Expression of the polymeric immunoglobulin receptor and excretion of secretory IgA in the postischemic kidney

Rice, James; Spence, Jeff S.; Megyesi, Judit; Goldblum, Randall M.; Safirstein, Robert

doi:10.1152/ajprenal.1999.276.5.f666

Cited by 9 publications

(11 citation statements)

References 35 publications

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“…We reported decreased pIgR mRNA and protein levels in the kidney in other models of renal stress compared with control, including water-loading (11) and ischemia-reperfusion injury (12). As several factors have been reported to increase transcription of the pIgR, including glucocorticoids (37) and proinflammatory cytokines (38), and E. coli bacterial infection increases cytokines (39) that are known to increase pIgR expression (8,40), we expected to see an increase in pIgR expression in the kidney in our ascending pyelonephritis model.…”

Section: Regulation Of Pigr Rna and Protein Expression In The Kidney mentioning

confidence: 97%

“…We have demonstrated that pIgR mRNA levels and pIgR protein levels are decreased in the rat kidney by renal ischemia (12). The significance of decreased pIgR protein levels induced by ischemia in the mucosal defense of the kidney is suggested by the frequent association of UTI with acute renal failure (13) and with the early (postischemic) renal transplant period (14).…”

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confidence: 97%

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Pyelonephritic Escherichia coli Expressing P Fimbriae Decrease Immune Response of the Mouse Kidney

Rice¹,

Peng²,

Spence³

et al. 2005

Journal of the American Society of Nephrology

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P fimbriae are proteinaceous appendages on the surface of Escherichia coli bacteria that mediate adherence to uroepithelial cells. E. coli that express P fimbriae account for the majority of ascending urinary tract infections in women with normal urinary tracts. The hypothesis that P fimbriae on uropathic E. coli attach to renal epithelia and may regulate the immune response to establish infection was investigated. The polymeric Ig receptor (pIgR), produced by renal epithelia, transports IgA into the urinary space. Kidney pIgR and urine IgA levels were analyzed in a mouse model of ascending pyelonephritis, using E. coli with (P؉) and without (P؊) P fimbriae, to determine whether P(؉) E. coli regulate epithelial pIgR expression and IgA transport into the urine. (P؉) E. coli establish infection and persist to a greater amount than P(؊) E. coli. P(؉)-infected mice downregulate pIgR mRNA and protein levels compared with P(؊)-infected or PBS controls at >48 h. The decrease in pIgR was associated with decreased urinary IgA levels in the P(؉)-infected group at 48 h. pIgR mRNA and protein also decline in P(؉) E. coli-infected LPS-hyporesponsive mice. These studies identify a novel virulence mechanism of E. coli that express P fimbriae. It is proposed that P fimbriae decrease pIgR expression in the kidney and consequently decrease IgA transport into the urinary space. This may explain, in part, how E. coli that bear P fimbriae exploit the immune system of human hosts to establish ascending pyelonephritis. Escherichia coli that express P fimbriae are the most common cause for upper urinary tract infections (UTI) or pyelonephritis (1). The P fimbriae mediate adherence to uroepithelial cells by binding to the Gal␣(1 to 4)Gal disaccharide on the apical surface of renal epithelial cells, glomeruli, and endothelia (2). The expression of P fimbriae on E. coli is important in establishing pyelonephritis, as P fimbriae-specific antibodies prevent the adherence of bacteria to uroepithelial cells in vitro (3) and protect animals from ascending E. coli pyelonephritis in vivo (4). Although P fimbriae are not the sole virulence factor on uropathic E. coli, pyelonephritis with P(ϩ) E. coli strains are more often associated with kidney histopathology than P(Ϫ) E. coli (5). In addition to its role as an adhesin, E. coli that express P fimbriae may determine the pattern of the local immune response via interaction with its P-specific glycosphingolipid receptors present on uroepithelial cells (6) and/or by signaling via inflammatory cytokines (7).The secretions that protect the mucosal surface of renal epithelia contain an array of host defense factors, including secretory immunoglobulins, of which IgA is the major class. The polymeric Ig receptor (pIgR) is responsible for transporting these secretory immunoglobulins (S-Ig) in vesicles from the basolateral to the apical surface of epithelial cells (8 -10), including renal tubule cells. The extracellular portion of the pIgR, termed secretory component (SC), is cleaved at the apical surface ...

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Section: Regulation Of Pigr Rna and Protein Expression In The Kidney mentioning

confidence: 97%

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confidence: 97%

Pyelonephritic Escherichia coli Expressing P Fimbriae Decrease Immune Response of the Mouse Kidney

Rice¹,

Peng²,

Spence³

et al. 2005

Journal of the American Society of Nephrology

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“…dIgA is typically produced by plasma cells located in the lamina propria, near the basolateral surface of mucosal epithelia. pIgR has been found in mouse and rat kidney tubule epithelial cells (19), and pIgR expression can be regulated by water deprivation, vasopressin administration, or renal ischemia-reperfusion in rats (20,21). dIgA can be found in urine, suggesting that it can reach the urinary space by pIgR-mediated transcytosis (21).…”

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confidence: 99%

“…pIgR has been found in mouse and rat kidney tubule epithelial cells (19), and pIgR expression can be regulated by water deprivation, vasopressin administration, or renal ischemia-reperfusion in rats (20,21). dIgA can be found in urine, suggesting that it can reach the urinary space by pIgR-mediated transcytosis (21). pIgR expression has been shown to be regulated by IL-4, TNF-␣, and IFN-␥ in airway, intestinal, and mammary gland epithelial cells (22), and a STAT6 binding domain has been identified in intron 1 of the pIgR gene (23,24).…”

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confidence: 99%

Exploitation of the Polymeric Immunoglobulin Receptor for Antibody Targeting to Renal Cyst Lumens in Polycystic Kidney Disease

Olsan

Matsushita

Rezaei

et al. 2015

Journal of Biological Chemistry

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“…82,83 One study that investigated the tubular expression of secretory component failed to demonstrate positivity for this receptor in rat glomeruli. 84 Human specimens have not yet been investigated carefully.…”

Section: Secretory Componentmentioning

confidence: 99%

IgA-Nephropathy: how does IgA activate the mesangial cell?

Westerhuis

Kitahara

Floege

2001

Clinical and Experimental Nephrology

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Immunoglobulin (Ig)A-nephropathy (IgAN), the most common glomerulonephritis worldwide, is immunohistochemically characterized by the deposition of IgA in the renal mesangium. The mechanism of binding and deposition of IgA in the kidney is still not clear. It has been demonstrated that IgA-binding to mesangial cells (MCs) is followed by cell activation, as indicated by the enhanced expression of proinflammatory cytokines, the nuclear transcriptional factor (NF)kB, or the protooncogene c-jun. The binding of IgA to MC is mediated via the Fc part of the immunoglobulin, as demonstrated by blocking experiments using Fc-fragments of IgA. The known myeloid Fc receptor for IgA (FcαRI/CD89), as well as other known receptors able to bind IgA (asialoglycoprotein receptor, mannose receptor, secretory component), are not expressed on MC. However the hepatic asialoglycoprotein receptor, as well as the myeloid FcαRI, play an important role in the clearance of IgA from the circulation. In patients with IgAN, this function seems to be impaired, possibly as a consequence of reduced glycosylation of the hinge region of IgA1 which affects IgA-receptor interactions. This could lead to increased plasma levels of IgA, resulting in increased binding of IgA to MC via a hitherto unidentified Fc receptor for IgA. Recently, the expression of mRNA transcripts with partial identity to CD89 was reported on human MC in vitro. These transcripts could be part of this new receptor, with partial homology to recently discovered genes that map to chromosome 19Q13.4 and encode a family of type I transmembrane proteins.

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Expression of the polymeric immunoglobulin receptor and excretion of secretory IgA in the postischemic kidney

Cited by 9 publications

References 35 publications

Pyelonephritic Escherichia coli Expressing P Fimbriae Decrease Immune Response of the Mouse Kidney

Pyelonephritic Escherichia coli Expressing P Fimbriae Decrease Immune Response of the Mouse Kidney

Exploitation of the Polymeric Immunoglobulin Receptor for Antibody Targeting to Renal Cyst Lumens in Polycystic Kidney Disease

IgA-Nephropathy: how does IgA activate the mesangial cell?

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