Abstract

BackgroundCockroach exposure is a major risk factor for the development of asthma. Inhalation of fecal remnants (frass) is the likely sensitizing agent; however isolated frass has not been tested for its ability to induce experimental asthma in mice.MethodsMice (Balb/c or C57Bl/6) were sensitized and challenged with GC frass or GC frass devoid of proteases and measurements of airway inflammation and hyperresponsiveness were performed (interleukin (IL)-5, -13, and interferon gamma (IFNγ) levels in bronchoalveolar lavage fluid, serum IgE levels, airway hyperresponsiveness, cellular infiltration, and mucin production).ResultsSensitization and challenge of Balb/c mice with GC frass resulted in increased airway inflammation and hyperresponsiveness. C57Bl/6 mice were not susceptible to this model of sensitization; however they were sensitized to GC frass using a more aggressive sensitization and challenge protocol. In mice that were sensitized by inhalation, the active serine proteases in GC frass played a role in airway hyperresponsiveness as these mice had less airway hyperresponsiveness to acetylcholine and less mucin production. Proteases did not play a role in mediating the allergic inflammation in mice sensitized via intraperitoneal injection.ConclusionWhile both strains of mice were able to induce experimental asthma following GC frass sensitization and challenge, the active serine proteases in GC frass only play a role in airway hyperresponsiveness in Balb/c mice that were susceptible to sensitization via inhalation. The differences in the method of sensitization suggest genetic differences between strains of mice.

Highlights

  • The principal domestic cockroach species that commonly infests homes in the United States are the German cockroaches (GC; Blattella germanica)

  • No mucin was detected in PBS treated Balb/c mice, while 49 ± 1% of the airways stained positive for mucin in mice sensitized and challenged with GC frass

  • 88 ± 3% of the cells in the airway were positive for mucin. These data demonstrate that Balb/c mice are susceptible to GC frass-induced allergic inflammation and airway hyperresponsiveness following sensitization and challenge by intratracheal inhalation, while C57Bl/6 mice only had increases in TH2 cytokine levels, but no increase in IgE or airway hyperresponsiveness

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Summary

Introduction

The principal domestic cockroach species that commonly infests homes in the United States are the German cockroaches (GC; Blattella germanica). Cockroaches (CR) produce a variety of substances that may be allergenic including exoskeleton, secretions, egg castings and fecal remnants (frass). The sensitization route of CR exposure is not fully understood, it is likely that inhalation of frass is a main route of exposure. While frass contains high levels of the cockroach allergens Bla g1 and Bla g2 [4], it contains active serine proteases [5,6], coliforms [7], pheromones, and a number of proteins and other components. While frass is the most likely source of GC allergen exposure, isolated GC frass has never been used as a sensitizing agent to induce the experimental asthma phenotype in mice. Inhalation of fecal remnants (frass) is the likely sensitizing agent; isolated frass has not been tested for its ability to induce experimental asthma in mice

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