Mechanisms of lactobacillus–mediated protection against acute respiratory virus infection

Wednesday, October 26, 2011 — Poster Session IV
2:00 p.m. – 4:00 p.m.	Natcher Conference Center	NIAID	IMMUNO/INFLAM-7

Authors

• KE Garcia-Crespo
• SJ Gabryszewski
• KD Dyer
• HF Rosenberg

Abstract

Previously, we showed that lactobacilli, targeted to the respiratory epithelium, are effective at suppressing virus-induced inflammation and protecting against lethal disease. Lactobacilli do not colonize the lungs, but are cleared rapidly, with production of chemoattractants CXCL1 and CCL3 and transient recruitment of neutrophils. At peak, typically 24 hrs after intranasal inoculation with 108cfu Lactobacillus reuteri, neutrophils represent 70% of the total lung cells, declining to 12% by day 4; few to no clinical symptoms are detected. To evaluate the role of neutrophils (and other leukocytes) in promoting protection, we examined lactobacillus-priming followed by infection (pneumonia virus of mice, PVM) using specific cell-deletion methods. Innate eosinophil deficiency or depletion of alveolar macrophages had no impact on survival of lactobacillus-primed, PVM-infected mice. Neutrophil recruitment persisted despite multiple attempts at antibody-mediated ablation (anti-Ly6G). Transient neutrophil recruitment was also observed in response to intranasal inoculation with isolated bacterial peptidoglycan, but this alone did not promote protection against PVM infection, results suggesting that neutrophil recruitment, while prominent, may not be a crucial component of lactobacillus-mediated protection. Our goal is to understand the mechanisms via which lactobacilli promote broad-spectrum mucosal immunomodulation and provide protection against respiratory virus infection in the absence of specific antiviral vaccines.

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