Transient neutrophil infiltration after allergen challenge is dependent on specific antibodies and FcγIII receptors

Christian Taube, Azzeddine Dakhama, Yeong Ho Rha, Katsuyuki Takeda, Anthony Joetham, Jung Won Park, Annette Balhorn, Toshiyuki Takai, Katie R. Poch, Jerry A. Nick, Erwin W. Gelfand

Research output: Contribution to journalArticle

36 Citations (Scopus)

Abstract

Following allergen challenge of sensitized mice, neutrophils are the first inflammatory cells found in bronchoalveolar lavage (BAL) fluid. To determine the underlying mechanism for their accumulation, mice were sensitized to OVA on days 0 and 14, and received, on day 28, a single intranasal challenge (s.i.n.) with either OVA or ragweed. Eight hours after the s.i.n., BAL fluid was obtained. BALB/c mice sensitized and challenged with OVA showed significantly higher total cell counts and numbers of neutrophils in BAL fluid compared to the OVA-sensitized and ragweed-challenged or nonsensitized mice. Levels of neutrophil chemokines in BAL fluid supernatants were markedly elevated in the sensitized and OVA-challenged mice; FcεRI-deficient mice showed comparable numbers of neutrophils and neutrophil chemokines in BAL fluid after s.i.n. But in sensitized mice lacking the Fc common γ-chain and B cell-deficient mice, the number of neutrophils and levels of neutrophil chemokines in BAL fluid were significantly lower. Further, mice lacking the FcγRIII did not develop this early neutrophil influx. Neutrophil infiltration could be induced in naive mice following intranasal instillation of allergen combined with allergen-specific IgG1. In addition, macrophages from sensitized mice were stimulated with allergen and activated to produce neutrophil chemokines. These results demonstrate that neutrophil influx after allergen challenge requires prior sensitization, is allergen-specific, is mediated through FcγRIII, and is dependent on the presence of Ab.

Original languageEnglish
Pages (from-to)4301-4309
Number of pages9
JournalJournal of Immunology
Volume170
Issue number8
Publication statusPublished - 2003 Apr 15

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Neutrophil Infiltration
Allergens
Neutrophils
Bronchoalveolar Lavage Fluid
Antibodies
Chemokines
Ambrosia
Cell Count
B-Lymphocytes
Immunoglobulin G
Macrophages

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

Cite this

Taube, C., Dakhama, A., Rha, Y. H., Takeda, K., Joetham, A., Park, J. W., ... Gelfand, E. W. (2003). Transient neutrophil infiltration after allergen challenge is dependent on specific antibodies and FcγIII receptors. Journal of Immunology, 170(8), 4301-4309.
Taube, Christian ; Dakhama, Azzeddine ; Rha, Yeong Ho ; Takeda, Katsuyuki ; Joetham, Anthony ; Park, Jung Won ; Balhorn, Annette ; Takai, Toshiyuki ; Poch, Katie R. ; Nick, Jerry A. ; Gelfand, Erwin W. / Transient neutrophil infiltration after allergen challenge is dependent on specific antibodies and FcγIII receptors. In: Journal of Immunology. 2003 ; Vol. 170, No. 8. pp. 4301-4309.
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abstract = "Following allergen challenge of sensitized mice, neutrophils are the first inflammatory cells found in bronchoalveolar lavage (BAL) fluid. To determine the underlying mechanism for their accumulation, mice were sensitized to OVA on days 0 and 14, and received, on day 28, a single intranasal challenge (s.i.n.) with either OVA or ragweed. Eight hours after the s.i.n., BAL fluid was obtained. BALB/c mice sensitized and challenged with OVA showed significantly higher total cell counts and numbers of neutrophils in BAL fluid compared to the OVA-sensitized and ragweed-challenged or nonsensitized mice. Levels of neutrophil chemokines in BAL fluid supernatants were markedly elevated in the sensitized and OVA-challenged mice; FcεRI-deficient mice showed comparable numbers of neutrophils and neutrophil chemokines in BAL fluid after s.i.n. But in sensitized mice lacking the Fc common γ-chain and B cell-deficient mice, the number of neutrophils and levels of neutrophil chemokines in BAL fluid were significantly lower. Further, mice lacking the FcγRIII did not develop this early neutrophil influx. Neutrophil infiltration could be induced in naive mice following intranasal instillation of allergen combined with allergen-specific IgG1. In addition, macrophages from sensitized mice were stimulated with allergen and activated to produce neutrophil chemokines. These results demonstrate that neutrophil influx after allergen challenge requires prior sensitization, is allergen-specific, is mediated through FcγRIII, and is dependent on the presence of Ab.",
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Taube, C, Dakhama, A, Rha, YH, Takeda, K, Joetham, A, Park, JW, Balhorn, A, Takai, T, Poch, KR, Nick, JA & Gelfand, EW 2003, 'Transient neutrophil infiltration after allergen challenge is dependent on specific antibodies and FcγIII receptors', Journal of Immunology, vol. 170, no. 8, pp. 4301-4309.

Transient neutrophil infiltration after allergen challenge is dependent on specific antibodies and FcγIII receptors. / Taube, Christian; Dakhama, Azzeddine; Rha, Yeong Ho; Takeda, Katsuyuki; Joetham, Anthony; Park, Jung Won; Balhorn, Annette; Takai, Toshiyuki; Poch, Katie R.; Nick, Jerry A.; Gelfand, Erwin W.

In: Journal of Immunology, Vol. 170, No. 8, 15.04.2003, p. 4301-4309.

Research output: Contribution to journalArticle

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T1 - Transient neutrophil infiltration after allergen challenge is dependent on specific antibodies and FcγIII receptors

AU - Taube, Christian

AU - Dakhama, Azzeddine

AU - Rha, Yeong Ho

AU - Takeda, Katsuyuki

AU - Joetham, Anthony

AU - Park, Jung Won

AU - Balhorn, Annette

AU - Takai, Toshiyuki

AU - Poch, Katie R.

AU - Nick, Jerry A.

AU - Gelfand, Erwin W.

PY - 2003/4/15

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N2 - Following allergen challenge of sensitized mice, neutrophils are the first inflammatory cells found in bronchoalveolar lavage (BAL) fluid. To determine the underlying mechanism for their accumulation, mice were sensitized to OVA on days 0 and 14, and received, on day 28, a single intranasal challenge (s.i.n.) with either OVA or ragweed. Eight hours after the s.i.n., BAL fluid was obtained. BALB/c mice sensitized and challenged with OVA showed significantly higher total cell counts and numbers of neutrophils in BAL fluid compared to the OVA-sensitized and ragweed-challenged or nonsensitized mice. Levels of neutrophil chemokines in BAL fluid supernatants were markedly elevated in the sensitized and OVA-challenged mice; FcεRI-deficient mice showed comparable numbers of neutrophils and neutrophil chemokines in BAL fluid after s.i.n. But in sensitized mice lacking the Fc common γ-chain and B cell-deficient mice, the number of neutrophils and levels of neutrophil chemokines in BAL fluid were significantly lower. Further, mice lacking the FcγRIII did not develop this early neutrophil influx. Neutrophil infiltration could be induced in naive mice following intranasal instillation of allergen combined with allergen-specific IgG1. In addition, macrophages from sensitized mice were stimulated with allergen and activated to produce neutrophil chemokines. These results demonstrate that neutrophil influx after allergen challenge requires prior sensitization, is allergen-specific, is mediated through FcγRIII, and is dependent on the presence of Ab.

AB - Following allergen challenge of sensitized mice, neutrophils are the first inflammatory cells found in bronchoalveolar lavage (BAL) fluid. To determine the underlying mechanism for their accumulation, mice were sensitized to OVA on days 0 and 14, and received, on day 28, a single intranasal challenge (s.i.n.) with either OVA or ragweed. Eight hours after the s.i.n., BAL fluid was obtained. BALB/c mice sensitized and challenged with OVA showed significantly higher total cell counts and numbers of neutrophils in BAL fluid compared to the OVA-sensitized and ragweed-challenged or nonsensitized mice. Levels of neutrophil chemokines in BAL fluid supernatants were markedly elevated in the sensitized and OVA-challenged mice; FcεRI-deficient mice showed comparable numbers of neutrophils and neutrophil chemokines in BAL fluid after s.i.n. But in sensitized mice lacking the Fc common γ-chain and B cell-deficient mice, the number of neutrophils and levels of neutrophil chemokines in BAL fluid were significantly lower. Further, mice lacking the FcγRIII did not develop this early neutrophil influx. Neutrophil infiltration could be induced in naive mice following intranasal instillation of allergen combined with allergen-specific IgG1. In addition, macrophages from sensitized mice were stimulated with allergen and activated to produce neutrophil chemokines. These results demonstrate that neutrophil influx after allergen challenge requires prior sensitization, is allergen-specific, is mediated through FcγRIII, and is dependent on the presence of Ab.

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