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Pilot 22 – Investigating Mechanisms of Vaccine Response Deficiency in Cystic Fibrosis<\/h1>\n

P.I.:<\/b> Jim Kublin, MD, MPH<\/b><\/span><\/a>
\n<\/span>Principal Staff Scientist, Vaccine and Infectious Disease Division, Fred Hutch<\/p>\n

In this project, we will determine whether the cystic fibrosis transmembrane conductance regulator (CFTR) protein plays a role in vaccine response. This is a question of high significance for the treatment and management of infection in cystic fibrosis (CF) patients, which our work and others have shown display sub-optimal responses to common childhood vaccines. The community of microorganisms residing in the gastrointestinal tract of CF infants (termed the microbiome) is dramatically altered compared to infants not experiencing CF. The microbiome is an important determinant of our immune development, however whether the CF-associated microbiome contributes to immune-dysregulation is unknown. In this project, we will determine whether the microbiome plays a role in mediating the immune alterations observed in a CF mouse model by studying these mice in completely bacteria-free conditions. In addition, we will isolate specific species of bacteria that we have found to be associated with high or low vaccine response in CF infants and determine how they modulate a vaccine response by introducing them into a mouse model. Identifying how specific gastrointestinal bacteria contribute to vaccine response deficiency and wider immune dysfunction in CF has the potential to offer novel therapeutic options to benefit patients. Our proposal integrates clinical and preclinical approaches to interrogate the mechanisms underlying vaccine response deficiency and the role of the microbiome in CF by utilizing and developing novel innovative approaches. These are objectives of high relevance and significance to patients with CF.<\/p>\n

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Pilot 22 – Investigating Mechanisms of Vaccine Response Deficiency In Cystic Fibrosis<\/p>\n

P.I.: Jim Kublin, MD, MPH
\nPrincipal Staff Scientist, Vaccine and Infectious Disease Division, Fred Hutch<\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_et_pb_use_builder":"on","_et_pb_old_content":"

P.I.: Steven Kahn, MB, ChB<\/a>
Professor of Medicine
Metabolism, Endocrinology and Nutrition<\/p>

Kristina Utzschneider, MD<\/a>
Associate Professor of Medicine
Metabolism, Endocrinology and Nutrition<\/p>

With the increased life expectancy of patients with cystic fibrosis (CF), other co-morbidities have become apparent in these patients. One of these is abnormal glucose metabolism, where CF-related diabetes (CFRD) is common. More recently, another abnormality of glucose metabolism has been recognized; namely late hypoglycemia following oral glucose loading. In this study, we propose to test the hypothesis that the post-glucose load hypoglycemia observed in patients with CF results from a deficient counterregulatory hormone response and\/or an insulin response that is exaggerated and delayed. This increased insulin response could be the result of an exaggerated incretin hormone response or altered gastric emptying. To address this hypothesis, we will perform a 3-hour oral glucose tolerance test during which we will measure counterregulatory, islet and incretin hormone responses and determine the rate of gastric emptying using acetaminophen. To determine whether patients with CF and late hypoglycemia also have episodes of hypoglycemia during daily living that includes mixed meals, we will use a continuous glucose monitoring system (CGMS) to examine 24-hour glucose profiles for 3 days. All these measures will be compared between patients with CF who develop late hypoglycemia, CF patients who do not develop hypoglycemia, and age and body mass index-matched healthy controls. The findings from this study will provide important new information regarding the mechanism(s) responsible for the late hypoglycemia observed in patients with CF and the data could be used as the basis for future grant applications. The ultimate goal is to gain insight into the condition of late hypoglycemia in order to better manage patients with CF.<\/p>","_et_gb_content_width":"","_monsterinsights_skip_tracking":false,"_monsterinsights_sitenote_active":false,"_monsterinsights_sitenote_note":"","_monsterinsights_sitenote_category":0,"footnotes":"","_links_to":"","_links_to_target":""},"categories":[12],"tags":[],"_links":{"self":[{"href":"https:\/\/depts.washington.edu\/cfrtc\/wp-json\/wp\/v2\/posts\/2303"}],"collection":[{"href":"https:\/\/depts.washington.edu\/cfrtc\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/depts.washington.edu\/cfrtc\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/depts.washington.edu\/cfrtc\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/depts.washington.edu\/cfrtc\/wp-json\/wp\/v2\/comments?post=2303"}],"version-history":[{"count":2,"href":"https:\/\/depts.washington.edu\/cfrtc\/wp-json\/wp\/v2\/posts\/2303\/revisions"}],"predecessor-version":[{"id":3188,"href":"https:\/\/depts.washington.edu\/cfrtc\/wp-json\/wp\/v2\/posts\/2303\/revisions\/3188"}],"wp:attachment":[{"href":"https:\/\/depts.washington.edu\/cfrtc\/wp-json\/wp\/v2\/media?parent=2303"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/depts.washington.edu\/cfrtc\/wp-json\/wp\/v2\/categories?post=2303"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/depts.washington.edu\/cfrtc\/wp-json\/wp\/v2\/tags?post=2303"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}