118
One kidney disease of interest is Alport Syndrome that is caused by gene mutations and subsequent increase in laminin α1β1γ1 protein expression of adult mice,
possibly facilitated by lipid dysregulation in lipid binding to the protein [74, 75].
IMS has recently been used for characterization of lipid species in mice in control
and in an Alport model. Nominally isobaric lipid species are differentiated with
high resolving power instrumentation. Three lipid species within 7 mDa of each
other were identified and shown to have different spatial distribution within the
mouse kidney (Fig. 7.5) [75]. Two
13
C isotopes of phospholipids (PI(36:4) and
PI(36:3)) did not change between the kidneys of wild-type and Alport model mice.
Interestingly, the sulfatide species SulfoHexCer(18:2/24:0) of m/z 888.6267 showed
an increase in intensity in the kidney tubules of the Alport model, lending support to
the hypothesis of the role of lipid changes in disease progression. Characterization
of diseases such as Alport syndrome on a molecular level can lead to more informed
and effective treatment strategies.
7.8 Applications to Infectious Disease
Due to the ability of IMS to molecularly probe complex tissue environments without the need for antigen-specific tags, this technology has been applied to a wide
variety of biological and medical issues. For example, one such area is the application to the field of infectious diseases. Antibiotic-resistant bacteria exposure are not
confined to healthcare settings. Isolated from many community settings, resistant
strains of Staphylococcus aureus are a public health threat causing an estimated
20,000 deaths per year in the United States alone. Infections by S. aureus have the
Fig. 7.5 Ion images of mice kidney comparing wild-type (top) to kidney from Alport model
mouse (bottom). Three nominally isobaric ions are mapped showing no change in distribution for
selected phospholipids (m/z 888.5561 and m/z 888.5709) whereas the sulfatide species SulfoHexCer
(18:2/24:0) at m/z 888.6267 is increased in the Alport model compared to the wild-type. (Reprinted
with permission from Ref. [75]. Copyright 2019 American Oil Chemists’ Society)
J. C. McMillen et al.
One kidney disease of interest is Alport Syndrome that is caused by gene mutations and subsequent increase in laminin α1β1γ1 protein expression of adult mice,
possibly facilitated by lipid dysregulation in lipid binding to the protein [74, 75].
IMS has recently been used for characterization of lipid species in mice in control
and in an Alport model. Nominally isobaric lipid species are differentiated with
high resolving power instrumentation. Three lipid species within 7 mDa of each
other were identified and shown to have different spatial distribution within the
mouse kidney (Fig. 7.5) [75]. Two
13
C isotopes of phospholipids (PI(36:4) and
PI(36:3)) did not change between the kidneys of wild-type and Alport model mice.
Interestingly, the sulfatide species SulfoHexCer(18:2/24:0) of m/z 888.6267 showed
an increase in intensity in the kidney tubules of the Alport model, lending support to
the hypothesis of the role of lipid changes in disease progression. Characterization
of diseases such as Alport syndrome on a molecular level can lead to more informed
and effective treatment strategies.
7.8 Applications to Infectious Disease
Due to the ability of IMS to molecularly probe complex tissue environments without the need for antigen-specific tags, this technology has been applied to a wide
variety of biological and medical issues. For example, one such area is the application to the field of infectious diseases. Antibiotic-resistant bacteria exposure are not
confined to healthcare settings. Isolated from many community settings, resistant
strains of Staphylococcus aureus are a public health threat causing an estimated
20,000 deaths per year in the United States alone. Infections by S. aureus have the
Fig. 7.5 Ion images of mice kidney comparing wild-type (top) to kidney from Alport model
mouse (bottom). Three nominally isobaric ions are mapped showing no change in distribution for
selected phospholipids (m/z 888.5561 and m/z 888.5709) whereas the sulfatide species SulfoHexCer
(18:2/24:0) at m/z 888.6267 is increased in the Alport model compared to the wild-type. (Reprinted
with permission from Ref. [75]. Copyright 2019 American Oil Chemists’ Society)
J. C. McMillen et al.
