BackgroundThe human gastrointestinal tract (GIT) represents one of the most densely populated microbial ecosystems studied to date. Although this microbial consortium has been recognized to have a crucial impact on human health, its precise composition is still subject to intense investigation. Among the GIT microbiota, bifidobacteria represent an important commensal group, being among the first microbial colonizers of the gut. However, the prevalence and diversity of members of the genus Bifidobacterium in the infant intestinal microbiota has not yet been fully characterized, while some inconsistencies exist in literature regarding the abundance of this genus.Methods/Principal FindingsIn the current report, we assessed the complexity of the infant intestinal bifidobacterial population by analysis of pyrosequencing data of PCR amplicons derived from two hypervariable regions of the 16 S rRNA gene. Eleven faecal samples were collected from healthy infants of different geographical origins (Italy, Spain or Ireland), feeding type (breast milk or formula) and mode of delivery (vaginal or caesarean delivery), while in four cases, faecal samples of corresponding mothers were also analyzed.ConclusionsIn contrast to several previously published culture-independent studies, our analysis revealed a predominance of bifidobacteria in the infant gut as well as a profile of co-occurrence of bifidobacterial species in the infant’s intestine.

SUMMARYThe prevalence of food allergic diseases is rising and poses an increasing clinical problem. Peanut allergy affects around 1% of the population and is a common food allergy associated with severe clinical manifestations. The exact route of primary sensitization is unknown although the gastrointestinal immune system is likely to play an important role. Exposure of the gastrointestinal tract to soluble antigens normally leads to a state of antigen-specific systemic hyporesponsiveness (oral tolerance). A deviation from this process is thought to be responsible for food-allergic diseases. In this study, we have developed a murine model to investigate immunoregulatory processes after ingestion of peanut protein and compared this to a model of oral tolerance to chicken egg ovalbumin (OVA). We demonstrate that oral tolerance induction is highly dose dependent and differs for the allergenic proteins peanut and OVA. Tolerance to peanut requires a significantly higher oral dose than tolerance to OVA. Low doses of peanut are more likely to induce oral sensitization and increased production of interleukin-4 and specific immunoglobulin E upon challenge. When tolerance is induced both T helper 1 and 2 responses are suppressed. These results show that oral tolerance to peanut can be induced experimentally but that peanut proteins have a potent sensitizing effect. This model can now be used to define regulatory mechanisms following oral exposure to allergenic proteins on local, mucosal and systemic immunity and to investigate the immunomodulating effects of non-oral routes of allergen exposure on the development of allergic sensitization to peanut and other food allergens.

The purpose of this brief communication is to highlight emerging evidence to existing guidelines regarding potential benefits of supporting early, rather than delayed, peanut introduction during the period of complementary food introduction in infants. This document should be considered as interim guidance based on consensus among the following organizations: American Academy of Allergy

The purpose of this brief communication is to highlight emerging evidence to existing guidelines regarding potential benefits of supporting early, rather than delayed, peanut introduction during the period of complementary food introduction in infants. This document should be considered as interim guidance based on consensus among the following organizations: American Academy of Allergy

OBJECTIVE.A prospective study was designed to evaluate the effects of hormone replacement therapy on mammographic density in postmenopausal women. The possible association of breast pain with increased mammographic density was evaluated. SUBJECTS AND METHODS. Thirty-three postmenopausal women undergoing hormone replacement therapy for a mean of 11 months had mammography before and after commencing treatment. As a control, 31 postmenopausal women who never had hormone therapy also had baseline and follow-up mammograms after a mean of 13 months. Subjects were asked whether breast pain, which they graded as mild, moderate, or severe, had developed since their entry into the study. Baseline and follow-up mammograms were assessed objectively and subjectively for interval changes in density. The presence of breast pain was correlated with changes in density on the mammograms.RESULTS. A subjective increase in mammographic density was seen in nine (27%) of the women taking hormones and in none of the control subjects (p = .002). Changes were focal in four, multifocal in four, and diffuse in one. An increase in density was seen with all types of treatment used, and was noted as early as 4 months after the start of treatment.Seven (78%) of nine patients with mammographic changes had breast pain, which they classed as moderate or severe, that had developed since the start of treatment. In five patients with mild or moderate breast pain, an increase in density was not shown on mammograms.Of the 21 women taking hormones who did not have breast pain, increased density on follow-up mammograms was shown in only two (p = .004). None of the patients in the control group had breast pain.CONCLUSION. Focal, multifocal, or diffuse mammographic increases in density occur in a significant percentage of women undergoing hormone replacement therapy. A large proportion of these women have breast pain. Increased mammographic density appears to be associated with breast pain in women receiving hormones. This has implications for mammography in women receiving hormone replacement therapy.