scholarly journals Selective Immunoglobulin A Deficiency, Helicobacter pylori Infection, and Strongyloidiasis in a Patient with Adenocarcinoma of the Stomach

2020 ◽  
Vol 13 (3) ◽  
pp. 1325-1329
Author(s):  
Bassel Mazen Dakkak ◽  
Yahia Imam ◽  
Khalid Ahmed ◽  
Ahmed Osman Saleh ◽  
Dina Soliman ◽  
...  

Selective immunoglobulin A (IgA) deficiency is one of many congenital immunodeficiencies. It is associated with several medical condition. It has been shown to be associated with some types of malignancies, some autoimmune disorders, and even with some infections. Here we report a young male with selective IgA deficiency who also tested positive for <i>Helicobacter pylori</i> and strongyloidiasis at the time when he was diagnosed with stomach adenocarcinoma. The presence of IgA deficiency with multiple etiological possibilities such as infections and cancer makes this case unusual.

2021 ◽  
Author(s):  
de la Cruz Peña Maria José ◽  
Luis Ignacio Gonzalez-Granado ◽  
Inmaculada Garcia-Heredia ◽  
Lucia Maestre Carballa ◽  
Manuel Martinez-Garcia

Abstract Immunoglobulin A (IgA) is the dominant antibody found in our mucosal secretions and has long been recognized to play an important role in protecting our epithelium from pathogens. Recently, IgA has been shown to be involved in gut homeostatic regulation by `recognizing´and shaping our commensal microbes. Paradoxically, yet selective IgA-deficiency is often described as asymptomatic and there is a paucity of studies only focused on the mice and human gut microbiome context fully ignoring other niches of our body and our commensal viruses. Here, we used as a model the human oral cavity and employed a holistic view and studied the impact of IgA deficiency on both the human virome and microbiome. Unexpectedly, metagenomic and experimental data in human IgA deficiency indicate minimal-moderate changes in microbiome and virome composition compared to healthy control group and point out to a rather functional, resilient oral commensal viruses and microbes. However, a significant depletion (2-fold) of bacterial cells (p-value < 0.01) and viruses was observed in IgA-deficiency. Our results challenge the view of an irreplaceable IgA role for regulating the composition and function of our commensal microbiota and pose the question whether other “back-up” Ig-independent mechanisms might exist for maintaining a functional commensal microbiome.


2017 ◽  
Vol 47 ◽  
pp. 592-598 ◽  
Author(s):  
Mustafa ERKOÇOĞLU ◽  
Ayşe METİN ◽  
Ayşenur KAYA ◽  
Celal ÖZCAN ◽  
Ayşegül AKAN ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Maria José de la Cruz Peña ◽  
Luis Ignacio Gonzalez-Granado ◽  
Inmaculada Garcia-Heredia ◽  
Lucia Maestre Carballa ◽  
Manuel Martinez-Garcia

AbstractImmunoglobulin A (IgA) is the dominant antibody found in our mucosal secretions and has long been recognized to play an important role in protecting our epithelium from pathogens. Recently, IgA has been shown to be involved in gut homeostatic regulation by ‘recognizing’ and shaping our commensal microbes. Paradoxically, yet selective IgA-deficiency is often described as asymptomatic and there is a paucity of studies only focused on the mice and human gut microbiome context fully ignoring other niches of our body and our commensal viruses. Here, we used as a model the human oral cavity and employed a holistic view and studied the impact of IgA deficiency and also common variable IgA and IgM immunodeficiencies (CVID), on both the human virome and microbiome. Unexpectedly, metagenomic and experimental data in human IgA deficiency and CVID indicate minimal-moderate changes in microbiome and virome composition compared to healthy control group and point out to a rather functional, resilient oral commensal viruses and microbes. However, a significant depletion (two fold) of bacterial cells (p-value < 0.01) and viruses was observed in IgA-deficiency. Our results demonstrate that, within the limits of our cohort, IgA role is not critical for maintaining a rather functional salivary microbiome and suggest that IgA is not a major influence on the composition of abundant commensal microbes.


2021 ◽  
Vol 12 ◽  
Author(s):  
Che Kang Lim ◽  
Paola G. Bronson ◽  
Jezabel Varade ◽  
Timothy W. Behrens ◽  
Lennart Hammarström

Immunoglobulin A Deficiency (IgAD) is a polygenic primary immune deficiency, with a strong genetic association to the human leukocyte antigen (HLA) region. Previous genome-wide association studies (GWAS) have identified five non-HLA risk loci (IFIH1, PVT1, ATG13-AMBRA1, AHI1 and CLEC16A). In this study, we investigated the genetic interactions between different HLA susceptibility haplotypes and non-MHC genes in IgAD. To do this, we stratified IgAD subjects and healthy controls based on HLA haplotypes (N = 10,993), and then performed GWAS to identify novel genetic regions contributing to IgAD susceptibility. After replicating previously published HLA risk haplotypes, we compared individuals carrying at least one HLA risk allele (HLA-B*08:01-DRB1*03:01-DQB1*02:01 or HLA-DRB1*07:01-DQB1*02:02 or HLA-DRB1*01-DQB1*05:01) with individuals lacking an HLA risk allele. Subsequently, we stratified subjects based on the susceptibility alleles/haplotypes and performed gene-based association analysis using 572,856 SNPs and 24,125 genes. A significant genome-wide association in STXBP6 (rs4097492; p = 7.63 × 10−9) was observed in the cohort carrying at least one MHC risk allele. We also identified a significant gene-based association for B3GNT6 (PGene = 2.1 × 10–6) in patients not carrying known HLA susceptibility alleles. Our findings indicate that the etiology of IgAD differs depending on the genetic background of HLA susceptibility haplotypes.


2006 ◽  
Vol 74 (1) ◽  
pp. 248-256 ◽  
Author(s):  
Shingo Yamanishi ◽  
Tadasu Iizumi ◽  
Eri Watanabe ◽  
Masumi Shimizu ◽  
Shigeru Kamiya ◽  
...  

ABSTRACT Besides various gastroduodenal diseases, Helicobacter pylori infection may be involved in autoimmune disorders like rheumatoid arthritis (RA) or idiopathic thrombocytopenic purpura. Such autoimmune disorders are often associated with autoreactive antibodies produced by B-1 cells, a subpopulation of B lymphocytes. These B-1 cells are mainly located in the pleural cavity or mucosal compartment. The existence of H. pylori urease-specific immunoglobulin A (IgA)-producing B cells in the mucosal compartment and of their specific IgM in the sera of acutely infected volunteers suggests the possibility that urease stimulates mucosal innate immune responses. Here, we show for the first time that purified H. pylori urease predominantly stimulates the B-1-cell population rather than B-2 cells, which produce antigen-specific conventional antibodies among splenic B220+ B cells. The fact that such stimulation of B-1 cells was not affected by the addition of polymyxin B indicates that the effect of purified H. pylori urease was not due to the contamination with bacterial lipopolysaccharide. Furthermore, the production of various B-1-cell-related autoreactive antibodies such as IgM-type rheumatoid factor, anti-single-stranded DNA antibody, and anti-phosphatidyl choline antibody was observed when the splenic B cells were stimulated with purified H. pylori urease in vitro. These findings suggest that H. pylori components, urease in particular, may be among the environmental triggars that initiate various autoimmune diseases via producing autoreactive antibodies through the activation of B-1 cells. The findings shown here offer important new insights into the pathogenesis of autoimmune disorders related to H. pylori infection.


2021 ◽  
Vol 74 (6) ◽  
pp. 1510-1514
Author(s):  
Hanna M. Sylenko ◽  
Petro M. Skrypnykov ◽  
Yurii I. Sylenko ◽  
Olena A. Pisarenko

The aim: To present data on the possibility of occurrence and active progression of generalized periodontitis in persons with secretory immunoglobulin A deficiency and possible methods of its correction. Мaterials and methods: Analytical elaboration of scientific and medical literature based on the immunological aspect of generalized periodontitis. Conclusions: The deficiency of secretory immunoglobulin A may occur in cases of primary or secondary insufficiency of the immune system. Selective IgA deficiency is an example of primary insufficiency of the immune system. Secondary immunodeficiency disorders is a clinical and immunological syndrome that develops against the background of a previously normally functioning immune system, characterized by a steady decrease in quantitative or functional indicators of specific or(and) nonspecific factors of immunoresistance. Insufficient awareness of dentists about certain aspects of the etiology and pathogenesis of generalized periodontitis leads to deterioration of treatment results.


2021 ◽  
Vol 10 (17) ◽  
pp. 3809
Author(s):  
Izabela Morawska ◽  
Sara Kurkowska ◽  
Dominika Bębnowska ◽  
Rafał Hrynkiewicz ◽  
Rafał Becht ◽  
...  

Selective IgA deficiency (sIgAD) is the most common primary immunodeficiency disease (PID), with an estimated occurrence from about 1:3000 to even 1:150, depending on population. sIgAD is diagnosed in adults and children after the 4th year of age, with immunoglobulin A level below 0.07 g/L and normal levels of IgM and IgG. Usually, the disease remains undiagnosed throughout the patient’s life, due to its frequent asymptomatic course. If symptomatic, sIgAD is connected to more frequent viral and bacterial infections of upper respiratory, urinary, and gastrointestinal tracts, as well as autoimmune and allergic diseases. Interestingly, it may also be associated with other PIDs, such as IgG subclasses deficiency or specific antibodies deficiency. Rarely sIgAD can evolve to common variable immunodeficiency disease (CVID). It should also be remembered that IgA deficiency may occur in the course of other conditions or result from their treatment. It is hypothesized that allergic diseases (e.g., eczema, rhinitis, asthma) are more common in patients diagnosed with this particular PID. Selective IgA deficiency, although usually mildly symptomatic, can be difficult for clinicians. The aim of the study is to summarize the connection between selective IgA deficiency and atopic diseases.


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