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LPS/TLR4 Pathway Regulates IgA1 Secretion to Induce IgA Nephropathy.

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Title: LPS/TLR4 Pathway Regulates IgA1 Secretion to Induce IgA Nephropathy.
Authors: Haidong He, Meilin Shen, Yuyan Tang, Weiqian Sun, Xudong Xu
Source: Alternative Therapies in Health & Medicine. Jan2024, Vol. 30 Issue 1, p419-425. 7p.
Subjects: IGA glomerulonephritis, GLOMERULONEPHRITIS, IMMUNOGLOBULIN A, IMMUNE complex diseases, NEPHRITIS
Abstract: Context • Studies have reported that the incidence and severity of IgA nephropathy (IgAN) are closely related to the imbalance of the intestinal flora. Imbalance of the intestinal flora may cause abnormalities, such as intestinal mucosal immunity or mesenteric B1 lymphocyte subsets. These can lead to an increase in immunoglobulin A (IgA) production and IgA structural changing, which can eventually cause IgA1 deposition in the glomerular mesangial area and nephritis. Objective • The study intended to explore whether the LPS/ TLR4 pathway regulates mesenteric B cells, secreting Gd-IgA1 to induce IgA nephropathy. Design • The research team designed an animal study. Setting • The study took place at Department of Nephrology, Minhang Hospital, Fudan University. Animals • The animals were 60 specific pathogen free (SPF) C57BL/6 (B6, H-2b) male mice from that were 6-8 weeks old and weighed 20-25 grams. Intervention • The research team established a mouse model of IgA nephropathy. The team created five groups of mice: (1) the NC group, a normal negative control group without induced nephropathy and with no treatments; (2) the IgA nephropathy (IgAN) group, a positive control group with induced nephropathy and with no treatments; (3) the IgAN+anti-TLR4 group, an intervention group, with induced nephropathy and with a TLR4- antibody (anti-TLR4) treatment; (4) the IgAN+GEC group, an intervention group, with induced nephropathy and with treatment with glutamine enteric-coated capsules (GEC); and (5) the IgAN+anti-TLR4+GEC group, an intervention group, with induced nephropathy and with treatment with anti-TLR4 and GEC. Outcome Measures • The research team collected the blood and urine of all the mice and used an enzyme-linked immunoassay (ELISA) to analyze the levels of blood creatinine, urine protein, and urea nitrogen (BUN). The team also used the ELISA to analyze signal molecules for serum inflammation: interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), monocyte chemotactic protein 1 (MCP-1), cyclooxygenase-2 (COX2), and galactose-deficient IgA1(Gd-IgA1). The team analyzed the distribution and content of IgA+B220+B lymphocytes in the intestinal tissues of all the mice, using tissue immunofluorescence tracking technology, and used hematoxylin-eosin (HE) staining to analyze the pathological damage in the kidney tissue. For analysis of glomerular IgA deposition, the team used a tissue immunofluorescence technique, and for detection of protein expression—toll-like receptor 4 (TLR4), B-cell activating factor (BAFF), and a proliferation-inducing ligand (APRIL)—in mesenteric lymphoid tissues, the team used western blot analysis. Results • For the five groups of mice, the amount or degree of the physiological indicators and inflammatory factors that ELISA detected, the B lymphocytes and IgA sedimentation that immunofluorescence tracing measured, the kidney pathological that HE staining detected, and the expression of immune-related proteins that western blotting measured, all showed a common trend: IgAN group> IgAN+ glomerular endothelial cells (GEC) group> IgAN+anti-TLR4 group> IgAN+anti-TLR4+GEC group> NC group. Conclusions • The TLR4 antibody and GEC for the treatment of the intestinal tract can regulate and repair intestinal function, so that IgAN can also be relieved at the same time. The results supported the hypothesis that a relationship exists between IgAN and the LPS/TLR4 pathway that regulates mesenteric B cells to secrete low-glycosylated poly-IgA1, which provides a new potential therapeutic plan for IgA nephritis. [ABSTRACT FROM AUTHOR]
Copyright of Alternative Therapies in Health & Medicine is the property of InnoVisions Professional Media and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: LPS/TLR4 Pathway Regulates IgA1 Secretion to Induce IgA Nephropathy.
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  Data: <searchLink fieldCode="AR" term="%22Haidong+He%22">Haidong He</searchLink><br /><searchLink fieldCode="AR" term="%22Meilin+Shen%22">Meilin Shen</searchLink><br /><searchLink fieldCode="AR" term="%22Yuyan+Tang%22">Yuyan Tang</searchLink><br /><searchLink fieldCode="AR" term="%22Weiqian+Sun%22">Weiqian Sun</searchLink><br /><searchLink fieldCode="AR" term="%22Xudong+Xu%22">Xudong Xu</searchLink>
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  Data: <searchLink fieldCode="JN" term="%22Alternative+Therapies+in+Health+%26+Medicine%22">Alternative Therapies in Health & Medicine</searchLink>. Jan2024, Vol. 30 Issue 1, p419-425. 7p.
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  Data: <searchLink fieldCode="DE" term="%22IGA+glomerulonephritis%22">IGA glomerulonephritis</searchLink><br /><searchLink fieldCode="DE" term="%22GLOMERULONEPHRITIS%22">GLOMERULONEPHRITIS</searchLink><br /><searchLink fieldCode="DE" term="%22IMMUNOGLOBULIN+A%22">IMMUNOGLOBULIN A</searchLink><br /><searchLink fieldCode="DE" term="%22IMMUNE+complex+diseases%22">IMMUNE complex diseases</searchLink><br /><searchLink fieldCode="DE" term="%22NEPHRITIS%22">NEPHRITIS</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Context • Studies have reported that the incidence and severity of IgA nephropathy (IgAN) are closely related to the imbalance of the intestinal flora. Imbalance of the intestinal flora may cause abnormalities, such as intestinal mucosal immunity or mesenteric B1 lymphocyte subsets. These can lead to an increase in immunoglobulin A (IgA) production and IgA structural changing, which can eventually cause IgA1 deposition in the glomerular mesangial area and nephritis. Objective • The study intended to explore whether the LPS/ TLR4 pathway regulates mesenteric B cells, secreting Gd-IgA1 to induce IgA nephropathy. Design • The research team designed an animal study. Setting • The study took place at Department of Nephrology, Minhang Hospital, Fudan University. Animals • The animals were 60 specific pathogen free (SPF) C57BL/6 (B6, H-2b) male mice from that were 6-8 weeks old and weighed 20-25 grams. Intervention • The research team established a mouse model of IgA nephropathy. The team created five groups of mice: (1) the NC group, a normal negative control group without induced nephropathy and with no treatments; (2) the IgA nephropathy (IgAN) group, a positive control group with induced nephropathy and with no treatments; (3) the IgAN+anti-TLR4 group, an intervention group, with induced nephropathy and with a TLR4- antibody (anti-TLR4) treatment; (4) the IgAN+GEC group, an intervention group, with induced nephropathy and with treatment with glutamine enteric-coated capsules (GEC); and (5) the IgAN+anti-TLR4+GEC group, an intervention group, with induced nephropathy and with treatment with anti-TLR4 and GEC. Outcome Measures • The research team collected the blood and urine of all the mice and used an enzyme-linked immunoassay (ELISA) to analyze the levels of blood creatinine, urine protein, and urea nitrogen (BUN). The team also used the ELISA to analyze signal molecules for serum inflammation: interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), monocyte chemotactic protein 1 (MCP-1), cyclooxygenase-2 (COX2), and galactose-deficient IgA1(Gd-IgA1). The team analyzed the distribution and content of IgA+B220+B lymphocytes in the intestinal tissues of all the mice, using tissue immunofluorescence tracking technology, and used hematoxylin-eosin (HE) staining to analyze the pathological damage in the kidney tissue. For analysis of glomerular IgA deposition, the team used a tissue immunofluorescence technique, and for detection of protein expression—toll-like receptor 4 (TLR4), B-cell activating factor (BAFF), and a proliferation-inducing ligand (APRIL)—in mesenteric lymphoid tissues, the team used western blot analysis. Results • For the five groups of mice, the amount or degree of the physiological indicators and inflammatory factors that ELISA detected, the B lymphocytes and IgA sedimentation that immunofluorescence tracing measured, the kidney pathological that HE staining detected, and the expression of immune-related proteins that western blotting measured, all showed a common trend: IgAN group> IgAN+ glomerular endothelial cells (GEC) group> IgAN+anti-TLR4 group> IgAN+anti-TLR4+GEC group> NC group. Conclusions • The TLR4 antibody and GEC for the treatment of the intestinal tract can regulate and repair intestinal function, so that IgAN can also be relieved at the same time. The results supported the hypothesis that a relationship exists between IgAN and the LPS/TLR4 pathway that regulates mesenteric B cells to secrete low-glycosylated poly-IgA1, which provides a new potential therapeutic plan for IgA nephritis. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
  Group: Ab
  Data: <i>Copyright of Alternative Therapies in Health & Medicine is the property of InnoVisions Professional Media and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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RecordInfo BibRecord:
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      – Code: eng
        Text: English
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        PageCount: 7
        StartPage: 419
    Subjects:
      – SubjectFull: IGA glomerulonephritis
        Type: general
      – SubjectFull: GLOMERULONEPHRITIS
        Type: general
      – SubjectFull: IMMUNOGLOBULIN A
        Type: general
      – SubjectFull: IMMUNE complex diseases
        Type: general
      – SubjectFull: NEPHRITIS
        Type: general
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      – TitleFull: LPS/TLR4 Pathway Regulates IgA1 Secretion to Induce IgA Nephropathy.
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            NameFull: Haidong He
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            NameFull: Meilin Shen
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            NameFull: Yuyan Tang
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              Text: Jan2024
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              Y: 2024
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