Mannheimia haemolytica biofilm formation on bovine respiratory epithelial cells

Abstract

Mannheimia haemolytica is the most important bacterial agent associated with the bovine respiratory disease complex (BRDC), which causes worldwide economic losses to the cattle industry. M. haemolytica cells initially colonize the tonsillar crypts in the upper respiratory tract of cattle, from where they can subsequently descend into the lungs to cause disease. Many bacteria exist as biofilms inside their hosts. We hypothesize that M. haemolytica colonization of cattle during its commensal state may include biofilm formation. To begin to assess this possibility, we developed an in vitro system to study biofilm formation directly on bovine respiratory epithelial cells. Using fixed primary bovine bronchial epithelial cells, we observed M. haemolytica biofilm formation after a 48h incubation period at 37°C. Addition of mucin, the main component of mucus present in the upper respiratory tract, decreased M. haemolytica biofilm formation on bovine epithelial cells. We investigated the effects of prior viral infection of the epithelial cells on subsequent biofilm formation by M. haemolytica and found negligible effects. Utilization of this model system will provide new insights into the potential role of biofilm formation by M. haemolytica in the pathogenesis of BRDC.

Dual and Triple Epithelial Coculture Model Systems with Donor-Derived Microbiota and THP-1 Macrophages To Mimic Host-Microbe Interactions in the Human Sinonasal Cavities

“…In biofilm-mediated diseases, and also as observed in CRS patients, chronic disease, extreme resistance to antibiotic treatment, and repeated acute exacerbations are characteristic of biofilm formation (67,68). Biofilm formation in our model system can be determined through microscopy or biofilm-staining procedures (69,70). The distribution of specific (known) subpopulations of the bacterial community in the model system can be assessed using fluorescence in situ hybridization, similar to the elegant approach of Welch et al (71,72) to study biogeography in host environments.…”

Pathogenesis, Host Innate Immune Response, and Aerosol Transmission of Influenza D Virus in Cattle

“…BRD is triggered by the presence of one or several viruses and/or bacteria (2) that are favored by a set of predisposing factors such as altered state of the host immune system (3) and environmental factors (4). Respiratory viruses may induce the disease alone, as in the case of bovine respiratory syncytial virus (BRSV), or cause disease by initiating a cascade of subsequent events of immune suppression (3,5), damaging the respiratory epithelium (6) and the airway clearance mechanisms (7) and altering the local biofilms (8)(9)(10) and normal commensal flora, thus leading to complex secondary bacterial invasion (8,10,11). Several viruses are thought to initiate and contribute to BRD, including BRSV, bovine parainfluenza type 3 virus (BPI3), bovine coronavirus (BCoV), bovine herpesvirus 1 (BoHV-1), and bovine viral diarrhea virus (BVDV).…”

Global Transmission, Spatial Segregation, and Recombination Determine the Long-Term Evolution and Epidemiology of Bovine Coronaviruses

“…Little evidence of genetic mixing between the spatially segregated lineages was found, suggesting that BCoV genetic diversity is a result of a global transmission pathway that occurred during the last century. However, we found variation in evolution rates between the European and non-European lineages indicating differences in virus ecology.Viruses 2020, 12, 534 2 of 16 epithelium damage, [7] and altering commensal microbiota and local biofilm [8][9][10], thus leading to complex secondary bacterial infections [8,10,11].BCoV is a pneumoenteric virus frequently isolated from the fecal samples of diarrheic calves [12-15] and from upper and lower respiratory tract samples during BRD episodes worldwide [16][17][18][19]. While both forms of BCoV infection are widespread with high prevalence among cattle [12,13,15,20,21] and wild ruminants [22], the putative differences between strains isolated from enteric and respiratory tracts are still not clear, and it is unknown whether these differences are related to tissue tropism or simply to distinct times and locations of isolation.…”

“…Viruses 2020, 12, 534 2 of 16 epithelium damage, [7] and altering commensal microbiota and local biofilm [8][9][10], thus leading to complex secondary bacterial infections [8,10,11].…”