scholarly journals Strongyloides stercoralis Larvae in Bronchoalveolar Lavage Fluid in the Asthmatic Patient: A Case Report

2021 ◽  
Author(s):  
Seyed Amir Miratashi Yazdi ◽  
Elham Nazar

Strongyloides stercoralis is a common cause of gastrointestinal infection. Symptoms are usually mild, but in the setting of impaired host immunity, severe and disseminated illnesses may occur. The present report describes a male patient with a history of asthma and corticosteroid therapy, now presented with dyspnea and abdominal pain. Examinations show Strongyloides stercoralis larvae in Bronchoalveolar lavage fluid specimens. The patients who have undergone immunosuppressive therapy are highly indicated for Strongyloides stercoralis screening which prevents hyperinflation in endemic areas.

Author(s):  
Petra Um-Bergström ◽  
Melvin Pourbazargan ◽  
Bettina Levänen ◽  
Marika Ström ◽  
Eva Berggren-Broströom ◽  
...  

2021 ◽  
Vol 20 (1) ◽  
pp. 22-27
Author(s):  
Zhaowen Shi ◽  
Xuming Luo

Asthma is a state of hyperresponsiveness of airways with associated inflammation and obstruction to air track. Present report evaluated the protective effect of desoxyrhapontigenin against ovalbumin-induced rat model of asthma. In asthmatic rats, there was an increase in serum IL-4, IL-5, bronchoalveolar lavage fluid IgE, IL-4, IL-13, IL-17, transforming growth factor β1, and leucocyte count. On the contrary, there was a decrease in bronchoalveolar lavage fluid IFN-γ that was reversed by desoxyrhapontigenin but not dexomethasone. Also, the mRNA expression for NF-kBp65 and vascular endothelial growth factor increased without any change in IκBα in the asthmatic rat tissue. There was a pronounced increase in the histopathological score in asthmatic rat tissue that were diminished by desoxyrhapontigenin or dexomethasone. In conclusion, study reveals that treatment with desoxyrhapontigen may protect the bronchial asthma by modulating the inflammation and immune response in the lung tissue.


1997 ◽  
Vol 27 (4) ◽  
pp. 396-405 ◽  
Author(s):  
L. M. TERAN ◽  
M. G. CAMPOS ◽  
B. T. BEGISHVILLI ◽  
J.-M. SCHRODER ◽  
R. DJUKANOVIC ◽  
...  

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Asbjørn G. Petersen ◽  
Peter C. Lind ◽  
Anne-Sophie B. Jensen ◽  
Mark A. Eggertsen ◽  
Asger Granfeldt ◽  
...  

Abstract Background Senicapoc is a potent and selective blocker of KCa3.1, a calcium-activated potassium channel of intermediate conductance. In the present study, we investigated whether there is a beneficial effect of senicapoc in a large animal model of acute respiratory distress syndrome (ARDS). The primary end point was the PaO2/FiO2 ratio. Methods ARDS was induced in female pigs (42–49 kg) by repeated lung lavages followed by injurious mechanical ventilation. Animals were then randomly assigned to vehicle (n = 9) or intravenous senicapoc (10 mg, n = 9) and received lung-protective ventilation for 6 h. Results Final senicapoc plasma concentrations were 67 ± 18 nM (n = 9). Senicapoc failed to change the primary endpoint PaO2/FiO2 ratio (senicapoc, 133 ± 23 mmHg; vehicle, 149 ± 68 mmHg). Lung compliance remained similar in the two groups. Senicapoc reduced the level of white blood cells and neutrophils, while the proinflammatory cytokines TNFα, IL-1β, and IL-6 in the bronchoalveolar lavage fluid were unaltered 6 h after induction of the lung injury. Senicapoc-treatment reduced the level of neutrophils in the alveolar space but with no difference between groups in the cumulative lung injury score. Histological analysis of pulmonary hemorrhage indicated a positive effect of senicapoc on alveolar–capillary barrier function, but this was not supported by measurements of albumin content and total protein in the bronchoalveolar lavage fluid. Conclusions In summary, senicapoc failed to improve the primary endpoint PaO2/FiO2 ratio, but reduced pulmonary hemorrhage and the influx of neutrophils into the lung. These findings open the perspective that blocking KCa3.1 channels is a potential treatment to reduce alveolar neutrophil accumulation and improve long-term outcome in ARDS.


Lung Cancer ◽  
2003 ◽  
Vol 41 ◽  
pp. S286
Author(s):  
Guzin Gursoy ◽  
Sibel Alpar ◽  
Nazire Ucar ◽  
Tulay Bakirci ◽  
Ahmet Aydin ◽  
...  

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