Investigating the effects of particulate matter on house dust mite and ovalbumin allergic airway inflammation in mice

Alejandro R. Castañeda, Kent E Pinkerton

Research output: Contribution to journalArticlepeer-review

10 Scopus citations


Particulate matter (PM), a component of air pollution, has been shown to enhance allergen-mediated airway hypersensitivity and inflammation. Surprisingly, exposure to PMduring the sensitization to allergen is sufficient to produce immunological changes that result in heightened inflammatory effects upon future allergen exposures (challenge) in the absence of PM. This suggests that PM has the ability to modulate the allergic immune response, thereby acting as an adjuvant by enhancing the immunological memory formed during the adaptive immune response; however, the mechanisms through which this occurs remain elusive. Establishing a reproducible animal model to study the PM-mediated immunotoxicological effects that enhance allergy, may provide insights to understand how air pollution activates the immune system and thereby modulates the pathophysiology of asthma. The basic protocol can be used to study various characteristics of air pollution, such as PM size, source, or chemical composition, to help elucidate how such features may affect the allergic response in a mouse model of asthma. Using a BALB/c model of acute exposure (14 days), mice are first sensitized with allergen and PM, and then subsequently challenged with allergen only. The endpoints of this basic protocol include the assessment of inflammation via cells recovered from broncho-alveolar lavage (BAL), histopathological analysis, gene expression profiles, and protein quantification of inflammatory markers.

Original languageEnglish (US)
Pages (from-to)1-18
Number of pages18
JournalCurrent Protocols in Toxicology
StatePublished - May 1 2016


  • Air pollution
  • Airway inflammation
  • Allergen
  • Allergic mouse model
  • House dust mite (HDM)
  • Ovalbumin (OVA)
  • Particulate matter (PM)

ASJC Scopus subject areas

  • Toxicology


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