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Erratum Free access | 10.1172/JCI79744

α–Intercalated cells defend the urinary system from bacterial infection

Neal Paragas, Ritwij Kulkarni, Max Werth, Kai M. Schmidt-Ott, Catherine Forster, Rong Deng, Qingyin Zhang, Eugenia Singer, Alexander D. Klose, Tian Huai Shen, Kevin P. Francis, Sunetra Ray, Soundarapandian Vijayakumar, Samuel Seward, Mary E. Bovino, Katherine Xu, Yared Takabe, Fábio E. Amaral, Sumit Mohan, Rebecca Wax, Kaitlyn Corbin, Simone Sanna-Cherchi, Kiyoshi Mori, Lynne Johnson, Thomas Nickolas, Vivette D’Agati, Chyuan-Sheng Lin, Andong Qiu, Qais Al-Awqati, Adam J. Ratner, and Jonathan Barasch

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Published December 1, 2014 - More info

Published in Volume 124, Issue 12 on December 1, 2014
J Clin Invest. 2014;124(12):5521–5521. https://doi.org/10.1172/JCI79744.
Copyright © 2014, American Society for Clinical Investigation
Published December 1, 2014 - Version history
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α–Intercalated cells defend the urinary system from bacterial infection
Neal Paragas, … , Adam J. Ratner, Jonathan Barasch
Neal Paragas, … , Adam J. Ratner, Jonathan Barasch
Research Article

α–Intercalated cells defend the urinary system from bacterial infection

Abstract

α–Intercalated cells (A-ICs) within the collecting duct of the kidney are critical for acid-base homeostasis. Here, we have shown that A-ICs also serve as both sentinels and effectors in the defense against urinary infections. In a murine urinary tract infection model, A-ICs bound uropathogenic E. coli and responded by acidifying the urine and secreting the bacteriostatic protein lipocalin 2 (LCN2; also known as NGAL). A-IC–dependent LCN2 secretion required TLR4, as mice expressing an LPS-insensitive form of TLR4 expressed reduced levels of LCN2. The presence of LCN2 in urine was both necessary and sufficient to control the urinary tract infection through iron sequestration, even in the harsh condition of urine acidification. In mice lacking A-ICs, both urinary LCN2 and urinary acidification were reduced, and consequently bacterial clearance was limited. Together these results indicate that A-ICs, which are known to regulate acid-base metabolism, are also critical for urinary defense against pathogenic bacteria. They respond to both cystitis and pyelonephritis by delivering bacteriostatic chemical agents to the lower urinary system.

Authors

Neal Paragas, Ritwij Kulkarni, Max Werth, Kai M. Schmidt-Ott, Catherine Forster, Rong Deng, Qingyin Zhang, Eugenia Singer, Alexander D. Klose, Tian Huai Shen, Kevin P. Francis, Sunetra Ray, Soundarapandian Vijayakumar, Samuel Seward, Mary E. Bovino, Katherine Xu, Yared Takabe, Fábio E. Amaral, Sumit Mohan, Rebecca Wax, Kaitlyn Corbin, Simone Sanna-Cherchi, Kiyoshi Mori, Lynne Johnson, Thomas Nickolas, Vivette D’Agati, Chyuan-Sheng Lin, Andong Qiu, Qais Al-Awqati, Adam J. Ratner, Jonathan Barasch

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Original citation: J Clin Invest. 2014;124(7):2963–2976. doi:10.1172/JCI71630.

Citation for this erratum: J Clin Invest. 2014;124(12):5521. doi:10.1172/JCI79744.

There were errors in Table 1 and Figure 9D. In Table 1, the correct concentration for LCN2 is 1.80 mM. In Figure 9D, the red and blue bars were mislabeled. The correct figure panel appears below.

Figure 9

The JCI regrets the errors.

Footnotes

See the related article beginning on page 2963.

Version history
  • Version 1 (December 1, 2014): No description
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