Dataset Information

Lipopolysaccharide O-antigens-bacterial glycans made to measure.

ABSTRACT: Lipopolysaccharides are critical components of bacterial outer membranes. The more conserved lipid A part of the lipopolysaccharide molecule is a major element in the permeability barrier imposed by the outer membrane and offers a pathogen-associated molecular pattern recognized by innate immune systems. In contrast, the long-chain O-antigen polysaccharide (O-PS) shows remarkable structural diversity and fulfills a range of functions, depending on bacterial lifestyles. O-PS production is vital for the success of clinically important Gram-negative pathogens. The biological properties and functions of O-PSs are mostly independent of specific structures, but the size distribution of O-PS chains is particularly important in many contexts. Despite the vast O-PS chemical diversity, most are produced in bacterial cells by two assembly strategies, and the different mechanisms employed in these pathways to regulate chain-length distribution are emerging. Here, we review our current understanding of the mechanisms involved in regulating O-PS chain-length distribution and discuss their impact on microbial cell biology.

SUBMITTER: Whitfield C

PROVIDER: S-EPMC7397119 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature

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Lipopolysaccharide O-antigens-bacterial glycans made to measure.

Whitfield Chris C Williams Danielle M DM Kelly Steven D SD

The Journal of biological chemistry 20200518 31

Lipopolysaccharides are critical components of bacterial outer membranes. The more conserved lipid A part of the lipopolysaccharide molecule is a major element in the permeability barrier imposed by the outer membrane and offers a pathogen-associated molecular pattern recognized by innate immune systems. In contrast, the long-chain O-antigen polysaccharide (O-PS) shows remarkable structural diversity and fulfills a range of functions, depending on bacterial lifestyles. O-PS production is vital f ...[more]

PMID: 32424042

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Project description:Depending on the specific viral pathogen, commensal bacteria can promote or reduce the severity of viral infection and disease progression in their hosts. Influenza A virus (IAV) has a broad host range, comprises many subtypes, and utilizes different routes of transmission, including the fecal-oral route in wild birds. It has been previously demonstrated that commensal bacteria can interact with the host's immune system to protect against IAV pathogenesis. However, it is unclear whether bacteria and their products may be interacting directly with IAV to impact virion stability. Herein we show that gastrointestinal (GI) tract bacterial isolates in an in vitro system significantly reduce the stability of IAV. Moreover, bacterial lipopolysaccharide (LPS), found on the exterior surfaces of bacteria, was sufficient to significantly decrease the stability of both human and avian viral strains in a temperature-dependent manner, including at the relevant temperatures of their respective hosts and the external aquatic habitat. The subtype and host origin of the viruses were shown to affect the extent to which IAV was susceptible to LPS. Furthermore, using a receptor binding assay and transmission electron microscopy, we observed that LPS binds to and alters the morphology of influenza virions, suggesting that direct interaction with the viral surface contributes to the observed antiviral effect of LPS on influenza. IMPORTANCE Influenza A virus (IAV), transmitted primarily via the fecal-oral route in wild birds, encounters high concentrations of bacteria and their products. Understanding the extent to which bacteria affect the infectivity of IAV will lead to a broader understanding of viral ecology in reservoir hosts and may lead to insights for the development of therapeutics in respiratory infection. Herein we show that bacteria and lipopolysaccharide (LPS) interact with and destabilize influenza virions. Moreover, we show that LPS reduces the long-term persistence and freeze-thaw stability of IAV, which is important information for modeling the movement and emergence of novel strains from animal hosts. Our results, demonstrating that the subtype and host origin of a virus also influence its susceptibility to LPS, raise key questions about the fitness of viruses in reservoir hosts, their potential to transmit to humans, and the importance of bacterial-viral interactions in viral ecology.

Project description:BACKGROUND: In mammals it is well known that infections can lead to alterations in reproductive function. As part of the innate immune response, a number of cytokines and other immune factors is produced during bacterial infection or after treatment with lipopolysaccharide (LPS) and acts on the reproductive system. In fish, LPS can also induce an innate immune response but little is known about the activation of the immune system by LPS on reproduction in fish. Therefore, we conducted studies to examine the in vivo and in vitro effects of lipopolysaccharide (LPS) on the reproductive function of sexually mature female trout. METHODS: In saline- and LPS -injected brook trout, we measured the concentration of plasma steroids as well as the in vitro steroidogenic response (testosterone and 17alpha-hydroxyprogesterone) of ovarian follicles to luteinizing hormone (LH), the ability of 17alpha,20beta-dihydroxy-4-pregnen-3-one to induce germinal vesicle breakdown (GVBD) in vitro, and that of epinephrine to stimulate follicular contraction in vitro. We also examined the direct effects of LPS in vitro on steroid production, GVBD and contraction in brook trout ovarian follicles. The incidence of apoptosis was evaluated by TUNEL analysis. Furthermore, we examined the gene expression pattern in the ovary of saline- and LPS-injected rainbow trout by microarray analysis. RESULTS: LPS treatment in vivo did not affect plasma testosterone concentration or the basal in vitro production of steroids, although a small but significant potentiation of the effects of LH on testosterone production in vitro was observed in ovarian follicles from LPS-treated fish. In addition, LPS increased the plasma concentration of cortisol. LPS treatment in vitro did not affect the basal or LH-stimulated steroid production in brook trout ovarian follicles. In addition, we did not observe any effects of LPS in vivo or in vitro on GVBD or follicular contraction. Therefore, LPS did not appear to impair ovarian steroid production, oocyte final maturation or follicular contraction under the present experimental conditions. Interestingly, LPS administration in vivo induced apoptosis in follicular cells, an observation that correlated with changes in the expression of genes involved in apoptosis, as evidenced by microarray analysis. CONCLUSION: These results indicate that female trout are particularly resistant to an acute administration of LPS in terms of ovarian hormone responsiveness. However, LPS caused a marked increase in apoptosis in follicular cells, suggesting that the trout ovary could be sensitive to the pro-apoptotic effects of LPS-induced inflammatory cytokines.

Dataset Information

Lipopolysaccharide O-antigens-bacterial glycans made to measure.

Publications

Lipopolysaccharide O-antigens-bacterial glycans made to measure.

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