The Potential Role of an Aberrant Mucosal Immune Response to SARS-CoV-2 in the Pathogenesis of IgA Nephropathy.
The Potential Role of an Aberrant Mucosal Immune Response to SARS-CoV-2 in the Pathogenesis of IgA Nephropathy.
复制标题
对 SARS-CoV-2 的异常粘膜免疫反应在 IgA 肾病发病机制中的潜在作用
DOI:
10.3390/pathogens10070881
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发表时间:
2021-07-12
期刊:
影响因子:
--
通讯作者:
Zhu S
中科院分区:
文献类型:
--
作者:
Zhang Z;Zhang G;Guo M;Tao W;Liu X;Wei H;Jin T;Zhang Y;Zhu S
The outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has become a global concern. Immunoglobin A (IgA) contributes to virus neutralization at the early stage of infection. Longitudinal studies are needed to assess whether SARS-CoV-2-specific IgA production persists for a longer time in patients recovered from severe COVID-19 and its lasting symptoms that can have disabling consequences should also be alerted to susceptible hosts. Here, we tracked the anti-SARS-CoV-2 spike protein receptor-binding domain (RBD) antibody levels in a cohort of 88 COVID-19 patients. We found that 52.3% of the patients produced more anti-SARS-CoV-2 RBD IgA than IgG or IgM, and the levels of IgA remained stable during 4–41 days of infection. One of these IgA-dominant COVID-19 patients, concurrently with IgA nephropathy (IgAN), presented with elevated serum creatinine and worse proteinuria during the infection, which continued until seven months post-infection. The serum levels of anti-SARS-CoV-2 RBD and total IgA were higher in this patient than in healthy controls. Changes in the composition of the intestinal microbiota, increased IgA highly coated bacteria, and elevated concentration of the proinflammatory cytokine IL-18 were indicative of potential involvement of intestinal dysbiosis and inflammation to the systemic IgA level and, consequently, the disease progression. Collectively, our work highlighted the potential adverse effect of the mucosal immune response to SARS-CoV-2 infection, and that additional care should be taken with COVID-19 patients presenting with chronic diseases such as IgAN.
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影响因子:
12.2
作者:
Pascoal LB;Rodrigues PB;Genaro LM;Gomes ABDSP;Toledo-Teixeira DA;Parise PL;Bispo-Dos-Santos K;Simeoni CL;Guimarães PV;Buscaratti LI;Elston JGA;Marques-Souza H;Martins-de-Souza D;Ayrizono MLS;Velloso LA;Proenca-Modena JL;Moraes-Vieira PMM;Mori MAS;Farias AS;Vinolo MAR;Leal RF
通讯作者:
Leal RF
影响因子:
17.1
作者:
Sterlin D;Mathian A;Miyara M;Mohr A;Anna F;Claër L;Quentric P;Fadlallah J;Devilliers H;Ghillani P;Gunn C;Hockett R;Mudumba S;Guihot A;Luyt CE;Mayaux J;Beurton A;Fourati S;Bruel T;Schwartz O;Lacorte JM;Yssel H;Parizot C;Dorgham K;Charneau P;Amoura Z;Gorochov G
通讯作者:
Gorochov G
影响因子:
64.8
作者:
Gaebler C;Wang Z;Lorenzi JCC;Muecksch F;Finkin S;Tokuyama M;Cho A;Jankovic M;Schaefer-Babajew D;Oliveira TY;Cipolla M;Viant C;Barnes CO;Bram Y;Breton G;Hägglöf T;Mendoza P;Hurley A;Turroja M;Gordon K;Millard KG;Ramos V;Schmidt F;Weisblum Y;Jha D;Tankelevich M;Martinez-Delgado G;Yee J;Patel R;Dizon J;Unson-O'Brien C;Shimeliovich I;Robbiani DF;Zhao Z;Gazumyan A;Schwartz RE;Hatziioannou T;Bjorkman PJ;Mehandru S;Bieniasz PD;Caskey M;Nussenzweig MC
通讯作者:
Nussenzweig MC
影响因子:
32.4
作者:
Quast I;Tarlinton D
通讯作者:
Tarlinton D
影响因子:
29.7
作者:
Cerutti A;Chen K;Chorny A
通讯作者:
Chorny A