» Articles » PMID: 22249932

The B-cell Superantigen Finegoldia Magna Protein L Causes Pulmonary Inflammation by a Mechanism Dependent on MyD88 but Not B Cells or Immunoglobulins

Overview
Journal Inflamm Res
Date 2012 Jan 18
PMID 22249932
Citations 1
Authors
Affiliations
Soon will be listed here.
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.

Citing Articles

, an Anaerobic Gram-Positive Bacterium of the Normal Human Microbiota, Induces Inflammation by Activating Neutrophils.

Neumann A, Bjorck L, Frick I Front Microbiol. 2020; 11:65.

PMID: 32117109 PMC: 7025542. DOI: 10.3389/fmicb.2020.00065.

References
1.
Kroeger K, Sullivan B, Locksley R . IL-18 and IL-33 elicit Th2 cytokines from basophils via a MyD88- and p38alpha-dependent pathway. J Leukoc Biol. 2009; 86(4):769-78. PMC: 2752018. DOI: 10.1189/jlb.0708452. View

2.
Kurowska-Stolarska M, Stolarski B, Kewin P, Murphy G, Corrigan C, Ying S . IL-33 amplifies the polarization of alternatively activated macrophages that contribute to airway inflammation. J Immunol. 2009; 183(10):6469-77. DOI: 10.4049/jimmunol.0901575. View

3.
Jain D, Keslacy S, Tliba O, Cao Y, Kierstein S, Amin K . Essential role of IFNbeta and CD38 in TNFalpha-induced airway smooth muscle hyper-responsiveness. Immunobiology. 2008; 213(6):499-509. PMC: 2587232. DOI: 10.1016/j.imbio.2007.12.002. View

4.
Anderson A, Sporici R, Lambris J, Larosa D, Levinson A . Pathogenesis of B-cell superantigen-induced immune complex-mediated inflammation. Infect Immun. 2006; 74(2):1196-203. PMC: 1360360. DOI: 10.1128/IAI.74.2.1196-1203.2006. View

5.
Levinson A, Kozlowski L, Zheng Y, Wheatley L . B-cell superantigens: definition and potential impact on the immune response. J Clin Immunol. 1995; 15(6 Suppl):26S-36S. DOI: 10.1007/BF01540891. View