Tag: immune

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Baby’s Immune System Suffers With Maternal Obesity; Risks Rise For Asthma … – Medical Daily


Medical Daily

Baby's Immune System Suffers With Maternal Obesity; Risks Rise For Asthma …
Medical Daily
These results support the hypothesis that maternal obesity influences programming of the neonatal immune system, providing a potential link to increased incidence of chronic inflammatory diseases such as asthma and cardiovascular disease in the offspring.
Maternal obesity linked to reduced immunity in newborns that may last a lifetimeMedical News Today
Maternal Obesity May Harm Babies' Immune SystemNature World News
Obese Mothers Have Babies With Immune Systems Weakened Before Birth …International Business Times
UCR Today (press release)
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Breastfeeding Babies Influences Their Immune System And Susceptibility To … – Tech Times


The Inquisitr

Breastfeeding Babies Influences Their Immune System And Susceptibility To …
Tech Times
Mothers who breastfeed babies in the first month are helping influence the nature of bacteria in the infant's digestive system, which in turn boosts the immune system to provide protection against conditions like allergies or asthma, researchers say …
Breastfeeding Puts Children At Lower Risk For Allergies And Asthma, Says New …The Inquisitr
Breastfeeding Benefits Babies' Immune Systems Within First Month; Provides …Medical Daily
Research links infants' microbiome to development of immune system, allergic …Your Houston News
Medical News Today –Yumanewsnow
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Immune system research also may help reveal new asthma clues – Medical Xpress


Medical Xpress

Immune system research also may help reveal new asthma clues
Medical Xpress
New knowledge about the immune system may lead to better understanding of asthma and how best to treat it. A new method of developing vaccines could point the way forward in the fight against infectious diseases for which traditional vaccination has …
Developing Lifesaving Vaccines in a New WayNews from Rutgers

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IL-33 and Thymic Stromal Lymphopoietin Mediate Immune Pathology in Response to Chronic Airborne Allergen Exposure.

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IL-33 and Thymic Stromal Lymphopoietin Mediate Immune Pathology in Response to Chronic Airborne Allergen Exposure.

J Immunol. 2014 Jul 11;

Authors: Iijima K, Kobayashi T, Hara K, Kephart GM, Ziegler SF, McKenzie AN, Kita H

Abstract
Humans are frequently exposed to various airborne allergens in the atmospheric environment. These allergens may trigger a complex network of immune responses in the airways, resulting in asthma and other chronic airway diseases. In this study, we investigated the immunological mechanisms involved in the pathological changes induced by chronic exposure to multiple airborne allergens. Naive mice were exposed intranasally to a combination of common airborne allergens, including the house dust mite, Alternaria, and Aspergillus, for up to 8 wk. These allergens acted synergistically and induced robust eosinophilic airway inflammation, specific IgE Ab production, type 2 cytokine response, and airway hyperresponsiveness in 4 wk, followed by airway remodeling in 8 wk. Increased lung infiltration of T cells, B cells, and type 2 innate lymphoid cells was observed. CD4(+) T cells and type 2 innate lymphoid cells contributed to the sources of IL-5 and IL-13, suggesting involvement of both innate and adaptive immunity in this model. The lung levels of IL-33 increased quickly within several hours after allergen exposure and continued to rise throughout the chronic phase of inflammation. Mice deficient in IL-33R (Il1rl1(-/-)) and thymic stromal lymphopoietin receptor (Tslpr(-/-)) showed significant reduction in airway inflammation, IgE Ab levels, and airway hyperresponsiveness. In contrast, mice deficient in IL-25R or IL-1R showed minimal differences as compared with wild-type animals. Thus, chronic exposure to natural airborne allergens triggers a network of innate and adaptive type 2 immune responses and airway pathology, and IL-33 and thymic stromal lymphopoietin most likely play key roles in this process.

PMID: 25015831 [PubMed – as supplied by publisher]

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The role of gut microbiota in programming the immune phenotype.

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The role of gut microbiota in programming the immune phenotype.

J Dev Orig Health Dis. 2013 Jun 1;4(3)

Authors: Weng M, Walker WA

Abstract
The human fetus lives in a germ-free intrauterine environment and enters the outside world containing microorganisms from several sources, resulting in gut colonization. Full-term, vaginally born infants are completely colonized with a diverse array of bacterial families in clusters (Phyla) and species (>1000) by the first year of life. Colonizing bacteria communicating with the gut epithelium and underlying lymphoid tissues (‘bacterial-epithelial crosstalk’) result in a functional immune phenotype and no expression of disease (immune homeostasis). Appropriate colonization is influenced by the prebiotic effect of breast milk oligosaccharides. Adequate colonization results in an innate and adaptive mucosal immune phenotype via communication between molecular patterns on colonizing bacteria and pattern-recognition receptors (e.g., toll-like receptors) on epithelial and lymphoid cells. This ontogeny affects the immune system’s capacity to develop oral tolerance to innocuous bacteria and benign antigens. Inadequate intestinal colonization with premature delivery, delivery by Cesarean section and excessive use of perinatal antibiotics results in the absence of adequate bacterial-epithelial crosstalk and an increased incidence of immune-mediated diseases [e.g., asthma, allergy in general and necrotizing enterocolitis (NEC)]. Fortunately, infants with inadequate intestinal colonization can be restored to a bacterial balance with the intake of probiotics. This has been shown to prevent debilitating diseases such as NEC. Thus, understanding the role of gut microbiota in programming of the immune phenotype may be important in preventing disease expression in later childhood and adulthood.

PMID: 24353893 [PubMed – as supplied by publisher]

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Hay Fever and Asthma as Markers of Atopic Immune Response and Risk of Colorectal Cancer in Three Large Cohort Studies.

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Hay Fever and Asthma as Markers of Atopic Immune Response and Risk of Colorectal Cancer in Three Large Cohort Studies.

Cancer Epidemiol Biomarkers Prev. 2013 Mar 19;

Authors: Jacobs EJ, Gapstur SM, Newton CC, Turner MC, Campbell PT

Abstract
BACKGROUND: In a previous analysis of 12 cancers in the Cancer Prevention Study II (CPS-II) cohort including follow-up from 1982-2000, having both hay fever and asthma was associated with lower colorectal cancer mortality. The combination of these allergic conditions may be a marker for allergy-related immune responses that could inhibit colorectal carcinogenesis.METHODS: We examined the association of having both hay fever and asthma with colorectal cancer mortality among 1,023,191 participants in CPS-I, followed from 1959-1972, and 1,102,092 participants in CPS-II, now followed from 1982-2008. We also examined associations with colorectal cancer incidence among 174,917 participants in the CPS-II Nutrition Cohort, a subgroup of CPS-II followed from 1992-2007. During the follow-up, there were 5,644 colorectal cancer deaths in CPS-I, 13,558 colorectal cancer deaths in CPS-II, and 3,365 incident colorectal cancer cases in the CPS-II Nutrition Cohort. Cox proportional hazards regression was used to calculate multivariable-adjusted relative risks (RR) and 95% confidence intervals (CI).RESULTS: RRs for colorectal cancer mortality associated with having both asthma and hay fever, compared with neither condition, were 0.90 (95% CI, 0.74-1.09) in CPS-I, 0.79 (95% CI, 0.69-0.91) in CPS-II, and 0.83 (95% CI, 0.74-0.92) when results from both cohorts were combined in a meta-analysis. The corresponding RR for colorectal cancer incidence in the CPS-II Nutrition Cohort was 0.90 (95% CI, 0.71-1.14).CONCLUSION: These results support an association between having both hay fever and asthma and modestly lower colorectal cancer mortality.Impact: Research examining other potential markers of allergy-related immune response in relation to colorectal cancer is warranted. Cancer Epidemiol Biomarkers Prev; 22(4); 1-9. ©2013 AACR.

PMID: 23513040 [PubMed – as supplied by publisher]

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