Could streptococcal erythrogenic toxin B induce inflammation prior to the development of immune complex deposits in poststreptococcal glomerulonephritis?

Jesus Mosquera, Maritza Josefina Romero Lucas, Ninoska Viera, Jaimar Rincon, Adriana Pedreáñez

Research output: Contribution to journalShort survey

4 Citations (Scopus)

Abstract

Acute poststreptococcal glomerulonephritis (APSGN) is a consequence of the immune response to streptococcal antigens with further in situ antigen-antibody interaction and deposition of circulating immune complexes, resulting in the activation of complement and the inflammatory process. These events are related to a previous antibody response. However, early renal events, when circulating streptococcal antigens bind to the kidney during streptococcal infection, remain unknown. Cationic streptococcal erythrogenic toxin type B (ETB) and its precursor (ETBP) are largely produced by nephritogenic streptococci and have high affinity for anionic glomerular structures. Renal deposition of ETB/ETBP makes conceivable a possible interaction between these streptococcal proteins with intrinsic glomerular cells or infiltrating leukocytes. Since ETB/ETBP are chemotactic for leukocytes and capable of inducing proliferation, cytokine and chemokine production, expression of adhesion molecules and apoptosis in renal cells and leukocytes, the early presence of these proteins could be a relevant event before and during antigen-antibody interaction takes place in renal tissues.

Original languageEnglish (US)
JournalNephron - Experimental Nephrology
Volume105
Issue number2
DOIs
StatePublished - Jan 1 2007
Externally publishedYes

Fingerprint

Glomerulonephritis
Antigen-Antibody Complex
Inflammation
Kidney
Antigens
Leukocytes
Streptococcal Infections
Antibodies
Complement Activation
Streptococcus
Chemokines
Antibody Formation
Proteins
erythrogenic toxin
Apoptosis
Cytokines

Keywords

  • Cytokines
  • Glomerulonephritis
  • Hypercellularity
  • Proliferation
  • Streptococcal erythrotoxin

ASJC Scopus subject areas

  • Nephrology

Cite this

Could streptococcal erythrogenic toxin B induce inflammation prior to the development of immune complex deposits in poststreptococcal glomerulonephritis? / Mosquera, Jesus; Romero Lucas, Maritza Josefina; Viera, Ninoska; Rincon, Jaimar; Pedreáñez, Adriana.

In: Nephron - Experimental Nephrology, Vol. 105, No. 2, 01.01.2007.

Research output: Contribution to journalShort survey

@article{1c27b18b104c4d758f4f0ae73d10f802,
title = "Could streptococcal erythrogenic toxin B induce inflammation prior to the development of immune complex deposits in poststreptococcal glomerulonephritis?",
abstract = "Acute poststreptococcal glomerulonephritis (APSGN) is a consequence of the immune response to streptococcal antigens with further in situ antigen-antibody interaction and deposition of circulating immune complexes, resulting in the activation of complement and the inflammatory process. These events are related to a previous antibody response. However, early renal events, when circulating streptococcal antigens bind to the kidney during streptococcal infection, remain unknown. Cationic streptococcal erythrogenic toxin type B (ETB) and its precursor (ETBP) are largely produced by nephritogenic streptococci and have high affinity for anionic glomerular structures. Renal deposition of ETB/ETBP makes conceivable a possible interaction between these streptococcal proteins with intrinsic glomerular cells or infiltrating leukocytes. Since ETB/ETBP are chemotactic for leukocytes and capable of inducing proliferation, cytokine and chemokine production, expression of adhesion molecules and apoptosis in renal cells and leukocytes, the early presence of these proteins could be a relevant event before and during antigen-antibody interaction takes place in renal tissues.",
keywords = "Cytokines, Glomerulonephritis, Hypercellularity, Proliferation, Streptococcal erythrotoxin",
author = "Jesus Mosquera and {Romero Lucas}, {Maritza Josefina} and Ninoska Viera and Jaimar Rincon and Adriana Pedre{\'a}{\~n}ez",
year = "2007",
month = "1",
day = "1",
doi = "10.1159/000097602",
language = "English (US)",
volume = "105",
journal = "Nephron - Experimental Nephrology",
issn = "0028-2766",
publisher = "S. Karger AG",
number = "2",

}

TY - JOUR

T1 - Could streptococcal erythrogenic toxin B induce inflammation prior to the development of immune complex deposits in poststreptococcal glomerulonephritis?

AU - Mosquera, Jesus

AU - Romero Lucas, Maritza Josefina

AU - Viera, Ninoska

AU - Rincon, Jaimar

AU - Pedreáñez, Adriana

PY - 2007/1/1

Y1 - 2007/1/1

N2 - Acute poststreptococcal glomerulonephritis (APSGN) is a consequence of the immune response to streptococcal antigens with further in situ antigen-antibody interaction and deposition of circulating immune complexes, resulting in the activation of complement and the inflammatory process. These events are related to a previous antibody response. However, early renal events, when circulating streptococcal antigens bind to the kidney during streptococcal infection, remain unknown. Cationic streptococcal erythrogenic toxin type B (ETB) and its precursor (ETBP) are largely produced by nephritogenic streptococci and have high affinity for anionic glomerular structures. Renal deposition of ETB/ETBP makes conceivable a possible interaction between these streptococcal proteins with intrinsic glomerular cells or infiltrating leukocytes. Since ETB/ETBP are chemotactic for leukocytes and capable of inducing proliferation, cytokine and chemokine production, expression of adhesion molecules and apoptosis in renal cells and leukocytes, the early presence of these proteins could be a relevant event before and during antigen-antibody interaction takes place in renal tissues.

AB - Acute poststreptococcal glomerulonephritis (APSGN) is a consequence of the immune response to streptococcal antigens with further in situ antigen-antibody interaction and deposition of circulating immune complexes, resulting in the activation of complement and the inflammatory process. These events are related to a previous antibody response. However, early renal events, when circulating streptococcal antigens bind to the kidney during streptococcal infection, remain unknown. Cationic streptococcal erythrogenic toxin type B (ETB) and its precursor (ETBP) are largely produced by nephritogenic streptococci and have high affinity for anionic glomerular structures. Renal deposition of ETB/ETBP makes conceivable a possible interaction between these streptococcal proteins with intrinsic glomerular cells or infiltrating leukocytes. Since ETB/ETBP are chemotactic for leukocytes and capable of inducing proliferation, cytokine and chemokine production, expression of adhesion molecules and apoptosis in renal cells and leukocytes, the early presence of these proteins could be a relevant event before and during antigen-antibody interaction takes place in renal tissues.

KW - Cytokines

KW - Glomerulonephritis

KW - Hypercellularity

KW - Proliferation

KW - Streptococcal erythrotoxin

UR - http://www.scopus.com/inward/record.url?scp=33846440522&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33846440522&partnerID=8YFLogxK

U2 - 10.1159/000097602

DO - 10.1159/000097602

M3 - Short survey

VL - 105

JO - Nephron - Experimental Nephrology

JF - Nephron - Experimental Nephrology

SN - 0028-2766

IS - 2

ER -