Open AccessVitamin A deficiency execrates Lewis lung carcinoma via induction of type 2 innate lymphoid cells and alternatively activates macrophages
Author(s) -
Cui Weiwei,
Zhang Wenxin,
Yuan Xiaofeng,
Liu Shanshan,
Li Meng,
Niu Junqi,
Zhang Peng,
Li Dong
Publication year - 2019
Publication title -
food science and nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.614
H-Index - 27
ISSN - 2048-7177
DOI - 10.1002/fsn3.961
Subject(s) - lewis lung carcinoma , immune system , macrophage polarization , lung cancer , bronchoalveolar lavage , immunology , medicine , innate lymphoid cell , cancer , lung , innate immune system , cancer research , macrophage , biology , metastasis , biochemistry , in vitro
Background Lung carcinoma is still associated with high rates of morbidity and mortality despite the advances in cancer therapy achieved in last decades. Recent studies showed that immune responses played a crucial role in the developments of cancers including lung cancer. Type 1 immune response could promote classical activated macrophages (CAMs) with antitumor properties. On the contrast, type 2 immune response could lead to the polarization of alternatively activated macrophages (AAMs) which could promote the growth and metastasis of tumor. Our previous research showed that vitamin A deficiency could promote the type 2 immune response but not the type 1 immune response. Whether vitamin A deficiency has detrimental effect for lung carcinoma need further investigate. Aim To investigate the effect of vitamin A deficiency in lung cancer and the potential mechanisms. Methods Mice were fed with normal diet or vitamin A deficiency diet for 2 weeks, and then, Lewis lung cancer (LLC) cells dissolved in Matrigel Matrix were planted on the left lower lope of lungs. Mice were sacrificed 28 days after the plantation of tumor cells, the tumor size, cytokine profile in bronchoalveolar lavage fluid (BALF), numbers of type 2 innate lymphoid cells (ILC2s), and macrophage phenotypes in the lung were measured. The overall survival rate was also monitored throughout the experiments. Results Vitamin A deficiency diet fed tumor‐bearing mice have lower survival rate ( χ 2 = 6.862, p < 0.001), larger tumor size ( t = 2.651, p < 0.05), more ILC2s ( t = 7.680, p < 0.001), and AAMs ( t = 6.315, p < 0.001) in the lung tissue; also, type 2 cytokines concentrations in the BALF were higher compared to normal diet fed ones. Conclusion Vitamin A deficiency could promote the pathogeneses of lung carcinoma via induction of ILC2s and polarizing AAMs.