Publications by authors named "L Borish"

Humoral immune disorders such as common variable immunodeficiency and specific antibody deficiency are prevalent in clinical practice and require accurate functional testing of humoral immunity for diagnosis and to guide treatment approach. Traditionally, the 23-valent pneumococcal polysaccharide vaccine (PPSV23) has been used to assess polysaccharide antibody responses by measuring pre- and post-vaccination pneumococcal titers. However, the recent introduction of pneumococcal conjugate vaccines (PCVs), such as PCV13, PCV15, and PCV20, into the childhood and adult vaccine schedules has significantly reduced the number of unique serotypes available for testing and in turn has complicated the evaluation process.

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Cystic fibrosis (CF) causes life-shortening respiratory and systemic disease due to dysfunction of the cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel. Highly effective modulator therapies (HEMT) improve the lives of many people with cystic fibrosis (PwCF) by correcting the structure and function of the defective CFTR channel at the molecular level. Despite these advancements, a subset of patients-termed modulator-refractory CF-continues to experience two or more pulmonary exacerbations per year requiring hospitalization or intravenous antibiotics, regardless of other modulator benefits.

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Neutrophilic inflammation contributes to multiple chronic inflammatory airway diseases, including asthma and chronic rhinosinusitis with nasal polyps (CRSwNP), and is associated with an unfavorable prognosis. Here, using single-cell RNA sequencing (scRNA-seq) to profile human nasal mucosa obtained from the inferior turbinates, middle turbinates, and nasal polyps of CRSwNP patients, we identify two IL-1 signaling-induced cell subsets-LY6D club cells and IDO1 fibroblasts-that promote neutrophil recruitment by respectively releasing S100A8/A9 and CXCL1/2/3/5/6/8 into inflammatory regions. IL-1β, a pro-inflammatory cytokine involved in IL-1 signaling, induces the transdifferentiation of LY6D club cells and IDO1 fibroblasts from primary epithelial cells and fibroblasts, respectively.

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Introduction: Psoriasis is a papulosquamous condition characterized by type 1 (T1) inflammation, while chronic rhinosinusitis (CRS) concurrent with asthma is commonly a type 2 (T2) process. Since psoriasis is predictive for higher rates of CRS, our objective was to determine whether CRS with concurrent psoriasis would share its T1 pathogenic signature. In comparison to T1 CRS, a T2 process can be predicted by presence of more extensive sinus disease via Lund-MacKay score, reduced sense of smell, and greater concurrence of purulent drainage and pain/pressure.

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