Respiratory pathogens encounter various lines of defenses before infection of the host is established. The innate immune response represents an important first-line protection mechanism against potentially pathogenic microorganisms during early stages of infection of the naive host. Important players in this host defense system are ‘collectins’, a class of soluble innate immune proteins. Well-characterized members of the collectin family are the surfactant proteins A (SP-A) and D (SP-D). These collectins are expressed in the lung and also in extrapulmonary mucosal tissues. Collectins are secreted as multimers resulting in trimeric clustering of the lectin domains which enables recognition of evolutionary conserved sugar patterns present on the surface of a large variety of pathogens. Binding to collectins may lead to direct agglutination and neutralization of pathogens, to opsonization in order to present bound microbes directly to phagocytes, to modulation of the inflammatory response and to regulation of dendritic cell and T cell functions. In pulmonary tissue, this early acute-phase-like response can be regarded as a crucial layer of protection against a vast array of pathogens that escape the physical barriers and threaten to infect the delicate respiratory epithelium. An important clinical application may be the inhalation, or instillation of collectin-based drugs as part of surfactant therapy, to prevent and treat infectious and inflammatory diseases of newborn infants.

In the yeast Saccharomyces cerevisiae, hexose transporter (Hxt) proteins transport glucose across the plasma membrane. The Hxt proteins are encoded by a multigene family with 20 members, of which Hxt1-4p and Hxt6-7p are the major hexose transporters. The remaining Hxt proteins have other or unknown functions. In this study, expression of HXT5 under different experimental set-ups is determined. In glucose-grown batch cultures, HXT5 is expressed prior to glucose depletion. Independent of the carbon source used in batch cultures, HXT5 is expressed after 24 h of growth and during growth on ethanol or glycerol, which indicates that growth on glucose is not necessary for expression of HXT5. Increasing the temperature or osmolarity of the growth medium also induces expression of HXT5. In fed-batch cultures, expression of HXT5 is only observed at low glucose consumption rates, independent of the extracellular glucose concentration. The only common parameter in these experiments is that an increase of HXT5 expression is accompanied by a decrease of the growth rate of cells. To determine whether HXT5 expression is determined by the growth rate, cells were grown in a nitrogen-limited continuous culture, which enables modulation of only the growth rate of cells. Indeed, HXT5 is expressed only at low dilution rates. Therefore, our results indicate that expression of HXT5 is regulated by growth rates of cells, rather than by extracellular glucose concentrations, as is the case for the major HXTs. A possible function for Hxt5p and factors responsible for increased expression of HXT5 upon low growth rates is discussed.

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These data show impaired sensitization in offspring of scGOS/lcFOS/pAOS-supplemented mice. A number of the analyzed variables are differentially affected by whether supplementation occurs during pregnancy or lactation, and the outcome of dietary supplementation is affected by whether the mother has been sensitized to ovalbumin and CT.

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Maternal supplementation of mice with scGOS/lcFOS during pregnancy leads to a significant decrease in allergic symptoms in the offspring.

Autism spectrum disorder (ASD) is a range of neurodevelopmental conditions that affect communication and social behavior. Besides social deficits, systemic inflammation, gastrointestinal immune-related problems, and changes in the gut microbiota composition are characteristic for people with ASD. Animal models showed that these characteristics can induce ASD-associated behavior, suggesting an intimate relationship between the microbiota, gut, immune system and the brain in ASD. Multiple factors can contribute to the development of ASD, but mutations leading to enhanced activation of the mammalian target of rapamycin (mTOR) are reported frequently. Hyperactivation of mTOR leads to deficits in the communication between neurons in the brain and to immune impairments. Hence, mTOR might be a critical factor linking the gut-brain-immune axis in ASD. Pharmacological inhibition of mTOR is shown to improve ASD-associated behavior and immune functions, however, the clinical use is limited due to severe side reactions. Interestingly, studies have shown that mTOR activation can also be modified by nutritional stimuli, in particular by amino acids. Moreover, specific amino acids are demonstrated to inhibit inflammation, improve gut barrier function and to modify the microbiota composition. In this review we will discuss the gut-brain-immune axis in ASD and explore the potential of amino acids as a treatment option for ASD, either via modification of mTOR activity, the immune system or the gut microbiota composition.

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