When people are severely injured or have extensive surgery that does
not affect ingestion of solid or liquid food (nutrition), the person will
be fed through the alimentary tract (mouth, esophagus, stomach, small
bowel, large bowel, etc). Provision of nutrients via the alimentary tract
is known as enteral nutrition. If the alimentary tract is impaired in
any way or if parts of the tract including the bowels (small, large or
both) are missing, nutrients must be provided via a vein (the subclavian
vein). Provision of all nutrients that are necessary for life (in the
form of salts, amino acids, lipids, sugars and vitamins, etc.) via a vein
is known as total parenteral nutrition, or, TPN. People who have for one
reason or the other permanently lost bowel function must receive TPN for
as long as the person is alive. Patients who receive TPN for several months
or longer are termed, long-term TPN patients. My research interests are
currently focused upon the study of alterations in immune function of
patients on long-term TPN. Persons who require long-term feeding via TPN
may eventually suffer from frequent bouts of central line infections,
osteoporosis and liver disease. In collaboration with Dr. Mary Hise at
the University of Kansas Medical Center, the goal of the research is to
determine the mechanism by which feeding patients via the subclavian vein
appears to alter immune function of the patient. While these dysfunctional
events appear to be related to immune system dysfunction and/or imbalance,
and/or inflammatory sequealae, the cause of these harmful conditions is
not yet known. The research involves examination of patient immune profiles
including assessment of activity of various cytokines, immune responsiveness,
functional and flow cytometric analyses of the CD4+ and CD8+ T cell populations
and, in vitro cellular responses of peripheral blood lymphocytes. Additionally,
a mouse model for TPN treatment is under development. This model will
allow manipulation of experimental parameters including TPN content, genetics
of the mouse and expression of cellular molecules important to lymphocyte
interaction. This experimental approach, combined with patient data, will
allow determination of the mechanism by which long-term TPN treatment
induces alteration of immune function. Determination of the mechanism(s)
of this system will hopefully provide a clinical approach that will reduce
or alleviate the conditions associated with long-term TPN treatment.
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