[et_pb_section fullwidth=”on” specialty=”off”][et_pb_fullwidth_slider admin_label=”Fullwidth Slider” show_arrows=”on” show_pagination=”on” auto=”off” parallax=”off” parallax_method=”off” module_id=”interior”][et_pb_slide background_image=”https:\/\/depts.washington.edu\/cfrtc\/wp-content\/uploads\/2014\/12\/microscope.jpg” background_color=”#ffffff” alignment=”center” background_layout=”dark” \/][\/et_pb_fullwidth_slider][\/et_pb_section][et_pb_section][et_pb_row][et_pb_column type=”1_4″][et_pb_sidebar admin_label=”Fellowships Sidebar” orientation=”left” area=”et_pb_widget_area_11″ background_layout=”light” \/][\/et_pb_column][et_pb_column type=”3_4″][et_pb_text admin_label=”Current Fellow Long text” background_layout=”light” text_orientation=”left”]<\/p>\n
Fellow: Matthew Long, PhD
\nMicrobiology<\/p>\n
Mentor: \u00a0Anne Manicone, MD<\/a> Pulmonary macrophages have dichotomous roles in promoting and resolving inflammatory responses in the lung; and they do this in part by their ability to adopt different activation or polarized states. In an \u201cM1\u201d polarized state, they participate in clearance of bacteria and secretion of pro-inflammatory cytokines\/chemokines. They can also adopt an \u201cM2\u201d polarized state, and this activation state is important in promoting wound resolution, including clearance of debri and apoptotic neutrophils. A balance of M1 and M2 polarization is likely necessary for a normal inflammatory response to infection; and an imbalance in these activation states may contribute to lung disease. The functional role of M1 and M2 cells in regulating chronic inflammatory diseases is far from clear, and potentially an imbalance of M2 cells may contribute to lung disease. In fact, an increase in M2 cells has been reported in CF airways and these cells may impair bacterial clearance, promote immunoparalysis and lead to excessive airway fibrosis. Particularly in CF, macrophage polarization may be altered by chronic exposure to apoptotic neutrophils (a stimulus for M2 polarization) and to bacteria (a stimulus for M1 polarization). In addition, other factors specific to or associated with CF, such lack of a functional CFTR on macrophages may also contribute to altered macrophage polarization. In this fellowship grant application, we seek to uncover the functional consequences of M2 polarization, the signaling pathways involved, and the role of CFTR in mediating these key macrophage functions. This proposal will address basic yet unknown areas in macrophage biology by answering these fundamental questions: What are the signaling pathways driving M2 polarization and does CFTR contribute to these pathways? What are the functional consequences of M2 polarization on innate immunity and does CFTR alter these functions? Overall, these studies will add to our basic understanding of macrophage polarization and the contribution of CFTR in modulating these phenotypes so that novel strategies may be designed to modulate CF lung disease.<\/p>\n [\/et_pb_text][\/et_pb_column][\/et_pb_row][\/et_pb_section]<\/p>\n","protected":false},"excerpt":{"rendered":" Fellow: Matthew Long, PhD Mentor: Anne Manicone, MD P.I.: Ian de boer, MD<\/a>
\nAssociate Professor,\u00a0Pulmonary and Critical Care<\/p>\n
\nMicrobiology<\/p>\n
\nAssociate Professor
\nPulmonary and Critical Care <\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"closed","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_et_pb_use_builder":"on","_et_pb_old_content":"
Associate Professor of Medicine
Nephrology<\/p>