Macrophage inflammatory protein-2 is required for neutrophil passage across the epithelial barrier of the infected urinary tract
(1999) In Journal of Immunology 162(5). p.3037-3044- Abstract
- IL-8 is a major human neutrophil chemoattractant at mucosal infection sites. This study examined the C-X-C chemokine response to mucosal infection, and, specifically, the role of macrophage inflammatory protein (MIP)-2, one of the mouse IL-8 equivalents, for neutrophil-epithelial interactions. Following intravesical Escherichia coli infection, several C-X-C chemokines were secreted into the urine, but only MIP-2 concentrations correlated to neutrophil numbers. Tissue quantitation demonstrated that kidney MIP-2 production was triggered by infection, and immunohistochemistry identified the kidney epithelium as a main source of MIP-2. Treatment with anti-MIP-2 Ab reduced the urine neutrophil numbers, but the mice had normal tissue neutrophil... (More)
- IL-8 is a major human neutrophil chemoattractant at mucosal infection sites. This study examined the C-X-C chemokine response to mucosal infection, and, specifically, the role of macrophage inflammatory protein (MIP)-2, one of the mouse IL-8 equivalents, for neutrophil-epithelial interactions. Following intravesical Escherichia coli infection, several C-X-C chemokines were secreted into the urine, but only MIP-2 concentrations correlated to neutrophil numbers. Tissue quantitation demonstrated that kidney MIP-2 production was triggered by infection, and immunohistochemistry identified the kidney epithelium as a main source of MIP-2. Treatment with anti-MIP-2 Ab reduced the urine neutrophil numbers, but the mice had normal tissue neutrophil levels. By immunohistochemistry, the neutrophils were found in aggregates under the pelvic epithelium, but in control mice the neutrophils crossed the urothelium into the urine. The results demonstrate that different chemokines direct neutrophil migration from the bloodstream to the lamina propria and across the epithelium and that MIP-2 serves the latter function. These findings suggest that neutrophils cross epithelial cell barriers in a highly regulated manner in response to chemokines elaborated at this site. This is yet another mechanism that defines the mucosal compartment and differentiates the local from the systemic host response. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1115679
- author
- Hang, Long ; Haraoka, Masashi ; Agace, William LU ; Leffler, Hakon LU ; Burdick, Marie ; Strieter, Robert and Svanborg, Catharina LU
- organization
- publishing date
- 1999
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Journal of Immunology
- volume
- 162
- issue
- 5
- pages
- 3037 - 3044
- publisher
- American Association of Immunologists
- external identifiers
-
- pmid:10072556
- scopus:0033104826
- ISSN
- 1550-6606
- language
- English
- LU publication?
- yes
- id
- f1067d98-4a6e-4e5b-b8f9-f7cf90262538 (old id 1115679)
- alternative location
- http://www.jimmunol.org/cgi/content/full/162/5/3037
- date added to LUP
- 2016-04-01 16:50:01
- date last changed
- 2022-01-28 22:28:36
@article{f1067d98-4a6e-4e5b-b8f9-f7cf90262538,
abstract = {{IL-8 is a major human neutrophil chemoattractant at mucosal infection sites. This study examined the C-X-C chemokine response to mucosal infection, and, specifically, the role of macrophage inflammatory protein (MIP)-2, one of the mouse IL-8 equivalents, for neutrophil-epithelial interactions. Following intravesical Escherichia coli infection, several C-X-C chemokines were secreted into the urine, but only MIP-2 concentrations correlated to neutrophil numbers. Tissue quantitation demonstrated that kidney MIP-2 production was triggered by infection, and immunohistochemistry identified the kidney epithelium as a main source of MIP-2. Treatment with anti-MIP-2 Ab reduced the urine neutrophil numbers, but the mice had normal tissue neutrophil levels. By immunohistochemistry, the neutrophils were found in aggregates under the pelvic epithelium, but in control mice the neutrophils crossed the urothelium into the urine. The results demonstrate that different chemokines direct neutrophil migration from the bloodstream to the lamina propria and across the epithelium and that MIP-2 serves the latter function. These findings suggest that neutrophils cross epithelial cell barriers in a highly regulated manner in response to chemokines elaborated at this site. This is yet another mechanism that defines the mucosal compartment and differentiates the local from the systemic host response.}},
author = {{Hang, Long and Haraoka, Masashi and Agace, William and Leffler, Hakon and Burdick, Marie and Strieter, Robert and Svanborg, Catharina}},
issn = {{1550-6606}},
language = {{eng}},
number = {{5}},
pages = {{3037--3044}},
publisher = {{American Association of Immunologists}},
series = {{Journal of Immunology}},
title = {{Macrophage inflammatory protein-2 is required for neutrophil passage across the epithelial barrier of the infected urinary tract}},
url = {{http://www.jimmunol.org/cgi/content/full/162/5/3037}},
volume = {{162}},
year = {{1999}},
}