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  • Although the presence of histamine secreting bacteria has be

    2022-05-17

    Although the presence of histamine-secreting bacteria has been well documented in foods, their presence within the human gut microbiota has not been investigated in detail. We recently performed an analysis of fecal samples from 161 volunteers to quantify the presence of bacterial HDC, using primers that do not amplify human HDC. Microbial-specific HDC was detected in all fecal samples, however a wide inter-individual range was evident []. Interestingly, bacterial HDC gene levels were significantly elevated in adult patients with gonadotropin releasing hormone agonist compared to healthy controls. In addition, non-obese patients with asthma had the highest level of the bacterial HDC gene compared with obese patients with asthma. The difference in HDC positive bacteria between obese and non-obese asthma patients suggests that factors other than histamine secretion by microbes in the gut may be more important for the development of asthma in obese patients. The bacteria isolated from these fecal samples, which were able to secrete the highest levels of histamine, belong to E. coli, M. morganii and L. vaginalis species []. The level of histamine secretion depended on the strain and in vitro culture conditions that were used (e.g. pH and culture media composition). Of note, E. coli and M. morganii were commonly reported to be the causative isolates associated with cases of HFP. Intriguingly, increased levels of M. morganii were positively associated with more severe asthma symptoms. Based on these observations, one might speculate that increased levels of bacterial-derived histamine in certain adult asthma patients may contribute to histamine-mediated pathologies due to a higher systemic level of histamine, which then reduces the level required for host-derived histamine to drive allergic responses following allergen exposure. However, this hypothesis remains unproven. In addition, certain bacterial strains can degrade histamine and it is currently unknown if the levels of these bacteria are altered in inflammatory disorders such as asthma [42].
    Immune regulation by histamine-secreting bacteria Given the potent immunological effects associated with histamine signalling, it is not surprising that histamine from the microbiota may also influence immune responses. In vitro, culture supernatants from histamine-secreting bacteria were able to stimulate CHO cells, which possessed a H1R reporter. Specific activation of the H1R by bacterial-derived histamine was confirmed as activity was blocked using the H1R antagonist diphenhydramine []. In addition, Lactobacillus reuteri-derived histamine was shown to inhibit TLR-induced TNF-α production by human monocytoid cells via signalling through the H2R and downstream cAMP and PKA activity [43]. In murine models, it was recently shown that gut microbiota-derived histamine influences host–microbiome homeostasis via epithelial IL-18 secretion, co-modulating NLRP6 inflammasome signalling and downstream anti-microbial peptide secretion []. Administration of the histamine-secreting Lactobacillus strain 30A to mice resulted in rapid weight loss and reduced Peyer's patch cytokine secretion [45]. However, weight loss was exaggerated in H2R-deficient mice and IL-4, IL-6, and IL-17 secretion by Peyer's patches was increased, an opposite result to that observed for wild-type animals. This data suggests that histamine-derived from gut microbes can have immunological effects within the mucosa, but the nature of these effects is determined by the histamine receptor that is triggered. In a separate study, the suppression of intestinal inflammation by a Lactobacillus reuteri strain was shown to be dependent on histamine secretion by the bacterium and its activation of H2R [].
    Conclusions
    Conflict of interest
    References and recommended reading Papers of particular interest, published within the period of review, have been highlighted as:
    Acknowledgements The authors are supported by Swiss National Science Foundation grants (project numbers CRSII3_154488, 310030_144219 and 310030-127356) and Christine Kühne – Center for Allergy Research and Education (CK-CARE).