Reversed Helper/Suppressor T-Lymphocyte Ratio in Bronchoalveolar Lavage Fluid from Patients with Breast Cancer andPneumocystis cariniiPneumonia

1991 ◽  
Vol 143 (2) ◽  
pp. 437-440 ◽  
Author(s):  
James Siminski ◽  
Pamela Kidd ◽  
Gretchen D. Phillips ◽  
Carolyn Collins ◽  
Ganesh Raghu
2020 ◽  
Author(s):  
qing Zhang ◽  
jing Li ◽  
tao Huang ◽  
yifeng Zhang ◽  
wenwu Xu ◽  
...  

Abstract Background: Developments of pulmonary diseases, often accompanied by infections of bacteria, severely affect meat production and welfare of pigs. This study investigated the association of lung lesions and Mycoplasma levels inferred from 16S rRNA sequencing of bronchoalveolar lavage fluid with 57 immune cells and 25 hematological traits in 307 pigs at age of 240 days from an eight-breed heterogeneous cross.Result: At a false discovery rate threshold of 0.05, we found that the greater severity of lung lesions were significantly associated with higher CD8+ to CD3+ cell ratio (CD8+/CD3+), neutrophil to lymphocyte ratio (NLR), and standard deviation of red blood cell volume distribution width (RDW-SD), and lower CD4-CD8-/CD3+, CD3+CD4-CD8-/PBMCs, CD14-CD16-/PBMCs, mean corpuscular hemoglobin concentration (MCHC), lymphocyte count (LYM) and lymphocyte count percentage (LYMR), reflected an status of inflammation, immune suppression and hypoxia of the pigs accompanying the development of the lung lesion. The Mycoplasma abundance showed positive correlations with neutrophil count (NEU), neutrophil count percentage (NEUR), neutrophil-to-lymphocyte ratio (NLR), monocyte count (MON), RDW-CV, and RDW-SD, and negative correlations with MCHC, LYM, and LYMR, these correlations are largely consistent with those of lung lesions, supporting the comorbidity of lung lesions and Mycoplasma infection. We also observed a nonlinear association that the sharp increases in NEU and NEUR occurred only when Mycoplasma abundance raised to a level above the population-average. Conclusion: This study showed that the pigs from an eight-breed cross heterogeneous population reared under standardized housing conditions suffered lesion averagely covered 40% of lung, and the lung lesions were significantly linked to load of Mycoplasma in bronchoalveolar lavage fluid. We further demonstrated that the lung lesion and load of Mycoplasma perturb a large variety of immune and hematological traits. These associations provide helpful insights into the changes of host immune status in response to mycoplasma relevant lung diseases in pigs.


2002 ◽  
Vol 18 (5) ◽  
pp. 391-401 ◽  
Author(s):  
Denise A. Croix ◽  
Kathryn Board ◽  
Saverio Capuano ◽  
Michael Murphey-Corb ◽  
Constantine G. Haidaris ◽  
...  

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.


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