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Immunological and Inflammatory Responses to Organic Dust in Agriculture
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  • Pubmed ID:
  • Pubmed Central ID:
  • Description:
    Purpose of review

    Agriculture represents a major industry worldwide, and despite protection against the development of IgE-mediated diseases, chronic exposure to agriculture-related organic dusts is associated with an increased risk of developing respiratory disease. This article will review the literature regarding new knowledge of important etiologic agents in the dusts and focus on the immunologic responses following acute and repetitive organic dust exposures.

    Recent findings

    Although endotoxin remains important, there is an emerging role for non-endotoxin components such as peptidoglycans from Gram-positive bacteria. Pattern recognition receptors including Toll-like receptor 4 (TLR4), TLR2 and intracellular nucleotide oligomerization domain-like receptors are partially responsible for mediating the inflammatory consequences. Repeated organic dust exposures modulate innate and adaptive immune function with a resultant adaptation-like response. However, repetitive exposures cause lung parenchymal inflammation, chronic disease, and lung function decline over time.


    The immunological consequences of organic dust exposure in the farming industry are likely explained by the diversity of microbial motifs in dust that can elicit differing innate immune receptor signaling pathways. Whereas initial activation results in a robust inflammatory response, repetitive dust exposures modulate immunity. This can result in low-grade, chronic inflammation and/or protection against allergic disease.

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  • Funding:
    1 U54 OH010162-01/OH/NIOSH CDC HHS/United States
    ES015522-03S1/ES/NIEHS NIH HHS/United States
    K08 ES015522/ES/NIEHS NIH HHS/United States
    K08 ES015522-01/ES/NIEHS NIH HHS/United States
    K08 ES015522-05/ES/NIEHS NIH HHS/United States
    R01 ES019325/ES/NIEHS NIH HHS/United States
    R01 ES019325/ES/NIEHS NIH HHS/United States
    R01 ES019325-02/ES/NIEHS NIH HHS/United States
    R01 OH008539-01/OH/NIOSH CDC HHS/United States
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