Transcriptomic Response in the Spleen after Whole-Body Low-Dose X-Ray Irradiation.

As the use of medical radiation procedures continues to rise, it is imperative to further our understanding of the effects of this exposure. The spleen is not known as a particularly radiosensitive organ, although its tolerance to radiation is not well understood. Low-dose radiation exposure has been implicated in beneficial responses, particularly in cell death and DNA damage repair. In this study, adult male rats received 2, 20, 200 mGy or 4 Gy whole-body X-ray irradiation and the transcriptional response in the spleen was analyzed at 0.5, 4 and 24 h postirradiation. We analyzed expression of genes involved in apoptosis, cell cycle progression and DNA damage repair. As expected, 4 Gy irradiated animals demonstrated elevated expression of genes related to apoptosis at 0.5, 4 and 24 h postirradiation in the spleen. These animals also showed upregulation of DNA damage repair genes at 24 h postirradiation. Interestingly, the spleens of 20 mGy irradiated animals showed reduced apoptosis and cell cycle arrest compared to the spleens of sham-irradiated animals. These results further reveal that the cellular response in the spleen to whole-body irradiation differs between low- and high-dose irradiation.

Leukocytes in expressed breast milk of asthmatic mothers

Objective: Infants are born immunologically immature. However, breastfeeding mothers retain an immunological link to their infants. While it is generally accepted that infants are at an immunological advantage when compared with formula-fed infants, the benefit of long-term exclusive breastfeeding by atopic mothers remains controversial. Inconsistency in the conferral of benefit may be due to differences in the immunological constituents passed to the recipient infant. The aim of this investigation was to examine the profile of human milk cells and cytokines from asthmatic compared to non-asthmatic mothers. Methods: Twenty-five exclusively breastfeeding mothers with a clinical diagnosis of asthma were postpartum age matched in a double-control 2:1 design with 50 non-asthmatic controls. Each mother provided a single milk sample which was assayed for cell differential by flow cytometry, for ex vivo cytokine production in culture and for aqueous phase cytokines. Results: Milks from asthmatic mothers differed from non-asthmatics in that they contained a higher proportion of polymorphonuclear (PMN) cells and lower proportion of lymphocytes, predominantly CD3+/CD4+ T helper cells, reflected by a decrease in the chemokine CCL5 in the milk aqueous phase. More PMN and lymphocytes from asthmatic mothers expressed the adhesion molecule CD11b and lymphocytes the IgE receptor CD23, than those from non-asthmatic mothers. Conclusions: Changes to human milk leucocyte prevalence, activation state and cytokines due to maternal asthma may result in changes to immunological priming in the infant. Consequently, the protective effect of long-term breastfeeding may be altered in these mother-infant pairs (AU)

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Leukocytes in expressed breast milk of asthmatic mothers.

OBJECTIVE: Infants are born immunologically immature. However, breastfeeding mothers retain an immunological link to their infants. While it is generally accepted that infants are at an immunological advantage when compared with formula-fed infants, the benefit of long-term exclusive breastfeeding by atopic mothers remains controversial. Inconsistency in the conferral of benefit may be due to differences in the immunological constituents passed to the recipient infant. The aim of this investigation was to examine the profile of human milk cells and cytokines from asthmatic compared to non-asthmatic mothers. METHODS: Twenty-five exclusively breastfeeding mothers with a clinical diagnosis of asthma were postpartum age matched in a double-control 2:1 design with 50 non-asthmatic controls. Each mother provided a single milk sample which was assayed for cell differential by flow cytometry, for ex vivo cytokine production in culture and for aqueous phase cytokines. RESULTS: Milks from asthmatic mothers differed from non-asthmatics in that they contained a higher proportion of polymorphonuclear (PMN) cells and lower proportion of lymphocytes, predominantly CD3+/CD4+ T helper cells, reflected by a decrease in the chemokine CCL5 in the milk aqueous phase. More PMN and lymphocytes from asthmatic mothers expressed the adhesion molecule CD11b and lymphocytes the IgE receptor CD23, than those from non-asthmatic mothers. CONCLUSIONS: Changes to human milk leucocyte prevalence, activation state and cytokines due to maternal asthma may result in changes to immunological priming in the infant. Consequently, the protective effect of long-term breastfeeding may be altered in these mother-infant pairs.