The effect of short term microbial exposure and diversity on allergy, and how FcεRI expression on inflammatory cells modulates asthma

Abstract

This editorial introduces a new issue of Pediatric Allergy and Immunology. This issue reflects the extensive work provided by researchers and clinicians, and the whole editorial team and the reviewers. Altogether, they aim to provide the best of research and education in our field. Here, I have made a personal selection of articles I would like to introduce to you. The issues always start with an educational review, and this month Erik Melén and colleagues link asthma, most prevalent in allergic children, with chronic obstructive pulmonary disease, a disease better known to physicians treating adults.1 When reading this contribution, I realized again how important it is to define risk factors in children. This helps prevent progression of a disease most often considered as benign when well controlled in childhood, to a devastating chronic lung disease in adults. From the section on original research articles, I first selected the study published by Eila Kujansuu et al.2 They took advantage of an unusual event, an accidental mixing of sewage water with drinking water in Nokia Finland, and they hypothesized that according to the “hygiene hypothesis,” this short‐term exposure to water contaminated with bacte‐ ria could influence the emergence of sensitization and allergies in children. Over 100 exposed children were assessed for allergies and skin tested 2 to 5 years later, and compared to age‐matched, non‐exposed controls. The study showed that in particular children below 1 year of age at the time of the contamination, and children who suffered from gas‐ troenteritis at exposure, had lower skin test reactivity. This study suggests that a very short oral exposure to a high microbial load may influence sensitization later in life. Earlier studies published in PAI have also shown a protection by microbial exposure. The most studied type of exposure has been by living in a farming environment,3,4 although other environmental factors such as pollution may also intervene.5 While most studies such as the one commented on here are focusing on bacterial exposure, studies published in PAI have also highlighted that other microorganisms, such as fungi, can also modulate the immune system.6 My second selection is the article by Jennifer Wing‐Ki Yau and colleagues.7 This research group from Singapore has investigated the bacterial microbiome of the nose and the eye in relation to allergic rhinitis and conjunctivitis (ARC). The originality of this publication is largely related to the sample sites, the eyes, and the nose. Indeed, the gut microbiome has been the target of most studies in relation to allergies.8 Nevertheless, recent studies pub‐ lished in PAI have also investigated the microbiome of other sites such as the skin,9 or the airways.10 As relevant findings, Yau et al report a larger nasal microbial diversity in ARC patients than in controls, which was not seen for the ocular microbiome. This observation highlights the difference in terms of microbial diversity of the bacterial flora between these two very close sites. However, authors suggest an interaction of the microbiome of the nose and the eyes, as the microbial composition tends to become more similar in terms of bacterial communities in ARC patients when compared to healthy controls. This study with a relatively low number of patients opens a large field for future investigations in relation to local microbial flora and allergic diseases. The third highlighted contribution in this issue addresses asthma and atopy in school‐age children in relation to FcεRI expression on circulating cells. A research group from Western Australia with Jonatan Leffler as the first author has col‐ lected peripheral blood from 391 asthmatic children recruited in four cohorts and isolated for further studies basophils, monocytes, and various types of dendritic cells.11 FACS analysis defined cell types in relation to the expression of the IgE high‐affinity receptor FcεRI. In summary, they could show upregulated expression of FcεRI on both effector (baso‐ phil) and regulatory (myeloid, and especially various types of dendritic cells) populations, and that this upregulation was associated with current atopic asthma. The authors also suggest that FcεRI expression may be used to identify children with maximal susceptibility to allergic asthma and thus identify those who may benefit the most from intervention ther‐ apies targeting Th2‐mediated inflammation, such as with biologic agents.12 This publication adds additional insights into the mechanisms of asthma. Readers with a special research interest in the field might also refer to these recent original publications in PAI 13‐15 or to a recent review on oxidative stress and asthma.16 Eila Kujansuu