The B-cell superantigen Finegoldia magna protein L causes pulmonary inflammation by a mechanism dependent on MyD88 but not B cells or immunoglobulins

Amy L. Anderson, Yi Zheng, Decheng Song, David Larosa, Nico Van Rooijen, Gerold Kierstein, Sonja Kierstein, Angela Franciska Haczku, Arnold I. Levinson

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Objective and design: To determine whether Finegoldia magna protein L (PL) causes lung inflammation and, if so, whether the response is dependent on its immunoglobulin (Ig)-binding B-cell superantigenic property. Material: Pulmonary inflammatory reactions were analyzed at various time points after intratracheal administration of PL to various strains of mice. Results: PL caused peribronchial and perivascular inflammation that peaked at 18-24 h. Polymorphonuclear cells (PMNs) began to accumulate in bronchoalveolar lavage fluid (BALF) of PL-challenged mice by 4 h and accounted for >90% of leukocytes by 18-24 h. Inflammation was marked by the appearance of MIP-2, KC, TNF-α, and IL-6 in the BALF with peak levels attained 4 h after PL administration. PL-induced pulmonary inflammation was associated with increased airway hyper-reactivity following inhalation of methacholine. The inflammatory reaction was unabated in mice lacking B cells and immunoglobulins. In contrast, PL-induced inflammation was abrogated in MyD88-deficient mice. PL-induced responses required alveolar macrophages. Conclusions: These results strongly suggest that PL-induced lung inflammation is dependent on an innate MyD88-dependent pathway rather than the Ig-binding properties of this microbial B cell superantigen. We propose that this pulmonary inflammatory reaction is caused by the interaction of PL with a Toll-like receptor expressed on alveolar macrophages.

Original languageEnglish (US)
Pages (from-to)161-169
Number of pages9
JournalInflammation Research
Volume61
Issue number2
DOIs
StatePublished - Feb 2012
Externally publishedYes

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Superantigens
Immunoglobulins
Pneumonia
B-Lymphocytes
Proteins
Bronchoalveolar Lavage Fluid
Alveolar Macrophages
Inflammation
Peptococcus magnus L-protein
Lung
Methacholine Chloride
Toll-Like Receptors
Inhalation
Interleukin-6
Leukocytes

Keywords

  • In-vivo inflammation
  • Inflammatory mediators
  • Innate immunity
  • Leukocytes

ASJC Scopus subject areas

  • Pharmacology
  • Immunology

Cite this

The B-cell superantigen Finegoldia magna protein L causes pulmonary inflammation by a mechanism dependent on MyD88 but not B cells or immunoglobulins. / Anderson, Amy L.; Zheng, Yi; Song, Decheng; Larosa, David; Van Rooijen, Nico; Kierstein, Gerold; Kierstein, Sonja; Haczku, Angela Franciska; Levinson, Arnold I.

In: Inflammation Research, Vol. 61, No. 2, 02.2012, p. 161-169.

Research output: Contribution to journalArticle

Anderson, Amy L. ; Zheng, Yi ; Song, Decheng ; Larosa, David ; Van Rooijen, Nico ; Kierstein, Gerold ; Kierstein, Sonja ; Haczku, Angela Franciska ; Levinson, Arnold I. / The B-cell superantigen Finegoldia magna protein L causes pulmonary inflammation by a mechanism dependent on MyD88 but not B cells or immunoglobulins. In: Inflammation Research. 2012 ; Vol. 61, No. 2. pp. 161-169.
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abstract = "Objective and design: To determine whether Finegoldia magna protein L (PL) causes lung inflammation and, if so, whether the response is dependent on its immunoglobulin (Ig)-binding B-cell superantigenic property. Material: Pulmonary inflammatory reactions were analyzed at various time points after intratracheal administration of PL to various strains of mice. Results: PL caused peribronchial and perivascular inflammation that peaked at 18-24 h. Polymorphonuclear cells (PMNs) began to accumulate in bronchoalveolar lavage fluid (BALF) of PL-challenged mice by 4 h and accounted for >90{\%} of leukocytes by 18-24 h. Inflammation was marked by the appearance of MIP-2, KC, TNF-α, and IL-6 in the BALF with peak levels attained 4 h after PL administration. PL-induced pulmonary inflammation was associated with increased airway hyper-reactivity following inhalation of methacholine. The inflammatory reaction was unabated in mice lacking B cells and immunoglobulins. In contrast, PL-induced inflammation was abrogated in MyD88-deficient mice. PL-induced responses required alveolar macrophages. Conclusions: These results strongly suggest that PL-induced lung inflammation is dependent on an innate MyD88-dependent pathway rather than the Ig-binding properties of this microbial B cell superantigen. We propose that this pulmonary inflammatory reaction is caused by the interaction of PL with a Toll-like receptor expressed on alveolar macrophages.",
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