25-hydroxycholecalciferol reverses heat induced alterations in bone quality in finisher broilers associated with effects on intestinal integrity and inflammation

Background Alterations in ambient temperature have been associated with multiple detrimental effects on broilers such as intestinal barrier disruption and dysbiosis resulting in systemic inflammation. Inflammation and 25-hydroxycholecalciferol (25-OH-D3) have shown to play a negative and positive role, respectively, in the regulation of bone mass. Hence the potential of 25-OH-D3 in alleviating heat induced bone alterations and its mechanisms was studied. Results Heat stress (HS) directly induced a decrease in tibia material properties and bone mass, as demonstrated by lower mineral content, and HS caused a notable increase in intestinal permeability. Treatment with dietary 25-OH-D3 reversed the HS-induced bone loss and barrier leak. Broilers suffering from HS exhibited dysbiosis and increased expression of inflammatory cytokines in the ileum and bone marrow, as well as increased osteoclast number and activity. The changes were prevented by dietary 25-OH-D3 administration. Specifically, dietary 25-OH-D3 addition decreased abundance of B- and T-cells in blood, and the expression of inflammatory cytokines, especially TNF-α, in both the ileum and bone marrow, but did not alter the diversity and population or composition of major bacterial phyla. With regard to bone remodeling, dietary 25-OH-D3 supplementation was linked to a decrease in serum C-terminal cross-linked telopeptide of type I collagen reflecting bone resorption and a concomitant decrement in osteoclast-specific marker genes expression (e.g. cathepsin K), whereas it did not apparently change serum bone formation markers during HS. Conclusions These data underscore the damage of HS to intestinal integrity and bone health, as well as that dietary 25-OH-D3 supplementation was identified as a potential therapy for preventing these adverse effects.

RELATION BETWEEN BACTERIAL COLONIZATION IN LUNGS AND LEVELS OF 25-HYDROXYVITAMIN D AND ANTIMICROBIAL PEPTIDE LL-37 IN CHILDREN WITH CYSTIC FIBROSIS

The aim of the study was to assess the bacterial colonization in lungs of children with cystic fibrosis based on the antimicrobial peptide cathelicidin and 25-hydroxycholecalciferol in the serum. Study showed significant correlation between P. aeruginosa infection and cathelicidin and 25-hydroxycholecalciferol levels.

Differential Modulation of 25-hydroxycholecalciferol on Innate Immunity of Broiler Breeder Hens

Past immunological studies in broilers focused on juveniles within the rapid pre-slaughter growth period and may not reflect adult immune responses, particularly in breeders managed with chronic feed restriction (R). The study aimed to assess innate immune cell functions in respect to R vs. ad libitum (Ad) feed intake in breeder hens with and without dietary 25-hydroxycholecalciferol (25-OH-D3) supplementation. Ad-feed intake consistently suppressed IL-1β secretion, respiratory burst, and cell livability in peripheral heterophils and/or monocytes along the feeding trial from the age of 51 to 68 weeks. Supplemental 25-OH-D3 repressed IL-1β secretion and respiratory burst of both cells mostly in R-hens, but promoted monocyte phagocytosis, chemotaxis, and bacterial killing activity in Ad-hens in accompany with relieved hyperglycemia, hyperlipidemia, and systemic inflammation. Overnight cultures with leukocytes from R-hens confirmed the differential effects of 25-OH-D3 to rescue immune functions altered by glucose and/or palmitic acid exposure. Studies with specific inhibitors further manifested the operative mechanisms via glucolipotoxicity in a cell type- and function-dependent manner. The results concluded no predominant changes between R- vs. Ad-feed intake on leukocyte defense against pathogens despite some differential differences, but supplemental 25-OH-D3 exerts more pronounced effects in Ad-hens.

25 hydroxycholicalciferol levels during Pregnancy in Rural and Urban Population of South India

Maternal 25 dihydroxycholecalciferol is the storage form the vitamin D. It gets activated to 1,25, Dihydroxycholecalciferol (vitamin D3) in the kidneys. Pregnancy increases requirement for the vitamin D3. The 1,25 dihydroxycholecalciferol is produced by the fetal kidneys from maternal sources of 25 dihydroxycholecalciferol. Vitamin D3 is essential for intestinal calcium absorption and bone mineralization in fetus.104 venous blood samples were used to study 25 hydroxycholecalciferol and serum calcium levels. Experimental group involved venous blood samples from 100 ANC between 20-40 years. In the first trimester rural ANC cases had an average 25 hydroxycholecalciferol level of 50.9ng/ml. In Urban participants the average was 31.6nmol/L. Second Trimester ANC in rural sector had an average of 54nmol/L and in urban average was 45nmol/L. In third trimester rural participants had an average of 61nmol/L, urban participants had 28nmol/L. The urban participants in all the three trimesters had 25 hydroxycholecalciferol insufficiency. 25 hydroxycholecalciferol deficiency is higher percentage in first trimester, gradually reduces in second trimester and reaches towards normal limits in third trimester. The placental secretion compensates for the homeostasis and maintenance of normal calcium levels and during third trimester. Active fetal bone mineralization occurs in third trimester.