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Dysbiosis refers to a reduction in microbial diversity, combined with a loss of beneficial taxa, and an increase in pathogenic microorganisms. Dysbiosis of the intestinal microbiota can have a substantial effect on the nervous and immune systems, contributing to the onset of several inflammatory diseases.

Incomplete maturation of immune regulatory functions at birth is antecedent to the heightened risk for severe respiratory infections during infancy. Our forerunner animal model studies demonstrated that maternal treatment with the microbial-derived immune training agent OM-85 during pregnancy promotes accelerated postnatal maturation of mechanisms that regulate inflammatory processes in the offspring airways.

Our results suggest that reciprocal influences between alpha1-adrenoceptors and inflammatory cytokines may play a role in normal inflammatory responses

We have demonstrated that a single dose of a closely related commensal can delay onset of NTHi otitis media in vivo

The expression pattern of FcεRI on DC and basophils differentiates asthmatic from non-asthmatic atopic children

Dysregulated expression of IFN-dependent pathways after respiratory viral infections is a defining immunophenotypic feature of AVB-susceptible infants

Pregnancy is associated with an alternatively activated phenotype of alveolar macrophage before infection

This protocol adapted an experimental animal model of disease for sensitization to ovalbumin during the immediate post-weaning period beginning at 21 days of age

Our findings suggest that the proportion of degranulated basophils can also be associated with recurrent exacerbations

The co-exposure responses in the Th2high BN incorporated type I interferon/Th1, alternative macrophage activation/Th2 and Th17 signatures