Lactobacillus delbrueckii UFV-H2b20 increases IFN-γ production and CD39+CD73+ Treg cell numbers in lungs,and protects mice against experimental allergic asthma

Asthma is a disorder characterized by airflow obstruction, inflammation, declining airway function, bronchial hyperresponsiveness and tissue remodelling. Probiotics are defined as “live microorganisms that, when administered in adequate amounts, confer a health benefit on the host”. The use of probiotics is becoming increasingly studied and recent evidence has suggested that it may provide therapeutic benefits in asthma and other diseases. Lactobacillus delbrueckii UFV-H2b20 fulfils all the requirements to be classified as probiotic. Previous studies have already shown the ability of L. delbrueckii UFV-H2b20 to stimulate the immune system. Our objective was to evaluate the protective effects of L. delbrueckii UFV-H2b20 in experimental allergic asthma. We used a murine model of ovalbumin-induced allergic airway inflammation to mimic allergic asthma. Oral treatment with L. delbrueckii UFV-H2b20 improves respiratory parameters and inhibits the inflammatory response in the lungs by decreasing the numbers of inflammatory monocytes, eosinophils and alveolar macrophages, as well as IgE levels. Treatment increased the IFN-γ/IL-4 cytokine ratio. Levels of IL-10 in the lungs were also increased in treated animals. Our results also showed that the probiotic administration increases the number of CD39⁺CD73⁺ T regulatory lymphocytes in the lung, suggesting a role for purinergic signals in the regulation of inflammation promoted by the treatment. Understanding the mechanisms of modulation of the immune system by probiotics could allow the development of probiotic preparations that are safe and have a direct action. Our results suggest that oral administration of L. delbrueckii UFV-H2b20 could be helpful to treat chronic inflammatory airway diseases, such as asthma.     

Neuro-immune crosstalk and food allergy: Focus on enteric neurons and mucosal mast cells

The nervous system and the immune system individually play important roles in regulating the processes necessary to maintain physiological homeostasis, respond to acute stress and protect against external threats. These two regulating systems for maintaining the living body had often been assumed to function independently. Allergies develop as a result of an overreaction of the immune system to substances that are relatively harmless to the body, such as food, pollen and dust mites. Therefore, it has been generally supposed that the development and pathogenesis of allergies can be explained through an immunological interpretation. Recently, however, neuro-immune crosstalk has attracted increasing attention. Consequently, it is becoming clear that there is close morphological proximity and physiological and pathophysiological interactions between neurons and immune cells in various peripheral tissues. Thus, researchers are now beginning to appreciate that neuro-immune interactions may play a role in tissue homeostasis and the pathophysiology of immune-mediated disease, but very little information is available on the molecular basis of these interactions. Mast cells are a part of the innate immune system implicated in allergic reactions and the regulation of host–pathogen interactions. Mast cells are ubiquitous in the body, and these cells are often found in close proximity to nerve fibers in various tissues, including the lamina propria of the intestine. Mast cells and neurons are thought to communicate bidirectionally to modulate neurophysiological effects and mast cell functions, which suggests that neuro-immune interactions may be involved in the pathology of allergic diseases.     

Gut microbiome alterations in patients with wheat-dependent exercise-induced anaphylaxis

The intestinal microbiota plays a critical role in food allergy development. However, little is known regarding the structure and composition of the intestinal microbiota in patients with wheat-dependent exercise-induced anaphylaxis (WDEIA). We examined the gut microbiota alterations in patients with WDEIA and the microbiota’s association with WDEIA. Fecal samples were collected from 25 patients with WDEIA and 25 healthy controls. Environmental exposure factors were obtained, serum total IgE, IgE specific to wheat, gluten, and ω-5 gliadin were measured. Fecal samples were profiled using 16S rRNA gene sequencing. The relative abundances of the bacterial genera Blautia (P < 0.05), Erysipelatoclostridium (P < 0.01), Akkermansia (P < 0.05) and Lachnospiraceae_NK4A136_group (P < 0.05) were significantly increased, while those of Lactobacillus (P = 0.001) and Dialister (P < 0.05) were significantly decreased in subjects with WDEIA. The microbial diversity did not differ between WDEIA patients and healthy controls. IgE specific to ω-5 gliadin was positively associated with the Oscillospira (r = 0.48, P < 0.05) and negatively associated with Leuconostoc (r = −0.49, P < 0.05). Total IgE levels were significantly negatively correlated with Bifidobacterium (P < 0.05). The gut microbiome compositions in WDEIA patients differed from those of healthy controls. We identified a potential association between the gut microbiome and WDEIA development. Our findings may suggest new methods for preventing and treating WDEIA.