Mother-to-infant microbiota transmission and infant microbiota development across multiple body sites.

Early-life microbiota seeding and subsequent development is crucial to future health. Cesarean-section (CS) birth, as opposed to vaginal delivery, affects early mother-to-infant transmission of microbes. Here, we assess mother-to-infant microbiota seeding and early-life microbiota development across six maternal and four infant niches over the first 30 days of life in 120 mother-infant pairs.

The rearing environment persistently modulates mouse phenotypes from the molecular to the behavioural level.

The phenotype of an organism results from its genotype and the influence of the environment throughout development. Even when using animals of the same genotype, independent studies may test animals of different phenotypes, resulting in poor replicability due to genotype-by-environment interactions. Thus, genetically defined strains of mice may respond differently to experimental treatments depending on their rearing environment.

The effect of live attenuated influenza vaccine on pneumococcal colonisation densities among children aged 24-59 months in The Gambia: a phase 4, open label, randomised, controlled trial.

Background: Influenza and other respiratory viruses promote proliferation in the upper respiratory tract. We sought to investigate for what we believe is the first time, the effect of intranasal live attenuated influenza vaccine (LAIV) on nasopharyngeal density in a low-income to middle-income country population with high pneumococcal carriage rates.

Methods: In an open-label, randomised, controlled trial in The Gambia, 330 healthy children aged 24-59 months were randomly assigned 2:1 to receive one trivalent LAIV dose at enrolment (day 0, intervention) or at the end of active follow-up (day 21, control).

Supplemented nutrition decreases helminth burden and increases drug efficacy in a natural host-helminth system.

Gastrointestinal (GI) helminths are common parasites of humans, wildlife, and livestock, causing chronic infections. In humans and wildlife, poor nutrition or limited resources can compromise an individual's immune response, predisposing them to higher helminth burdens. This relationship has been tested in laboratory models by investigating infection outcomes following reductions of specific nutrients.

Infant respiratory syncytial virus prophylaxis and nasopharyngeal microbiota until 6 years of life: a subanalysis of the MAKI randomised controlled trial.

Background: Respiratory syncytial virus (RSV) infection during infancy is suggested to cause long-term wheeze. In turn, wheeze has been associated with bacterial dysbiosis of the respiratory tract. We investigated the effects of RSV prophylaxis with palivizumab in otherwise healthy preterm infants on respiratory microbiota composition at 1 year and 6 years of age.

Nasopharyngeal Microbiota Profiles in Rural Venezuelan Children Are Associated With Respiratory and Gastrointestinal Infections.

Background: Recent research suggests that the microbiota affects susceptibility to both respiratory tract infections (RTIs) and gastrointestinal infections (GIIs). In order to optimize global treatment options, it is important to characterize microbiota profiles across different niches and geographic/socioeconomic areas where RTI and GII prevalences are high.

Methods: We performed 16S sequencing of nasopharyngeal swabs from 209 Venezuelan Amerindian children aged 6 weeks-59 months who were participating in a 13-valent pneumococcal conjugate vaccine (PCV13) study.

Variation in Local and Systemic Pro-Inflammatory Immune Markers of Wild Wood Mice after Anthelmintic Treatment.

The immune system represents a host's main defense against infection to parasites and pathogens. In the wild, a host's response to immune challenges can vary due to physiological condition, demography (age, sex), and coinfection by other parasites or pathogens. These sources of variation, which are intrinsic to natural populations, can significantly impact the strength and type of immune responses elicited after parasite exposure and infection.

Age affects antibody levels and anthelmintic treatment efficacy in a wild rodent.

The role of the host immune system in determining parasite burdens and mediating within-host parasite interactions has traditionally been studied in highly controlled laboratory conditions. This does, however, not reflect the diversity of individuals living in nature, which is often characterised by significant variation in host demography, such as host age, sex, and infection history. Whilst studies using wild hosts and parasites are beginning to give insights into the complex relationships between immunity, parasites and host demography, the cause-and-effect relationships often remain unknown due to a lack of high resolution, longitudinal data.

Parasitic nematodes simultaneously suppress and benefit from coccidian coinfection in their natural mouse host.

Within-host interactions among coinfecting parasites are common and have important consequences for host health and disease dynamics. However, these within-host interactions have traditionally been studied in laboratory mouse models, which often exclude important variation and use unnatural host-parasite combinations. Conversely, the few wild studies of within-host interactions often lack knowledge of parasite exposure and infection history.

Loss of Microbial Topography between Oral and Nasopharyngeal Microbiota and Development of Respiratory Infections Early in Life.

The respiratory microbiota is increasingly being appreciated as an important mediator in the susceptibility to childhood respiratory tract infections (RTIs). Pathogens are presumed to originate from the nasopharyngeal ecosystem. To investigate the association between early life respiratory microbiota and development of childhood RTIs.

Antibodies and coinfection drive variation in nematode burdens in wild mice.

Coinfections with parasitic helminths and microparasites are highly common in nature and can lead to complex within-host interactions between parasite species which can cause negative health outcomes for humans, and domestic and wild animals. Many of these negative health effects worsen with increasing parasite burdens. However, even though many studies have identified several key factors that determine worm burdens across various host systems, less is known about how the immune response interacts with these factors and what the consequences are for the outcome of within-host parasite interactions.

The Immune and Non-Immune Pathways That Drive Chronic Gastrointestinal Helminth Burdens in the Wild.

Parasitic helminths are extremely resilient in their ability to maintain chronic infection burdens despite (or maybe because of) their hosts' immune response. Explaining how parasites maintain these lifelong infections, identifying the protective immune mechanisms that regulate helminth infection burdens, and designing prophylactics and therapeutics that combat helminth infection, while preserving host health requires a far better understanding of how the immune system functions in natural habitats than we have at present. It is, therefore, necessary to complement mechanistic laboratory-based studies with studies on wild populations and their natural parasite communities.

Lipopolysaccharide from Crypt-Specific Core Microbiota Modulates the Colonic Epithelial Proliferation-to-Differentiation Balance.

We identified a crypt-specific core microbiota (CSCM) dominated by strictly aerobic, nonfermentative bacteria in murine cecal and proximal colonic (PC) crypts and hypothesized that, among its possible functions, it may affect epithelial regeneration. In the present work, we isolated representative CSCM strains using selective media based upon our initial 16S rRNA-based molecular identification (i.e.

Expression of parasite genetic variation changes over the course of infection: implications of within-host dynamics for the evolution of virulence.

How infectious disease agents interact with their host changes during the course of infection and can alter the expression of disease-related traits. Yet by measuring parasite life-history traits at one or few moments during infection, studies have overlooked the impact of variable parasite growth trajectories on disease evolution. Here we show that infection-age-specific estimates of host and parasite fitness components can reveal new insight into the evolution of parasites.