Bifidobacterium breve (B. breve) may have a beneficial effect on allergic rhinitis (AR). The aim of the present study was to investigate whether microbial induction of regulatory T cells (Tregs) and adjustment of Th1 and Th2 responses by B. breve are associated with protection against allergic inflammation, and to identify a dose-response association in a murine AR model. Ovalbumin (OVA)-sensitized BALB/c mice were orally treated with different doses of B. breve [1010, 109, 107 and 105 colony forming units (CFU)]. Following nasal challenge with OVA, sneeze frequency, serum OVA-specific immunoglobulin E (IgE) and cytokine concentrations [interleukin (IL)-4, IL-10, IL-13 and interferon-γ], splenic percentage of cluster of differentiation (CD)4+CD25+ Tregs, and morphology of the nasal mucosa were examined. Oral treatment with live B. breve at doses of 107 CFU or higher alleviated nasal mucosal injury and suppressed sneezing upon repeated administration over a 6-week period. Furthermore, treatment with B. breve at these higher doses reduced the concentrations of serum OVA-specific IgE, IL-4 and IL-10, and increased the splenic percentage of CD4+CD25+ Tregs in rhinitic mice compared with those who did not receive probiotics. In contrast, treatment with B. breve at a lower dose did not indicate any effect on sneezing frequency or mucosal morphology in this animal model, even though the splenic percentage of CD4+CD25+ Tregs increased and the concentrations of serum OVA-specific IgE and IL-10 declined. B. breve exerts its anti-allergic effects by inhibiting type 2 helper T cell immune responses and enhancing CD4+CD25+ Treg activity. Sneezing was also reduced at a dose of 107 CFU or higher. The current study investigated the role of B. breve and aided in identifying the optimal dose of B. breve administration in the treatment of AR.

Lycium barbarum polysaccharide (LBP) has a variety of pharmacological and biological activities such as anti-inflammatory, antioxidation, anti-apoptosis, immune regulation and other pharmacological effects; however, the effect of LBP on infantile hemangioma (IH) was less reported. Primary human hemangioma endothelial cells (HemECs) were isolated from fresh surgical specimens of patients. HemECs was treated with LBP and the changes in proliferative and apoptotic signaling pathways were investigated by performing cell counting kit-8, cloning formation experiment, in vitro angiogenesis experiment, flow cytometry, Western blot, immunofluorescence, HE stain and real-time quantitative polymerase chain reaction. We found that LBP potently inhibited the proliferation of HemECs and achieved a low-micromolar IC50 (45 and 40 μg/ml, the half maximal inhibitory concentration) value and less angiogenesis, however, the IC50 had no effect on human umbilical vein endothelial cells (HUVECs) viability. LBP treatment induced apoptosis in HemECs, which was supported by positive Annexin-V-FITC staining, the activation of cleaved caspase-3 and Bcl-2-associated X protein (Bax) and the inhibition of B-cell lymphoma/leukemia-2 (Bcl-2). Moreover, the result demonstrated that LBP suppressed the expressions of proliferating cell nuclear antigen (PCNA), Ki67, vascular endothelial growth factor (VEGF), VEGFR2 and phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signal pathway. PI3K-specific agonist (IGF-1) had promotive effects on HemECs proliferation, which was reversed by LBP. Our study suggests that the effectiveness of LBP in IHs may be associated with its potent anti-proliferative and apoptotic activities in HemECs. Thus, our findings may provide an effective medicine for IHs treatment.