scholarly journals Potential role of aberrant mucosal immune response to SARS-CoV-2 in pathogenesis of IgA Nephropathy

2020 ◽  
Author(s):  
Zhao Zhang ◽  
Guorong Zhang ◽  
Meng Guo ◽  
Wanyin Tao ◽  
Xingzi Liu ◽  
...  
Keyword(s):  
Immune Response ◽  
Iga Nephropathy ◽  
Potential Role ◽  
Intestinal Inflammation ◽  
Clinical Manifestations ◽  
Mucosal Immune Response ◽  
Causal Pathogen ◽  
Global Concern ◽  
Antibody Levels

Aberrant mucosal immunity has been suggested to play a pivotal role in pathogenesis of IgA nephropathy (IgAN), the most common form of glomerulonephritis worldwide. The outbreak of severe acute respiratory syndrome coronavirus (SARS-CoV-2), the causal pathogen of coronavirus disease 2019 (COVID-19), has become a global concern. However, whether the mucosal immune response caused by SARS-CoV-2 influences the clinical manifestations of IgAN patients remains unknown. Here we tracked the SARS-CoV-2 anti-receptor binding domain (RBD) antibody levels in a cohort of 88 COVID-19 patients. We found that 52.3% of the COVID-19 patients produced more SARS-CoV-2 anti-RBD IgA than IgG or IgM, and the levels of the IgA were stable during 4-41 days of infection. Among these IgA-dominated COVID-19 patients, we found a severe COVID-19 patient concurrent with IgAN. The renal function of the patient declined presenting with increased serum creatinine during the infection and till 7 months post infection. This patient predominantly produced anti-RBD IgA as well as total IgA in the serum compared to that of healthy controls. The analysis of the IgA-coated microbiota as well as proinflammatory cytokine IL-18, which was mainly produced in the intestine, reveals intestinal inflammation, although no obvious gastrointestinal symptom was reported. The mucosal immune responses in the lung are not evaluated due to the lack of samples from respiratory tract. Collectively, our work highlights the potential adverse effect of the mucosal immune response towards SARS-CoV-2, and additional care should be taken for COVID-19 patients with chronic diseases like IgAN.

scholarly journals The Potential Role of an Aberrant Mucosal Immune Response to SARS-CoV-2 in the Pathogenesis of IgA Nephropathy

Pathogens ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 881
Author(s):  
Zhao Zhang ◽  
Guorong Zhang ◽  
Meng Guo ◽  
Wanyin Tao ◽  
Xingzi Liu ◽  
...  
Keyword(s):  
Immune Response ◽  
Iga Nephropathy ◽  
Early Stage ◽  
Elevated Serum ◽  
Serum Levels ◽  
Mucosal Immune Response ◽  
Elevated Concentration ◽  
Protein Receptor ◽  
Iga Production ◽  
Antibody Levels

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.

Role of mucosal immune response and histopathological study in European eel (Anguilla anguilla L.) intraperitoneal challenged by Vibrio anguillarum or Tenacibaculum soleae

2021 ◽  
Author(s):  
Emanuele Conforto ◽  
Luciano Vílchez-Gómez ◽  
Daniela Parrinello ◽  
Maria Giovanna Parisi ◽  
María Ángeles Esteban ◽  
...  
Keyword(s):  
Immune Response ◽  
Vibrio Anguillarum ◽  
Anguilla Anguilla ◽  
Mucosal Immune Response ◽  
Histopathological Study ◽  
European Eel

scholarly journals Haptoglobin and Its Related Protein, Zonulin—What Is Their Role in Spondyloarthropathy?

2021 ◽  
Vol 10 (5) ◽  
pp. 1131
Author(s):  
Magdalena Chmielińska ◽  
Marzena Olesińska ◽  
Katarzyna Romanowska-Próchnicka ◽  
Dariusz Szukiewicz
Keyword(s):  
Immune Response ◽  
Free Radicals ◽  
Immune System ◽  
Potential Role ◽  
Acute Phase Protein ◽  
Related Protein ◽  
Functional Differences ◽  
Phase Protein ◽  
Its Polymorphism

Haptoglobin (Hp) is an acute phase protein which supports the immune response and protects tissues from free radicals. Its concentration correlates with disease activity in spondyloarthropathies (SpAs). The Hp polymorphism determines the functional differences between Hp1 and Hp2 protein products. The role of the Hp polymorphism has been demonstrated in many diseases. In particular, the Hp 2-2 phenotype has been associated with the unfavorable course of some inflammatory and autoimmune disorders. Its potential role in modulating the immune system in SpA is still unknown. This article contains pathophysiological considerations on the potential relationship between Hp, its polymorphism and SpA.

scholarly journals Neuroinflammation and Its Impact on the Pathogenesis of COVID-19

2021 ◽  
Vol 8 ◽  
Author(s):  
Mohammed M. Almutairi ◽  
Farzane Sivandzade ◽  
Thamer H. Albekairi ◽  
Faleh Alqahtani ◽  
Luca Cucullo
Keyword(s):  
Immune System ◽  
Molecular Mechanisms ◽  
Potential Role ◽  
Immune Cell ◽  
Clinical Manifestations ◽  
Cell Infiltration ◽  
Cellular Mechanisms ◽  
Cytokine Levels

Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The clinical manifestations of COVID-19 include dry cough, difficult breathing, fever, fatigue, and may lead to pneumonia and respiratory failure. There are significant gaps in the current understanding of whether SARS-CoV-2 attacks the CNS directly or through activation of the peripheral immune system and immune cell infiltration. Although the modality of neurological impairments associated with COVID-19 has not been thoroughly investigated, the latest studies have observed that SARS-CoV-2 induces neuroinflammation and may have severe long-term consequences. Here we review the literature on possible cellular and molecular mechanisms of SARS-CoV-2 induced-neuroinflammation. Activation of the innate immune system is associated with increased cytokine levels, chemokines, and free radicals in the SARS-CoV-2-induced pathogenic response at the blood-brain barrier (BBB). BBB disruption allows immune/inflammatory cell infiltration into the CNS activating immune resident cells (such as microglia and astrocytes). This review highlights the molecular and cellular mechanisms involved in COVID-19-induced neuroinflammation, which may lead to neuronal death. A better understanding of these mechanisms will help gain substantial knowledge about the potential role of SARS-CoV-2 in neurological changes and plan possible therapeutic intervention strategies.

scholarly journals Cellular and molecular changes and immune response in the intestinal mucosa during Trichinella spiralis early infection in rats

2020 ◽  
Vol 13 (1) ◽  
Author(s):  
María Priscila Saracino ◽  
Cecilia Celeste Vila ◽  
Melina Cohen ◽  
María Virginia Gentilini ◽  
Guido Hernán Falduto ◽  
...  
Keyword(s):  
Immune Response ◽  
Lamina Propria ◽  
Trichinella Spiralis ◽  
Mucosal Immune Response ◽  
Mesenteric Lymph Nodes ◽  
Muscle Larvae ◽  
Gut Immunity ◽  
Gut Mucosa

Abstract Background: The main targets of the host’s immune system in Trichinella spiralis infection are the adult worms (AW), at the gut level, and the migrant or newborn larvae (NBL), at systemic and pulmonary levels. Most of the studies carried out in the gut mucosa have been performed on the Payer’s patches and/or the mesenteric lymph nodes but not on the lamina propria, therefore, knowledge on the gut immune response against T. spiralis remains incomplete. Methods This study aimed at characterizing the early mucosal immune response against T. spiralis, particularly, the events taking place between 1 and 13 dpi. For this purpose, Wistar rats were orally infected with muscle larvae of T. spiralis and the humoral and cellular parameters of the gut immunity were analysed, including the evaluation of the ADCC mechanism exerted by lamina propria cells. Results A marked inflammation and structural alteration of the mucosa was found. The changes involved an increase in goblet cells, eosinophils and mast cells, and B and T lymphocytes, initially displaying a Th1 profile, characterised by the secretion of IFN-γ and IL-12, followed by a polarization towards a Th2 profile, with a marked increase in IgE, IgG1, IL-4, IL-5 and IL-13 levels, which occurred once the infection was established. In addition, the helminthotoxic activity of lamina propria cells demonstrated the role of the intestine as a place of migrant larvae destruction, indicating that not all the NBLs released in the gut will be able to reach the muscles. Conclusions The characterization of the immune response triggered in the gut mucosa during T. spiralis infection showed that not only an effector mechanism is directed toward the AW but also towards the NBL as a cytotoxic activity was observed against NBL exerted by lamina propria cells.

scholarly journals The application of omics techniques to understand the role of the gut microbiota in inflammatory bowel disease

2019 ◽  
Vol 12 ◽  
pp. 175628481882225 ◽  
Author(s):  
Jonathan P. Segal ◽  
Benjamin H. Mullish ◽  
Mohammed Nabil Quraishi ◽  
Animesh Acharjee ◽  
Horace R. T. Williams ◽  
...  
Keyword(s):  
Systems Biology ◽  
Gut Microbiota ◽  
Potential Role ◽  
Intestinal Inflammation ◽  
Clinical Care ◽  
Complex Interaction ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
Compositional Changes

The aetiopathogenesis of inflammatory bowel diseases (IBD) involves the complex interaction between a patient’s genetic predisposition, environment, gut microbiota and immune system. Currently, however, it is not known if the distinctive perturbations of the gut microbiota that appear to accompany both Crohn’s disease and ulcerative colitis are the cause of, or the result of, the intestinal inflammation that characterizes IBD. With the utilization of novel systems biology technologies, we can now begin to understand not only details about compositional changes in the gut microbiota in IBD, but increasingly also the alterations in microbiota function that accompany these. Technologies such as metagenomics, metataxomics, metatranscriptomics, metaproteomics and metabonomics are therefore allowing us a deeper understanding of the role of the microbiota in IBD. Furthermore, the integration of these systems biology technologies through advancing computational and statistical techniques are beginning to understand the microbiome interactions that both contribute to health and diseased states in IBD. This review aims to explore how such systems biology technologies are advancing our understanding of the gut microbiota, and their potential role in delineating the aetiology, development and clinical care of IBD.

scholarly journals Potential role of soluble CD40 in the humoral immune response impairment of uraemic patients

Immunology ◽  
2003 ◽  
Vol 110 (1) ◽  
pp. 131-140 ◽  
Author(s):  
Cecile Contin ◽  
Vincent Pitard ◽  
Yahsou Delmas ◽  
Nadege Pelletier ◽  
Thierry Defrance ◽  
...  
Keyword(s):  
Immune Response ◽  
Humoral Immune Response ◽  
Potential Role ◽  
Humoral Immune

scholarly journals Antibody Is Critical for the Clearance of Murine Norovirus Infection

2008 ◽  
Vol 82 (13) ◽  
pp. 6610-6617 ◽  
Author(s):  
Karen A. Chachu ◽  
David W. Strong ◽  
Anna D. LoBue ◽  
Christiane E. Wobus ◽  
Ralph S. Baric ◽  
...  
Keyword(s):  
Immune Response ◽  
B Cells ◽  
Murine Norovirus ◽  
Wild Type ◽  
Human Norovirus ◽  
Mucosal Infection ◽  
Antibody Levels ◽  
Deficient Mice ◽  
Immune Antibody

ABSTRACT Human noroviruses cause more than 90% of epidemic nonbacterial gastroenteritis. However, the role of B cells and antibody in the immune response to noroviruses is unclear. Previous studies have demonstrated that human norovirus specific antibody levels increase upon infection, but they may not be protective against infection. In this report, we used murine norovirus (MNV), an enteric norovirus, as a model to determine the importance of norovirus specific B cells and immune antibody in clearance of norovirus infection. We show here that mice genetically deficient in B cells failed to clear primary MNV infection as effectively as wild-type mice. In addition, adoptively transferred immune splenocytes derived from B-cell-deficient mice or antibody production-deficient mice were unable to efficiently clear persistent MNV infection in RAG1−/− mice. Further, adoptive transfer of either polyclonal anti-MNV serum or neutralizing anti-MNV monoclonal antibodies was sufficient to reduce the level of MNV infection both systemically and in the intestine. Together, these data demonstrate that antibody plays an important role in the clearance of MNV and that immunoglobulin G anti-norovirus antibody can play an important role in clearing mucosal infection.

scholarly journals The Role of Galectin-1 and Galectin-3 in the Mucosal Immune Response to Citrobacter rodentium Infection

PLoS ONE ◽  
2014 ◽  
Vol 9 (9) ◽  
pp. e107933 ◽  
Author(s):  
Renata Curciarello ◽  
Alison Steele ◽  
Dianne Cooper ◽  
Thomas T. MacDonald ◽  
Laurens Kruidenier ◽  
...  
Keyword(s):  
Immune Response ◽  
Mucosal Immune Response ◽  
Citrobacter Rodentium ◽  
Galectin 3

scholarly journals Genetic Susceptibility to Chagas Disease: An Overview about the Infection and about the Association between Disease and the Immune Response Genes

2013 ◽  
Vol 2013 ◽  
pp. 1-13 ◽  
Author(s):  
Christiane Maria Ayo ◽  
Márcia Machado de Oliveira Dalalio ◽  
Jeane Eliete Laguila Visentainer ◽  
Pâmela Guimarães Reis ◽  
Emília Ângela Sippert ◽  
...  
Keyword(s):  
Immune Response ◽  
Chagas Disease ◽  
Chronic Infection ◽  
Genetic Factors ◽  
Clinical Course ◽  
Clinical Manifestations ◽  
Severity Of Disease ◽  
Host Genetic ◽  
Host Genetic Factors

Chagas disease, which is caused by the flagellate parasiteTrypanosoma cruzi, affects 8–10 million people in Latin America. The disease is endemic and is characterised by acute and chronic phases that develop in the indeterminate, cardiac, and/or gastrointestinal forms. The immune response during humanT. cruziinfection is not completely understood, despite its role in driving the development of distinct clinical manifestations of chronic infection. Polymorphisms in genes involved in the innate and specific immune response are being widely studied in order to clarify their possible role in the occurrence or severity of disease. Here we review the role of classic and nonclassic MHC,KIR, and cytokine host genetic factors on the infection byT. cruziand the clinical course of Chagas disease.

Sign in / Sign up

Export Citation Format

Share Document