TY - JOUR AU - Ogrinc, Katarina AU - Hernández, Sergio AU - Korva, Miša AU - Bogovič, Petra AU - Rojko, Tereza AU - Lusa, Lara AU - Chiumento, Geena AU - Strle, Franc AU - Strle, Klemen T1 - Unique Clinical, Immune, and Genetic Signature in Patients with Borrelial Meningoradiculoneuritis T2 - Emerging Infectious Disease journal PY - 2022 VL - 28 IS - 4 SP - 766 SN - 1080-6059 AB - Lyme neuroborreliosis (LNB) in Europe may manifest with painful meningoradiculoneuritis (also known as Bannwarth syndrome) or lymphocytic meningitis with or without cranial neuritis (peripheral facial palsy). We assessed host immune responses and the prevalence of TLR1 (toll-like receptor 1)–1805GG polymorphism to gain insights into the pathophysiology of these conditions. Regardless of LNB manifestation, most mediators associated with innate and adaptive immune responses were concentrated in cerebrospinal fluid; serum levels were unremarkable. When stratified by specific clinical manifestation, patients with meningoradiculoneuritis had higher levels of B-cell chemoattractants CXC motif chemokine ligand (CXCL) 12 and CXCL13 and T-cell–associated mediators CXCL9, CXCL10, and interleukin 17, compared with those without radicular pain. Moreover, these patients had a higher frequency of TLR1–1805GG polymorphism and more constitutional symptoms. These findings demonstrate that meningoradiculoneuritis is a distinct clinical entity with unique immune and genetic pathophysiology, providing new considerations for the study of LNB and borrelial meningoradiculitis. KW - Lyme disease KW - neuroborreliosis KW - meningoradiculoneuritis KW - peripheral facial palsy KW - meningitis/encephalitis KW - immune response KW - inflammation KW - cytokines KW - genetics KW - polymorphism KW - vector-borne infections KW - bacteria KW - Slovenia KW - United States DO - 10.3201/eid2804.211831 UR - https://wwwnc.cdc.gov/eid/article/28/4/21-1831_article ER - End of Reference