung injury in murine peritonitis

BACKGROUND: Acute lung injury is a frequent extraabdominal complication of bacterial peritonitis, and neutrophil plays an important role in this lung damage. Macrophage inflammatory protein 2 (MIP-2) serves the same chemotactic function as IL-8 which is a potent neutrophil chemotactic factor in humans, and we investigated the role of MIP-2 associated with neutrophil recruitment in the lung of murine peritonitis. METHODS: Cecal ligation and puncture (CLP) were performed on mice. MIP-2 levels in blood and lung tissue, MIP-2 mRNA expression in lung tissue and bronchoalveolar lavage fluid (BALF), and CD11b expression on peripheral blood neutrophil and BALF cells were determined after CLP. In addition, we investigated the effect of anti-MIP-2 antibody on the lung injury associated with peritonitis. RESULTS: MIP-2 mRNA expression was observed in lung tissue after CLP and numerous neutrophils were accumulated in the lung under those conditions. Anti-MIP-2 antibody contributed to the inhibition of the CD11b expression and chemotaxis of pulmonary neutrophils, lung edema, and thus the reduction in peritonitis-related mortality. CONCLUSIONS: MIP-2 plays a pivotal role in neutrophil recruitment in the lung following peritonitis, and control of neutrophil accumulation in the lung by neutralizing MIP-2 is recommended as a new therapeutic approach to the lung damage associated with peritonitis.