Effects of blood pathological changes before TAI on pregnancy of dairy cows with anestrus and estrus / [Efeitos de mudanças patológicas de plasma antes de (TAI) na gestação de vacas em anestro e estro]

The objective of this study was to investigate the influence of plasma pathological changes before timed artificial insemination (TAI) on pregnancy of cows. The contents of estrogen (E2), progesterone (P4), glucose (Glu), selenium (Se), brain-derived neurotrophic factor (BDNF), and histamine (HIS) in plasma of 48 Holstein cows were measured before TAI. According to the estrus detection, the cows were divided into estrus (E) and anestrus (A) groups. After pregnancy testing at 28 d after TAI, two groups of E and A were divided into positive pregnancy of E group (EP+), negative pregnancy of E group (EP-), positive pregnancy of A group (AP+), and negative pregnancy of A group (AP-). The contents of E2, P4, Glu, Se, BDNF and hIS significantly differed among the four groups (P<0.01). The ROC analysis was used to determine the risk of negative pregnancy test (-) after TAI was increased when plasma E2 was less than 46.45 pmol/L in cows before TAI. The changes in E2, P4,hIS, Glu, and BDNF in the blood of natural estrus and natural anestrus cows affected the pregnancy after TAI. the level of E2 in plasma may be used to assess the risk of negative pregnancy after TAI.(AU)

O objetivo do presente estudo foi investigar a influência de mudanças patológicas de plasma antes de inseminação artificial (TAI) na gestação de vacas. O conteúdo de estrogênio (E2), progesterona (P4), glucose (Glu), selênio (Se), fator neurotrófico derivado do cérebro (BDNF), e histamina (HIS) no plasma de 48 vacas Holstein foi medido antes de TAI. De acordo com a detecção de estro, as vacas foram divididas em dois grupos: estro (E) e anestro (A). Após teste de gestação 28 d após TAI, dois grupos de E e A foram formados em gestação positiva do grupo E (EP+), gestação negativa do grupo E (EP-), gestação positiva do grupo A (AP+), e gestação negativa do grupo A (AP-). Os valores de E2, P4, Glu, Se, BDNF e hIS foram significativamente diferentes entre os quatro grupos (P<0,01). A análise ROC foi utilizada para determinar o risco de teste de gestação negativo (-) após aumento de TAI quando plasma E2 estava abaixo de 46,45 pmol/L em vacas antes de TAI. Alterações em E2, P4,hIS, Glu e BDNF no sangue de estro natural e anestro natural em vacas afetou a gestação após TAI. O nível de E2 no plasma pode ser usado para avaliar o risco de gestação negativa após TAI.(AU)

15-Lipoxygenase 1 in nasal polyps promotes CCL26/eotaxin 3 expression through extracellular signal-regulated kinase activation.

BACKGROUND: 15-Lipoxygenase 1 (15LO1) is expressed in airway epithelial cells in patients with type 2-high asthma in association with eosinophilia. Chronic rhinosinusitis with nasal polyps (CRSwNP) is also associated with type 2 inflammation and eosinophilia. CCL26/eotaxin 3 has been reported to be regulated by 15LO1 in lower airway epithelial cells. However, its relation to 15LO1 in patients with CRSwNP or mechanisms for its activation are unclear. OBJECTIVE: We sought to evaluate 15LO1 and CCL26 expression in nasal epithelial cells (NECs) from patients with CRSwNP and healthy control subjects (HCs) and determine whether 15LO1 regulates CCL26 in NECs through extracellular signal-regulated kinase (ERK) activation. METHODS: 15LO1, CCL26, and phosphorylated ERK were evaluated in NECs from patients with CRSwNP and HCs. 15LO1/CCL26 and CCL26/cytokeratin 5 were colocalized by means of immunofluorescence. IL-13-stimulated NECs were cultured at an air-liquid interface with or without 15-lipoxygenase 1 gene (ALOX15) Dicer-substrate short interfering RNAs (DsiRNA) transfection, a specific 15LO1 enzymatic inhibitor, and 2 ERK inhibitors. Expression of 15LO1 and CCL26 mRNA and protein was analyzed by using quantitative RT-PCR, Western blotting, and ELISA. RESULTS: 15LO1 expression was increased in nasal polyp (NP) epithelial cells compared with middle turbinate epithelial cells from patients with CRSwNP and HCs. 15LO1 expression correlated with CCL26 expression and colocalized with CCL26 expression in basal cells of the middle turbinate and NPs from patients with CRSwNP. In primary NECs in vitro, IL-13 induced 15LO1 and CCL26 expression. 15LO1 knockdown and inhibition decreased IL-13-induced ERK phosphorylation and CCL26 expression. ERK inhibition (alone) similarly decreased IL-13-induced CCL26. Phosphorylated ERK expression was increased in NECs from CRSwNP subjects and positively correlated with both 15LO1 and CCL26 expression. CONCLUSIONS: 15LO1 expression is increased in NP epithelial cells and contributes to CCL26 expression through ERK activation. 15LO1 could be considered a novel therapeutic target for CRSwNP.