Shabtai Varsano

Generation of complement C3 and expression of cell membrane complement inhibitory proteins by human bronchial epithelium cell line

BACKGROUND The interrelationship between human airway epithelium and complement proteins may affect airway defence, airway function, and airway epithelial integrity. A study was undertaken to determine (1) whether unstimulated human bronchial epithelium generates complement proteins and expresses cell membrane complement inhibitory proteins (CIP) and (2) whether stimulation by proinflammatory cytokines affects the generation of complement and expression of cell membrane CIP by these cells. METHODS Human bronchial epithelium cell line BEAS-2B was cultured in a serum-free medium. Cells were incubated with and without proinflammatory cytokines to assess unstimulated and stimulated generation of complement C3, C1q and C5 (by ELISA), and to examine the expression of cell membrane CIP decay accelerating factor (DAF; CD55), membrane cofactor protein (MCP; CD46), and CD59 (protectin) by flow cytometry analysis. RESULTS Unstimulated human bronchial epithelial cell line BEAS-2B in serum-free medium generates complement C3 (mean 32 ng/106 cells/72 h, range 18–52) but not C1q and C5, and expresses cell membrane DAF, MCP, and CD59. Interleukin (IL)-1α (100 U/ml/72 h) and tumour necrosis factor (TNF-α; 1000 U/ml/72 h) increased generation of C3 up to a mean of 78% and 138%, respectively, above C3 generation by unstimulated cells. DAF was the only cell membrane CIP affected by cytokine stimulation. Interferon (IFN)-γ (10 U/ml/72 h) and TNF-α (1000 U/ml/72 h) increased DAF expression up to a mean of 116% and 45%, respectively, above that in unstimulated cells. MCP and CD59 expression was not consistently affected by IL-1α, TNF-α, or IFN-γ. CONCLUSIONS Local generation of complement C3 and expression of cell membrane CIP by human bronchial epithelium and its modulation by proinflammatory cytokines might be an additional regulatory mechanism of local airway defence and may affect airway function and epithelial integrity in health and disease.

Bilateral and Unilateral Spontaneous Massive Hemothorax as a Presenting Manifestation of Rare Tumors

Spontaneous true hemothorax is quite a rare manifestation of a presenting disease. This is a report of two patients, one with bilateral spontaneous massive hemothorax as a presenting manifestation of angiosarcoma involving the lungs and pleura, and the other with unilateral spontaneous hemothorax and hemorrhagic shock as a presenting manifestation of ‘cystic’ chondroblastoma. Differential diagnosis of spontaneous true hemothorax and its evaluation and management are discussed.

Pergolide-Induced Dyspnea, Bilateral Pleural Effusion and Peripheral Edema

A patient with severe Parkinson’s disease presented with increasing dyspnea, bilateral pleural effusion and peripheral edema that were refractory to diuretic therapy and were first misdiagnosed as signs of right-sided heart failure. Pergolide was the only culprit for this devastating condition and on its discontinuation all signs of fluid retention resolved. In this report, drug reactions to ergots and dopamine agonists are discussed.

Hypophosphatemia as a reversible cause of refractory ventilatory failure.

An 81-yr-old male with pulmonary emphysema was hospitalized because of malnutrition and hypoglycemia. This patient developed ventilatory failure requiring mechanical assistance 12 h after initiation of iv hyperalimentation. Severe hypophosphatemia (0.1 mg/dl), mild hypocalcemia, hypomagnesemia, and hypokalemia were subsequently and concomitantly documented. Repeated attempts to wean him from the respirator failed until hypophosphatemia was corrected. When difficulties are encountered in weaning patients from mechanical ventilation, attention should be directed toward detection of hypophosphatemia. This may be crucial in the presence of chronic lung disease.

Kaposi's sarcoma and angioimmunoblastic lymphadenopathy

Kaposis sarcoma (KS) and angioimmunoblastic lymphadenopathy (AILD) are exceptionally rare neoplastic diseases, although the former has recently been more frequently reported among certain populations, and is lately a topic for extensive medical and investigational interest. This case is unique in that it describes an association between KS and AILD. Such an association raises the question of a common pathogenic mechanism. The authors believe that predisposition to each of both diseases may be related to acquired immune deffiency which in turn may be induced by specific viral infections.

Human Nasal Epithelium Adsorbs Complement C3-Related Fragments and Expresses Cell Membrane Complement Regulatory Proteins†

Recent evidence suggests that complement is activated in human nasal airways in inflammatory states. Activated complement protects the nasal mucosa against microorganisms, but also has the potential to lyse the hosts normal cells. Complement‐mediated cell lysis depends on adsorption of complement to the cell membrane and on uninterrupted activation of the complement cascade upon the same cell membrane. In the present study, the authors investigated first whether key complement components, C3‐related fragments, are adsorbed to nasal epithelial cell membrane. Second, we investigated whether nasal epithelium expresses cell membrane complement regulatory proteins that are known as interruptors of complement activation.