HIV infection impairs the host response to Mycobacterium tuberculosis infection by altering surfactant protein D function in the human lung alveolar mucosa

IF 7.9 2区 医学 Q1 IMMUNOLOGY
Anwari Akhter , Juan I. Moliva , Abul K. Azad , Angélica Olmo-Fontánez , Andreu Garcia-Vilanova , Julia M. Scordo , Mikhail A. Gavrilin , Phillip T. Diaz , Janice J. Endsley , Susan T. Weintraub , Larry S. Schlesinger , Mark D. Wewers , Jordi B. Torrelles
{"title":"HIV infection impairs the host response to Mycobacterium tuberculosis infection by altering surfactant protein D function in the human lung alveolar mucosa","authors":"Anwari Akhter ,&nbsp;Juan I. Moliva ,&nbsp;Abul K. Azad ,&nbsp;Angélica Olmo-Fontánez ,&nbsp;Andreu Garcia-Vilanova ,&nbsp;Julia M. Scordo ,&nbsp;Mikhail A. Gavrilin ,&nbsp;Phillip T. Diaz ,&nbsp;Janice J. Endsley ,&nbsp;Susan T. Weintraub ,&nbsp;Larry S. Schlesinger ,&nbsp;Mark D. Wewers ,&nbsp;Jordi B. Torrelles","doi":"10.1016/j.mucimm.2023.12.003","DOIUrl":null,"url":null,"abstract":"<div><p>Tuberculosis is the leading cause of death for people living with HIV (PLWH). We hypothesized that altered functions of innate immune components in the human alveolar lining fluid of PLWH (HIV-ALF) drive susceptibility to <em>Mycobacterium tuberculosis</em> (<em>M.tb</em>) infection. Our results indicate a significant increase in oxidation of innate proteins and chemokine levels and significantly lower levels and function of complement components and Th1/Th2/Th17 cytokines in HIV-ALF versus control-ALF (non-HIV-infected people). We further found a deficiency of surfactant protein D (SP-D) and reduced binding of SP-D to <em>M.tb</em> that had been exposed to HIV-ALF. Primary human macrophages infected with <em>M.tb</em> exposed to HIV-ALF were significantly less capable of controlling the infection, which was reversed by SP-D replenishment in HIV-ALF. Thus, based on the limited number of participants in this study, our data suggest that PLWH without antiretroviral therapy (ART) have declining host innate defense function in their lung mucosa, thereby favoring <em>M.tb</em> and potentially other pulmonary infections.</p></div>","PeriodicalId":18877,"journal":{"name":"Mucosal Immunology","volume":null,"pages":null},"PeriodicalIF":7.9000,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1933021923000995/pdfft?md5=5038782cf5b1e5d8d20c0cb80bf79121&pid=1-s2.0-S1933021923000995-main.pdf","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Mucosal Immunology","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1933021923000995","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Tuberculosis is the leading cause of death for people living with HIV (PLWH). We hypothesized that altered functions of innate immune components in the human alveolar lining fluid of PLWH (HIV-ALF) drive susceptibility to Mycobacterium tuberculosis (M.tb) infection. Our results indicate a significant increase in oxidation of innate proteins and chemokine levels and significantly lower levels and function of complement components and Th1/Th2/Th17 cytokines in HIV-ALF versus control-ALF (non-HIV-infected people). We further found a deficiency of surfactant protein D (SP-D) and reduced binding of SP-D to M.tb that had been exposed to HIV-ALF. Primary human macrophages infected with M.tb exposed to HIV-ALF were significantly less capable of controlling the infection, which was reversed by SP-D replenishment in HIV-ALF. Thus, based on the limited number of participants in this study, our data suggest that PLWH without antiretroviral therapy (ART) have declining host innate defense function in their lung mucosa, thereby favoring M.tb and potentially other pulmonary infections.

艾滋病病毒感染通过改变人体肺泡黏膜表面活性蛋白 D 的功能,损害宿主对结核分枝杆菌感染的反应。
结核病是艾滋病病毒感染者(PLWH)的主要死因。我们假设,艾滋病病毒感染者肺泡内衬液(HIV-ALF)中先天性免疫成分功能的改变会导致对结核分枝杆菌(M.tb)感染的易感性。我们的研究结果表明,与对照-ALF(非艾滋病毒感染者)相比,HIV-ALF 中的先天性蛋白氧化和趋化因子水平明显升高,补体成分和 Th1/Th2/Th17 细胞因子的水平和功能明显降低。我们还发现表面活性蛋白-D(SP-D)缺乏,SP-D与接触过HIV-ALF的M.tb的结合减少。原代人类巨噬细胞感染了暴露于 HIV-ALF 的 M.tb 后,控制感染的能力明显降低,而这种情况在补充了 HIV-ALF 中的 SP-D 后得到了逆转。因此,基于本研究中有限的参与人数,我们的数据表明,未接受抗逆转录病毒疗法的 PLWH 肺粘膜宿主先天防御功能下降,从而有利于 M.tb,并可能导致其他肺部感染。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Mucosal Immunology
Mucosal Immunology 医学-免疫学
CiteScore
16.60
自引率
3.80%
发文量
100
审稿时长
12 days
期刊介绍: Mucosal Immunology, the official publication of the Society of Mucosal Immunology (SMI), serves as a forum for both basic and clinical scientists to discuss immunity and inflammation involving mucosal tissues. It covers gastrointestinal, pulmonary, nasopharyngeal, oral, ocular, and genitourinary immunology through original research articles, scholarly reviews, commentaries, editorials, and letters. The journal gives equal consideration to basic, translational, and clinical studies and also serves as a primary communication channel for the SMI governing board and its members, featuring society news, meeting announcements, policy discussions, and job/training opportunities advertisements.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信