Liver Regeneration is Impaired in Macrophage Colony Stimulating Factor Deficient Mice After Partial Hepatectomy: The Role of M-CSF-Induced Macrophages

2011 ◽  
Vol 165 (1) ◽  
pp. 59-67 ◽  
Author(s):  
Hidetake Amemiya ◽  
Hiroshi Kono ◽  
Hideki Fujii
2009 ◽  
Vol 6 (4) ◽  
pp. 246-251 ◽  
Author(s):  
Miriam Navarro-Sobrino ◽  
Anna Rosell ◽  
Anna Penalba ◽  
Marc Ribo ◽  
Jose Alvarez-Sabin ◽  
...  

2006 ◽  
Vol 186 (2) ◽  
pp. 282-290 ◽  
Author(s):  
Fjoralba Babamusta ◽  
Debra L. Rateri ◽  
Jessica J. Moorleghen ◽  
Deborah A. Howatt ◽  
Xiang-An Li ◽  
...  

1996 ◽  
Vol 270 (4) ◽  
pp. L650-L658 ◽  
Author(s):  
M. Ikegami ◽  
T. Ueda ◽  
W. Hull ◽  
J. A. Whitsett ◽  
R. C. Mulligan ◽  
...  

Mice made granulocyte macrophage-colony stimulating factor (GM-CSF)-deficient by homologous recombination maintain normal steady-state hematopoiesis but have an alveolar accumulation of surfactant lipids and protein that is similar to pulmonary alveolar proteinosis in humans. We asked how GM-CSF deficiency alters surfactant metabolism and function in mice. Alveolar and lung tissue saturated phosphatidylcholine (Sat PC) were increased six- to eightfold in 7- to 9-wk-old GM-CSF-deficient mice relative to controls. Incorporation of radiolabeled palmitate and choline into Sat PC was higher in GM-CSF deficient mice than control mice, and no loss of labeled Sat PC occurred from the lungs of GM-CSF-deficient mice. Secretion of radiolabeled Sat PC to the alveolus was similar in GM-CSF-deficient and control mice. Labeled Sat PC and surfactant protein A (SP-A) given by tracheal instillation were cleared rapidly in control mice, but there was no measurable loss from the lungs of GM-CSF-deficient mice. The function of the surfactant from GM-CSF-deficient mice was normal when tested in preterm surfactant-deficient rabbits. GM-CSF deficiency results in a catabolic defect for Sat PC and SP-A.


2021 ◽  
Vol 7 (2) ◽  
pp. 93
Author(s):  
Made Indira Dianti Sanjiwani ◽  
Nyoman Budhi Wirananda Setiawan ◽  
Agus Indra Yudhistira Diva Putra ◽  
Agus Eka Darwinata

Tuberculosis is a global health problem with a total of 1.4 million cases in 2015. Over the last decade, several studies have demonstrated the potential role of gut-lung axis in the treatment of tuberculosis. The exact mechanism of the gut-lung axis on tuberculosis is still unknown, however modulation of the gut-lung axis can be performed via probiotic administration. The administered probiotics are capable of inducing an immunomodulating effect which helps in the process of tuberculosis infection. One of the molecules that can be activated with probiotics and plays a role in tuberculosis infection is granulocyte macrophage-colony stimulating factor (GM-CSF). GM-CSF can control intracellular production of M. tuberculosis, inflammation in granulomas, and lung tissue reparation. This article aimed to explore the role of the gut-lung axis, GM-CSF, and the potential of probiotic-based therapy on active tuberculosis infection. It was found that probiotics mediate the immune response via the activation of several inflammatory cytokines and interleukins related to lung infection, but not directly with the tuberculosis pathogen. Thus, probiotic-based therapy has the potential to increase immunity during active tuberculosis infection. Further studies to explore the other mechanisms of the gut-lung axis against tuberculosis through probiotic administration need to be performed.


2006 ◽  
Vol 34 (6) ◽  
pp. 766-774 ◽  
Author(s):  
Megan N. Ballinger ◽  
Robert Paine ◽  
Carlos H. C. Serezani ◽  
David M. Aronoff ◽  
Esther S. Choi ◽  
...  

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