Program Schedule

Lung Cellular Bioenergetics in Galectin-3 Deficient Mice Infected with Respiratory Syncytial Virus

Session: Poster Abstract Session: Microbial and Host Factors
Saturday, October 11, 2014
Room: The Pennsylvania Convention Center: IDExpo Hall BC
  • GAL_Poster_Alsuwaidi-Final.pdf (358.8 kB)
  • Background:

    Cellular bioenergetics includes all metabolic processes involved in energy conversion.  Cellular respiration implies delivery of O2 and metabolic fuels to the mitochondria, oxidation of reduced metabolic fuels and passage of electrons to O2.  Lung cellular bioenergetics (mitochondrial O2 consumption and ATP synthesis) are increased in C57BL/6 mice infected with respiratory syncytial virus (RSV).  This study investigated these biomarkers in galectin-3 deficient (Gal-3-/-) C57BL/6 mice infected with RSV.  Gal-3 (b-galactoside-binding lectin) is an immune modulator with pro-inflammatory activity.  Its absence is expected to ameliorate the disease.


    RSV A2 infection was induced by intranasal inoculation of wild-type and Gal-3-/- mice.  Lung fragments were then collected on days 3 and 5 after inoculation and analyzed for cellular bioenergetics (mitochondrial O2 consumption and ATP content).  Cellular respiration was measured using phosphorescence O2 analyzer.  Cellular ATP was measured using the luciferin/ luciferase system.


    In wild-type mice, the rate of respiration (mean ▒ SD, in ÁM O2 mg-1 min-1) in uninfected lungs was 0.08 ▒ 0.02 (n = 6) and in RSV-infected lungs was 0.14 ▒ 0.06 (n = 7, p = 0.002).  In Gal-3-/- mice, the rate of respiration in uninfected lungs was 0.06 ▒ 0.01 (n = 3) and in RSV-infected lungs was 0.06 ▒ 0.01 (n = 6, p = 0.272), see Figure.  Lung cellular ATP increased by 18% in wild-type mice infected with RSV and decreased by 16% in Gal-3-/- mice infected with RSV. 


    The increase in lung cellular bioenergetics is not observed in Gal-3 deficient mice.  Thus, Gal-3 plays a role in RSV-induced modulation of cellular metabolism. The impact of Gal-3 on RSV infection requires further investigation.

    Ahmed Alsuwaidi, MD1, Steven Varga, PhD2 and Abdul Kader Souid, MD, PhD1, (1)Pediatrics, United Arab Emirates University, Al Ain, United Arab Emirates, (2)Microbiology, University of Iowa, Iowa City, IA


    A. Alsuwaidi, None

    S. Varga, None

    A. K. Souid, None

    Findings in the abstracts are embargoed until 12:01 a.m. EDT, Oct. 8th with the exception of research findings presented at the IDWeek press conferences.

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