Macrophage inflammatory protein-1α (not T helper type 2 cytokines) is associated with severe forms of respiratory syncytial virus bronchiolitis

Roberto Garofalo, J. Patti, K. A. Hintz, V. Hill, P. L. Ogra, R. C. Welliver

Research output: Contribution to journalArticle

175 Citations (Scopus)

Abstract

It has been suggested that the pathogenesis of respiratory syncytial virus (RSV) infection is related to the development of T helper (Th) type 2 cytokine responses. The presence of Th1 and Th2 cytokines and the chemokines macrophage inflammatory protein (MIP)-1α and monocyte chemotactic protein (MCP)-1 were assessed by ELISA in nasopharyngeal secretions of infants with RSV infection. Infants with mild bronchiolitis had increased Th1 cytokines and reduced Th2 cytokines, compared with infants with upper respiratory tract illness alone. Severe bronchiolitis was characterized by a more balanced Th1-Th2 response that did not differ from that of infants with upper respiratory tract illness alone. In contrast, MIP-1α was markedly increased in infants with severe bronchiolitis. MIP-1α and MCP-1 levels also were inversely related to oxygen saturation (P<.005). Thus, the severity of RSV bronchiolitis appears to be related more to chemokine release than to Th2 cytokine production.

Original languageEnglish (US)
Pages (from-to)393-399
Number of pages7
JournalJournal of Infectious Diseases
Volume184
Issue number4
DOIs
StatePublished - Aug 15 2001
Externally publishedYes

Fingerprint

Macrophage Inflammatory Proteins
Bronchiolitis
Respiratory Syncytial Viruses
Cytokines
Respiratory Syncytial Virus Infections
Chemokine CCL2
Chemokines
Respiratory System
Enzyme-Linked Immunosorbent Assay
Oxygen

ASJC Scopus subject areas

  • Public Health, Environmental and Occupational Health
  • Immunology

Cite this

Macrophage inflammatory protein-1α (not T helper type 2 cytokines) is associated with severe forms of respiratory syncytial virus bronchiolitis. / Garofalo, Roberto; Patti, J.; Hintz, K. A.; Hill, V.; Ogra, P. L.; Welliver, R. C.

In: Journal of Infectious Diseases, Vol. 184, No. 4, 15.08.2001, p. 393-399.

Research output: Contribution to journalArticle

@article{f1a370a0418349a283c4acdd1dd7cea4,
title = "Macrophage inflammatory protein-1α (not T helper type 2 cytokines) is associated with severe forms of respiratory syncytial virus bronchiolitis",
abstract = "It has been suggested that the pathogenesis of respiratory syncytial virus (RSV) infection is related to the development of T helper (Th) type 2 cytokine responses. The presence of Th1 and Th2 cytokines and the chemokines macrophage inflammatory protein (MIP)-1α and monocyte chemotactic protein (MCP)-1 were assessed by ELISA in nasopharyngeal secretions of infants with RSV infection. Infants with mild bronchiolitis had increased Th1 cytokines and reduced Th2 cytokines, compared with infants with upper respiratory tract illness alone. Severe bronchiolitis was characterized by a more balanced Th1-Th2 response that did not differ from that of infants with upper respiratory tract illness alone. In contrast, MIP-1α was markedly increased in infants with severe bronchiolitis. MIP-1α and MCP-1 levels also were inversely related to oxygen saturation (P<.005). Thus, the severity of RSV bronchiolitis appears to be related more to chemokine release than to Th2 cytokine production.",
author = "Roberto Garofalo and J. Patti and Hintz, {K. A.} and V. Hill and Ogra, {P. L.} and Welliver, {R. C.}",
year = "2001",
month = "8",
day = "15",
doi = "10.1086/322788",
language = "English (US)",
volume = "184",
pages = "393--399",
journal = "Journal of Infectious Diseases",
issn = "0022-1899",
publisher = "Oxford University Press",
number = "4",

}

TY - JOUR

T1 - Macrophage inflammatory protein-1α (not T helper type 2 cytokines) is associated with severe forms of respiratory syncytial virus bronchiolitis

AU - Garofalo, Roberto

AU - Patti, J.

AU - Hintz, K. A.

AU - Hill, V.

AU - Ogra, P. L.

AU - Welliver, R. C.

PY - 2001/8/15

Y1 - 2001/8/15

N2 - It has been suggested that the pathogenesis of respiratory syncytial virus (RSV) infection is related to the development of T helper (Th) type 2 cytokine responses. The presence of Th1 and Th2 cytokines and the chemokines macrophage inflammatory protein (MIP)-1α and monocyte chemotactic protein (MCP)-1 were assessed by ELISA in nasopharyngeal secretions of infants with RSV infection. Infants with mild bronchiolitis had increased Th1 cytokines and reduced Th2 cytokines, compared with infants with upper respiratory tract illness alone. Severe bronchiolitis was characterized by a more balanced Th1-Th2 response that did not differ from that of infants with upper respiratory tract illness alone. In contrast, MIP-1α was markedly increased in infants with severe bronchiolitis. MIP-1α and MCP-1 levels also were inversely related to oxygen saturation (P<.005). Thus, the severity of RSV bronchiolitis appears to be related more to chemokine release than to Th2 cytokine production.

AB - It has been suggested that the pathogenesis of respiratory syncytial virus (RSV) infection is related to the development of T helper (Th) type 2 cytokine responses. The presence of Th1 and Th2 cytokines and the chemokines macrophage inflammatory protein (MIP)-1α and monocyte chemotactic protein (MCP)-1 were assessed by ELISA in nasopharyngeal secretions of infants with RSV infection. Infants with mild bronchiolitis had increased Th1 cytokines and reduced Th2 cytokines, compared with infants with upper respiratory tract illness alone. Severe bronchiolitis was characterized by a more balanced Th1-Th2 response that did not differ from that of infants with upper respiratory tract illness alone. In contrast, MIP-1α was markedly increased in infants with severe bronchiolitis. MIP-1α and MCP-1 levels also were inversely related to oxygen saturation (P<.005). Thus, the severity of RSV bronchiolitis appears to be related more to chemokine release than to Th2 cytokine production.

UR - http://www.scopus.com/inward/record.url?scp=0035882454&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035882454&partnerID=8YFLogxK

U2 - 10.1086/322788

DO - 10.1086/322788

M3 - Article

VL - 184

SP - 393

EP - 399

JO - Journal of Infectious Diseases

JF - Journal of Infectious Diseases

SN - 0022-1899

IS - 4

ER -