Abstract
Rhinovirus (RV) is the predominant virus causing respiratory tract infections. Bronchobini® is a low dose multi component, multi target preparation used to treat inflammatory respiratory diseases such as the common cold, described to ease severity of symptoms such as cough and viscous mucus production. The aim of the study was to assess the efficacy of Bronchobini® in RV infection and to elucidate its mode of action. Therefore, Bronchobini®’s ingredients (BRO) were assessed in an ex vivo model of RV infection using mouse precision-cut lung slices, an organotypic tissue capable to reflect the host immune response to RV infection. Cytokine profiles were assessed using enzyme-linked immunosorbent assay (ELISA) and mesoscale discovery (MSD). Gene expression analysis was performed using Affymetrix microarrays and ingenuity pathway analysis. BRO treatment resulted in the significant suppression of RV-induced antiviral and pro-inflammatory cytokine release. Transcriptome analysis revealed a multifactorial mode of action of BRO, with a strong inhibition of the RV-induced pro-inflammatory and antiviral host response mediated by nuclear factor kappa B (NFkB) and interferon signaling pathways. Interestingly, this was due to priming of these pathways in the absence of virus. Overall, BRO exerted its beneficial anti-inflammatory effect by priming the antiviral host response resulting in a reduced inflammatory response to RV infection, thereby balancing an otherwise excessive inflammatory response.
Highlights
Every year millions of people are affected by respiratory tract infections causing the common cold
RV, but not the replication-deficient virus inactivated by ultraviolet (UV) light irradiation, induced the production and release of key cytokines in the antiviral host response such as Interferon β (IFNβ), chemokine (C-X-C) motif ligand 10 (CXCL10), and IFNG (Figure 1)
This was not due to unspecific cytotoxic effects, as no increase in lactate dehydrogenase (LDH) release was observed (Figure S1), and tissue viability was maintained throughout the experiment
Summary
Every year millions of people are affected by respiratory tract infections causing the common cold. Nasal congestions, sore throat, headache, sneezing, and coughing [1,2] Despite this rather mild course of disease, and its usually self-limiting progression with recovery in approximately 7–10 days, the common cold continues to be one of the most frequent respiratory disease and has a high socioeconomic impact due to the high prevalence [3,4]. Major group rhinoviruses comprising about 90% of RV serotypes A and all of group B use the human intercellular adhesion molecule 1 (ICAM1). I.e., the remaining serotypes of group A, use receptors of the low density lipoprotein receptor (LDLR) family [13,14,15]. In contrast to major group RV using ICAM1, the LDLR-mediated infection with minor group serotypes, e.g., RV1b, has been described to be applicable in mouse models [19,20,21]
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