Cytokine-induced neutrophil chemoattractant production by primary rat alveolar type II cells

Tawni L. Crippen, Kirk C. Klasing, Dallas M. Hyde

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

This study was designed to determine the production of the chemokine cytokine-induced neutrophil chemoattractant (CINC) by primary rat alveolar type II (ATII) cells upon stimulation with exogenous and endogenous proinflammatory factors. Cultures of primary rat ATII cells were exposed to lipopolysaccharide (LPS), interleukin-1 beta (IL-1 β) or tumor necrosis factor-alpha (TNF α) over a 16 hour period and the production of CINC both apically and basolaterally was measured by ELISA. Compared to unstimulated (UNS) cultures, LPS, IL-1 β and TNF α were found to significantly increase the level of CINC detected in culture by two, four and sixteen hours post stimulation, respectively. ATII cells also demonstrated a polar secretion of CINC. The accumulation of CINC basolaterally was significantly more than apically; 133%, 45%, 117% and 123% for UNS, IL-1 β, LPS and TNF α respectively. We demonstrated that primary rat ATII cells may participate in the chemokine network during inflammation by the production of CINC upon stimulation with endogenous and exogenous factors.

Original languageEnglish (US)
Pages (from-to)575-586
Number of pages12
JournalInflammation
Volume19
Issue number5
DOIs
StatePublished - Oct 1995

Fingerprint

Alveolar Epithelial Cells
Chemotactic Factors
Neutrophils
Cytokines
Interleukin-1beta
Lipopolysaccharides
Tumor Necrosis Factor-alpha
Chemokines
Enzyme-Linked Immunosorbent Assay
Inflammation

ASJC Scopus subject areas

  • Medicine(all)
  • Immunology
  • Cell Biology

Cite this

Cytokine-induced neutrophil chemoattractant production by primary rat alveolar type II cells. / Crippen, Tawni L.; Klasing, Kirk C.; Hyde, Dallas M.

In: Inflammation, Vol. 19, No. 5, 10.1995, p. 575-586.

Research output: Contribution to journalArticle

Crippen, Tawni L. ; Klasing, Kirk C. ; Hyde, Dallas M. / Cytokine-induced neutrophil chemoattractant production by primary rat alveolar type II cells. In: Inflammation. 1995 ; Vol. 19, No. 5. pp. 575-586.
@article{d66167831a524e1fbb109dce4f821182,
title = "Cytokine-induced neutrophil chemoattractant production by primary rat alveolar type II cells",
abstract = "This study was designed to determine the production of the chemokine cytokine-induced neutrophil chemoattractant (CINC) by primary rat alveolar type II (ATII) cells upon stimulation with exogenous and endogenous proinflammatory factors. Cultures of primary rat ATII cells were exposed to lipopolysaccharide (LPS), interleukin-1 beta (IL-1 β) or tumor necrosis factor-alpha (TNF α) over a 16 hour period and the production of CINC both apically and basolaterally was measured by ELISA. Compared to unstimulated (UNS) cultures, LPS, IL-1 β and TNF α were found to significantly increase the level of CINC detected in culture by two, four and sixteen hours post stimulation, respectively. ATII cells also demonstrated a polar secretion of CINC. The accumulation of CINC basolaterally was significantly more than apically; 133{\%}, 45{\%}, 117{\%} and 123{\%} for UNS, IL-1 β, LPS and TNF α respectively. We demonstrated that primary rat ATII cells may participate in the chemokine network during inflammation by the production of CINC upon stimulation with endogenous and exogenous factors.",
author = "Crippen, {Tawni L.} and Klasing, {Kirk C.} and Hyde, {Dallas M.}",
year = "1995",
month = "10",
doi = "10.1007/BF01539137",
language = "English (US)",
volume = "19",
pages = "575--586",
journal = "Inflammation",
issn = "0360-3997",
publisher = "Springer New York",
number = "5",

}

TY - JOUR

T1 - Cytokine-induced neutrophil chemoattractant production by primary rat alveolar type II cells

AU - Crippen, Tawni L.

AU - Klasing, Kirk C.

AU - Hyde, Dallas M.

PY - 1995/10

Y1 - 1995/10

N2 - This study was designed to determine the production of the chemokine cytokine-induced neutrophil chemoattractant (CINC) by primary rat alveolar type II (ATII) cells upon stimulation with exogenous and endogenous proinflammatory factors. Cultures of primary rat ATII cells were exposed to lipopolysaccharide (LPS), interleukin-1 beta (IL-1 β) or tumor necrosis factor-alpha (TNF α) over a 16 hour period and the production of CINC both apically and basolaterally was measured by ELISA. Compared to unstimulated (UNS) cultures, LPS, IL-1 β and TNF α were found to significantly increase the level of CINC detected in culture by two, four and sixteen hours post stimulation, respectively. ATII cells also demonstrated a polar secretion of CINC. The accumulation of CINC basolaterally was significantly more than apically; 133%, 45%, 117% and 123% for UNS, IL-1 β, LPS and TNF α respectively. We demonstrated that primary rat ATII cells may participate in the chemokine network during inflammation by the production of CINC upon stimulation with endogenous and exogenous factors.

AB - This study was designed to determine the production of the chemokine cytokine-induced neutrophil chemoattractant (CINC) by primary rat alveolar type II (ATII) cells upon stimulation with exogenous and endogenous proinflammatory factors. Cultures of primary rat ATII cells were exposed to lipopolysaccharide (LPS), interleukin-1 beta (IL-1 β) or tumor necrosis factor-alpha (TNF α) over a 16 hour period and the production of CINC both apically and basolaterally was measured by ELISA. Compared to unstimulated (UNS) cultures, LPS, IL-1 β and TNF α were found to significantly increase the level of CINC detected in culture by two, four and sixteen hours post stimulation, respectively. ATII cells also demonstrated a polar secretion of CINC. The accumulation of CINC basolaterally was significantly more than apically; 133%, 45%, 117% and 123% for UNS, IL-1 β, LPS and TNF α respectively. We demonstrated that primary rat ATII cells may participate in the chemokine network during inflammation by the production of CINC upon stimulation with endogenous and exogenous factors.

UR - http://www.scopus.com/inward/record.url?scp=0029115225&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029115225&partnerID=8YFLogxK

U2 - 10.1007/BF01539137

DO - 10.1007/BF01539137

M3 - Article

C2 - 8543372

AN - SCOPUS:0029115225

VL - 19

SP - 575

EP - 586

JO - Inflammation

JF - Inflammation

SN - 0360-3997

IS - 5

ER -