Vitamin A deficiency and vitamin A supplementation affect innate and T cell immune responses to rotavirus A infection in a conventional sow model.
Vitamin A deficiency and vitamin A supplementation affect innate and T cell immune responses to rotavirus A infection in a conventional sow model.
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DOI：
10.3389/fimmu.2023.1188757
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发表时间：
2023
影响因子：
7.3
通讯作者：
中科院分区：
文献类型：
--
作者：
轮状病毒A（RVA）每年导致约200，000例5岁以下儿童的疟疾死亡，主要发生在低收入和中等收入国家。风险因素包括营养状况、社会因素、母乳喂养状况和免疫缺陷。我们评估了维生素A（VA）缺乏/VA补充和RVA暴露（回忆）对RVA血清阳性妊娠和哺乳母猪先天性和T细胞免疫应答的影响，以及RVA攻击后仔猪的被动保护。从妊娠第30天（GD）开始，对母猪饲喂VA缺乏（VAD）或充足（VAS）饲料。VAD母猪的一个子集从GD接受VA补充|76例（30，000 IU/天，VAD+VA）。在GD~90时，用猪RVA G5 P [7]（OSU菌株）或最小必需培养基（模拟物）接种母猪（6组）：VAD+RVA; VAS+RVA; VAD+VA+RVA; VAD模拟物; VAS模拟物和VAD+ VA模拟物。在几个时间点采集母猪的血液、乳汁和肠道相关组织，以检查先天性[自然杀伤（NK）细胞、树突状（DC）细胞]、T细胞应答和肠道-乳腺（MG）-免疫轴运输相关基因的变化。在母猪接种后和仔猪攻毒后评价RVA的临床体征。我们观察到VAD+RVA母猪中NK细胞、总的和MHCII+浆细胞样DC、常规DC、CD 103 + DC和CD 4 +/CD 8+和T调节细胞（T细胞）以及NK细胞活性的频率降低。VAD+RVA母猪肠系膜淋巴结和回肠多聚体IG受体和视黄酸受体α（RARα）基因表达下调。有趣的是，在VAD模拟母猪中，RVA特异性产生IFN-γ的CD 4 +/CD 8 + T细胞增加，与IL-22增加一致，表明这些母猪中存在炎症。补充VA至VAD+RVA母猪恢复NK细胞和pDC的频率以及NK活性，但不恢复组织cDC和血液T细胞。总之，与我们最近观察到的VAD母猪B细胞应答降低导致其仔猪被动免疫保护降低相似，VAD损害了母猪的先天性和T细胞应答，而补充VA可恢复部分但非全部应答。我们的数据重申了在妊娠和哺乳期母亲中保持足够的VA水平和RVA免疫的重要性，以实现最佳的免疫应答，肠道MG免疫细胞轴的有效功能，并改善其仔猪的被动保护。
Rotavirus A (RVA) causes ~200,000 diarrheal deaths annually in children <5yrs, mostly in low- and middle-income countries. Risk factors include nutritional status, social factors, breastfeeding status, and immunodeficiency. We evaluated the effects of vitamin A (VA) deficiency/VA supplementation and RVA exposure (anamnestic) on innate and T cell immune responses in RVA seropositive pregnant and lactating sows and passive protection of their piglets post-RVA challenge. Sows were fed VA deficient (VAD) or sufficient (VAS) diets starting at gestation day (GD)30. A subset of VAD sows received VA supplementation from GD|76 (30,000IU/day, VAD+VA). Sows (6 groups) were inoculated with porcine RVA G5P[7] (OSU strain) or Minimal Essential Medium (mock) at GD~90: VAD+RVA; VAS+RVA; VAD+VA+RVA; VAD-mock; VAS-mock; and VAD+VA-mock. Blood, milk, and gut-associated tissues were collected from sows at several time points to examine innate [natural killer (NK), dendritic (DC) cells], T cell responses and changes in genes involved in the gut-mammary gland (MG)-immunological axis trafficking. Clinical signs of RVA were evaluated post inoculation of sows and post-challenge of piglets. We observed decreased frequencies of NK cells, total and MHCII+ plasmacytoid DCs, conventional DCs, CD103+ DCs and CD4+/CD8+ and T regulatory cells (Tregs) and NK cell activity in VAD+RVA sows. Polymeric Ig receptor and retinoic acid receptor alpha (RARα) genes were downregulated in mesenteric lymph nodes and ileum of VAD+RVA sows. Interestingly, RVA-specific IFN-γ producing CD4+/CD8+ T cells were increased in VAD-Mock sows, coinciding with increased IL-22 suggesting inflammation in these sows. VA supplementation to VAD+RVA sows restored frequencies of NK cells and pDCs, and NK activity, but not tissue cDCs and blood Tregs. In conclusion, similar to our recent observations of decreased B cell responses in VAD sows that led to decreased passive immune protection of their piglets, VAD impaired innate and T cell responses in sows, while VA supplementation to VAD sows restored some, but not all responses. Our data reiterate the importance of maintaining adequate VA levels and RVA immunization in pregnant and lactating mothers to achieve optimal immune responses, efficient function of the gut-MG-immune cell-axis and to improve passive protection of their piglets.
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影响因子：
30.3
作者：
Bonakdar, Maryam;Czuba, Lindsay C.;Han, Geongoo;Zhong, Guo;Luong, Hien;Isoherrannen, Nina;Vaishnava, Shipra
通讯作者：
Vaishnava, Shipra
抗原呈递给 B 细胞。
DOI：
10.3410/b2-87
发表时间：
2010-12-17
期刊：
F1000 biology reports
影响因子：
--
作者：
Harwood NE;Batista FD
通讯作者：
Batista FD
影响因子：
4.3
作者：
Bhaskaram, P.;Rao, K. Visweswara
通讯作者：
Rao, K. Visweswara
影响因子：
2.7
作者：
Collins, P. J.;Martella, V.;O'Shea, H.
通讯作者：
O'Shea, H.
影响因子：
3.3
作者：
Domingues Molinari, Bruna Leticia;Possatti, Flavia;Alfieri, Amauri Alcindo
通讯作者：
Alfieri, Amauri Alcindo