{"title":"更正:热门阅读。","authors":"","doi":"10.4049/jimmunol.2400459","DOIUrl":null,"url":null,"abstract":"<p><p>Top Reads. 2024. J. Immunol. 213:245. A third summary for the article titled \"Obesity inhibits alveolar macrophage responses to Pseudomonas aeruginosa pneumonia via upregulation of PGE2 in male, but not female mice\" by Gabrielle P. Entrup, Aayush Unadkat, Helen I. Warheit-Niemi, Brooke Thomas, Stephen J. Gurczynski, Yuxiao Cui, Andrew M. Smith, Katherine A. Gallagher, Bethany B. Moore, and Kanakadurga Singer was inadvertently excluded from the Top Reads' summary in the August 1, 2024 issue and appears below. Obesity Inhibits Alveolar Macrophage Responses to Pneumonia Obesity is associated with increased morbidity and mortality during bacterial pneumonia. Cyclooxygenase-2 (COX-2) and PGE2 have been shown to be upregulated in patients who are obese. In this study, we investigated the role of obesity and PGE2 in bacterial pneumonia and how inhibition of PGE2 improves antibacterial functions of macrophages. C57BL/6J male and female mice were fed either a normal diet (ND) or high-fat diet (HFD) for 16 wk. After this time, animals were infected with Pseudomonas aeruginosa in the lung. In uninfected animals, alveolar macrophages were extracted for either RNA analysis or to be cultured ex vivo for functional analysis. HFD resulted in changes in immune cell numbers in both noninfected and infected animals. HFD animals had increased bacterial burden compared with ND animals; however, male HFD animals had higher bacterial burden compared with HFD females. Alveolar macrophages from HFD males had decreased ability to phagocytize and kill bacteria and were shown to have increased cyclooxygenase-2 and PGE2. Treating male, but not female, alveolar macrophages with PGE2 leads to increases in cAMP and decreased bacterial phagocytosis. Treatment with lumiracoxib-conjugated nanocarriers targeting alveolar macrophages improves bacterial phagocytosis and clearance in both ND and HFD male animals. Our study highlights that obesity leads to worse morbidity during bacterial pneumonia in male mice because of elevated PGE2. In addition, we uncover a sex difference in both obesity and infection, because females produce high basal PGE2 but because of a failure to signal via cAMP do not display impaired phagocytosis. This has been corrected in the online version of the article, which now differs from the print version as originally published.</p>","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":null,"pages":null},"PeriodicalIF":3.6000,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Correction: Top Reads.\",\"authors\":\"\",\"doi\":\"10.4049/jimmunol.2400459\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Top Reads. 2024. J. Immunol. 213:245. A third summary for the article titled \\\"Obesity inhibits alveolar macrophage responses to Pseudomonas aeruginosa pneumonia via upregulation of PGE2 in male, but not female mice\\\" by Gabrielle P. Entrup, Aayush Unadkat, Helen I. Warheit-Niemi, Brooke Thomas, Stephen J. Gurczynski, Yuxiao Cui, Andrew M. Smith, Katherine A. Gallagher, Bethany B. Moore, and Kanakadurga Singer was inadvertently excluded from the Top Reads' summary in the August 1, 2024 issue and appears below. Obesity Inhibits Alveolar Macrophage Responses to Pneumonia Obesity is associated with increased morbidity and mortality during bacterial pneumonia. Cyclooxygenase-2 (COX-2) and PGE2 have been shown to be upregulated in patients who are obese. In this study, we investigated the role of obesity and PGE2 in bacterial pneumonia and how inhibition of PGE2 improves antibacterial functions of macrophages. C57BL/6J male and female mice were fed either a normal diet (ND) or high-fat diet (HFD) for 16 wk. After this time, animals were infected with Pseudomonas aeruginosa in the lung. In uninfected animals, alveolar macrophages were extracted for either RNA analysis or to be cultured ex vivo for functional analysis. HFD resulted in changes in immune cell numbers in both noninfected and infected animals. HFD animals had increased bacterial burden compared with ND animals; however, male HFD animals had higher bacterial burden compared with HFD females. Alveolar macrophages from HFD males had decreased ability to phagocytize and kill bacteria and were shown to have increased cyclooxygenase-2 and PGE2. Treating male, but not female, alveolar macrophages with PGE2 leads to increases in cAMP and decreased bacterial phagocytosis. Treatment with lumiracoxib-conjugated nanocarriers targeting alveolar macrophages improves bacterial phagocytosis and clearance in both ND and HFD male animals. Our study highlights that obesity leads to worse morbidity during bacterial pneumonia in male mice because of elevated PGE2. In addition, we uncover a sex difference in both obesity and infection, because females produce high basal PGE2 but because of a failure to signal via cAMP do not display impaired phagocytosis. 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引用次数: 0
摘要
热门阅读。2024.J. Immunol.213:245.Gabrielle P. Entrup、Aayush Unadkat、Helen I. Warheit-Niemi、Brooke Thomas、Stephen J. Gurczynski、Yuxiao Cui、Andrew M. Smith、J.Warheit-Niemi, Brooke Thomas, Stephen J. Gurczynski, Yuxiao Cui, Andrew M. Smith, Katherine A. Gallagher, Bethany B. Moore, and Kanakadurga Singer "不慎被排除在 2024 年 8 月 1 日刊的热门阅读摘要之外,现刊登如下。肥胖抑制肺泡巨噬细胞对肺炎的反应 肥胖与细菌性肺炎发病率和死亡率的增加有关。研究表明,肥胖患者体内的环氧化酶-2 (COX-2) 和 PGE2 上调。在这项研究中,我们探讨了肥胖和 PGE2 在细菌性肺炎中的作用,以及抑制 PGE2 如何改善巨噬细胞的抗菌功能。C57BL/6J 雄性和雌性小鼠以正常饮食(ND)或高脂饮食(HFD)喂养 16 周。之后,动物肺部感染铜绿假单胞菌。在未感染的动物中,提取肺泡巨噬细胞用于 RNA 分析或体内外培养用于功能分析。高脂血症导致非感染动物和感染动物的免疫细胞数量发生变化。与 ND 动物相比,HFD 动物的细菌负荷增加;但与 HFD 雌性动物相比,HFD 雄性动物的细菌负荷更高。雄性高脂血症动物的肺泡巨噬细胞吞噬和杀死细菌的能力下降,而且环氧化酶-2 和 PGE2 的含量增加。用 PGE2 处理雄性(而非雌性)肺泡巨噬细胞会导致 cAMP 增加和细菌吞噬能力下降。以肺泡巨噬细胞为靶标的鲁米拉考昔布结合纳米载体可提高ND和HFD雄性动物的细菌吞噬和清除能力。我们的研究强调,由于 PGE2 升高,肥胖会导致雄性小鼠在细菌性肺炎期间发病率升高。此外,我们还发现了肥胖和感染中的性别差异,因为雌性小鼠会产生较高的基础 PGE2,但由于不能通过 cAMP 发出信号,因此不会显示出吞噬功能受损。这一点已在文章的网络版中更正,现在的网络版与最初发表的印刷版不同。
Top Reads. 2024. J. Immunol. 213:245. A third summary for the article titled "Obesity inhibits alveolar macrophage responses to Pseudomonas aeruginosa pneumonia via upregulation of PGE2 in male, but not female mice" by Gabrielle P. Entrup, Aayush Unadkat, Helen I. Warheit-Niemi, Brooke Thomas, Stephen J. Gurczynski, Yuxiao Cui, Andrew M. Smith, Katherine A. Gallagher, Bethany B. Moore, and Kanakadurga Singer was inadvertently excluded from the Top Reads' summary in the August 1, 2024 issue and appears below. Obesity Inhibits Alveolar Macrophage Responses to Pneumonia Obesity is associated with increased morbidity and mortality during bacterial pneumonia. Cyclooxygenase-2 (COX-2) and PGE2 have been shown to be upregulated in patients who are obese. In this study, we investigated the role of obesity and PGE2 in bacterial pneumonia and how inhibition of PGE2 improves antibacterial functions of macrophages. C57BL/6J male and female mice were fed either a normal diet (ND) or high-fat diet (HFD) for 16 wk. After this time, animals were infected with Pseudomonas aeruginosa in the lung. In uninfected animals, alveolar macrophages were extracted for either RNA analysis or to be cultured ex vivo for functional analysis. HFD resulted in changes in immune cell numbers in both noninfected and infected animals. HFD animals had increased bacterial burden compared with ND animals; however, male HFD animals had higher bacterial burden compared with HFD females. Alveolar macrophages from HFD males had decreased ability to phagocytize and kill bacteria and were shown to have increased cyclooxygenase-2 and PGE2. Treating male, but not female, alveolar macrophages with PGE2 leads to increases in cAMP and decreased bacterial phagocytosis. Treatment with lumiracoxib-conjugated nanocarriers targeting alveolar macrophages improves bacterial phagocytosis and clearance in both ND and HFD male animals. Our study highlights that obesity leads to worse morbidity during bacterial pneumonia in male mice because of elevated PGE2. In addition, we uncover a sex difference in both obesity and infection, because females produce high basal PGE2 but because of a failure to signal via cAMP do not display impaired phagocytosis. This has been corrected in the online version of the article, which now differs from the print version as originally published.
期刊介绍:
The JI publishes novel, peer-reviewed findings in all areas of experimental immunology, including innate and adaptive immunity, inflammation, host defense, clinical immunology, autoimmunity and more. Special sections include Cutting Edge articles, Brief Reviews and Pillars of Immunology. The JI is published by The American Association of Immunologists (AAI)