Assessment of Pathological and Physiological Changes in Mouse Lung Through Bronchoalveolar Lavage

Di, Y. Peter

doi:10.1007/978-1-62703-739-6_3

Cited by 7 publications

(6 citation statements)

References 33 publications

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“…AM is the majority of BAL cells, Crowell RE claimed that AM is approximately 78% of BAL cells. The standard protocol recommends Cut the abdominal aorta beneath intestines to drain blood, to eliminate red blood cell accumulation in the alveolar region to have fewer red blood cell (RBC) in BAL fluid and interstitial lung tissues [33] . In our study, we did not get rid of RBC, because AM has to be collected in shortest time to keep AM viable, another reason is that RBC could not adhere to the plate, it will be washed when we purified the AM.…”

Section: Discussionmentioning

confidence: 99%

PI3K/Akt Signaling Pathway Modulates Influenza Virus Induced Mouse Alveolar Macrophage Polarization to M1/M2b

et al. 2014

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Macrophages polarized to M1 (pro-inflammation) or M2 (anti-inflammation) phenotypes in response to environmental signals. In this study, we examined the polarization of alveolar macrophage (AM), following induction by different influenza virus strains (ST169 (H1N1), ST602 (H3N2) and HKG9 (H9N2)). Macrophages from other tissues or cell line exert alternative responding pattern, and AM is necessary for investigating the respiratory system. AM polarized toward the M1 phenotype after 4 hours of infection by all three virus strains, and AM to presented M2b phenotype after 8 hours induction, and immunosuppressive phenotype after 24 hours of induction. Protein expression assay showed similar results as the gene expression analysis for phenotype verification. The ELISA assay showed that TNF-α secretion was up-regulated after 4 and 8 hours of infection by influenza viruses, and it returned to basal levels after 24 hours of infection. IL-10 expression was elevated after 8 and 24 hours of infection. Immunofluorescence showed that iNOS expression was up-regulated but not Arg1 expression. Influenza virus notably increased phospho-Akt but not phospho-Erk1/2 or phospho-p38, and the AM polarization pattern have been changed by LY294002 (PI3K inhibitor). In conclusion, our results demonstrate the dynamic polarization of AM induced by influenza viruses, and suggested that PI3K/Akt signaling pathway modulates AM polarization to M1/M2b.

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Section: Discussionmentioning

confidence: 99%

PI3K/Akt Signaling Pathway Modulates Influenza Virus Induced Mouse Alveolar Macrophage Polarization to M1/M2b

et al. 2014

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“…After 24 hours of treatment, mice were anesthetized with 2.5% tribromoethanol (Avertin). The trachea was cannulated, the lungs were lavaged twice using 1 ml saline, and the BAL samples collected as previously described 51 . The number of live immune cells in the BAL was determined by a Vision Cell Analyzer automatic cell counter (Nexcelom, Lawrence, MA).…”

Section: Methodsmentioning

confidence: 99%

In vivo therapeutic efficacy of frog skin-derived peptides against Pseudomonas aeruginosa-induced pulmonary infection

Chen

Mangoni

2017

Sci Rep

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Pseudomonas aeruginosa is an opportunistic and frequently drug-resistant pulmonary pathogen especially in cystic fibrosis sufferers. Recently, the frog skin-derived antimicrobial peptide (AMP) Esc(1–21) and its diastereomer Esc(1–21)-1c were found to possess potent in vitro antipseudomonal activity. Here, they were first shown to preserve the barrier integrity of airway epithelial cells better than the human AMP LL-37. Furthermore, Esc(1–21)-1c was more efficacious than Esc(1–21) and LL-37 in protecting host from pulmonary bacterial infection after a single intra-tracheal instillation at a very low dosage of 0.1 mg/kg. The protection was evidenced by 2-log reduction of lung bacterial burden and was accompanied by less leukocytes recruitment and attenuated inflammatory response. In addition, the diastereomer was more efficient in reducing the systemic dissemination of bacterial cells. Importantly, in contrast to what reported for other AMPs, the peptide was administered at 2 hours after bacterial challenge to better reflect the real life infectious conditions. To the best of our knowledge, this is also the first study investigating the effect of AMPs on airway-epithelia associated genes upon administration to infected lungs. Overall, our data highly support advanced preclinical studies for the development of Esc(1–21)-1c as an efficacious therapeutic alternative against pulmonary P. aeruginosa infections.

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“…FVB/NJ female mice were injected intratracheally with 50 μL of PBS at different concentrations of UBM, ranging from 1 to 10 mg/kg. Lung tissues were lavaged as described 25 and harvested 24 h after UBM administration and analyzed for toxicity by total protein, lactic acid dehydrogenase, total leukocytes, and differential cell counts in bronchoalveolar lavage (BAL) as well as by gene expression using real-time polymerase chain reaction (PCR) analysis.…”

Section: Methodsmentioning

confidence: 99%

Treatment with a Urinary Bladder Matrix Alters the Innate Host Response to Pneumonia Induced by Escherichia coli

Lin

Zhu

Yang

et al. 2021

ACS Biomater. Sci. Eng.

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Escherichia coli has become the prominent cause of nosocomial pneumonia in recent years. In the meantime, some strains of E. coli have developed resistance to commonly used antibacterial drugs. The urinary bladder matrix (UBM) is a biologically derived scaffold material that has been used to promote site-appropriate tissue remodeling in a variety of body systems, partially through the modulation of the innate immune response. In this study, we seek to determine UBM efficacy in preventing bacterial pneumonia in mouse lungs using the Gram-negative bacterial strain E. coli. Our results show that the UBM prevented bacterial biofilm formation in both abiotic and biotic conditions through experimentation on polystyrene plates and culture on the apical surface of differentiated airway epithelial cells. Intratracheal treatment with UBM led to host protection from E. coli-induced respiratory infection in a murine pneumonia model. Transcriptomic analysis revealed the involvement of the enhanced host immune response in UBM-treated mice. Additionally, UBM-treated macrophages had an increased iNOS expression and enhanced phagocytosis activity. Therefore, the protection against E. coli-induced infection and the antibacterial function observed by UBM is potentially through both the anti-biofilm activity and enhanced host immunity following UBM treatment. Taken together, our results support further investigation of UBM as an alternative treatment to attenuate bacterial-induced respiratory infection.

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Assessment of Pathological and Physiological Changes in Mouse Lung Through Bronchoalveolar Lavage

Cited by 7 publications

References 33 publications

PI3K/Akt Signaling Pathway Modulates Influenza Virus Induced Mouse Alveolar Macrophage Polarization to M1/M2b

PI3K/Akt Signaling Pathway Modulates Influenza Virus Induced Mouse Alveolar Macrophage Polarization to M1/M2b

In vivo therapeutic efficacy of frog skin-derived peptides against Pseudomonas aeruginosa-induced pulmonary infection

Treatment with a Urinary Bladder Matrix Alters the Innate Host Response to Pneumonia Induced by Escherichia coli

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