NLRP12 was originally suggested to form an inflammasome with PYCARD. However, more recently, NLRP12 has been characterized as a negative regulator of both canonical and noncanonical NF-kB signaling. NLRP12 was shown to interact with and inhibit the accumulation of hyperphosphorylated IRAK1, downstream of TLR signaling, to attenuate canonical NF-kB signaling. Similarly, NLRP12 associates with NIK in the non-canonical NF-kB pathway, which results in the rapid proteosomal degradation of the kinase. NF-kB regulates a variety of inflammatory pathways that may directly contribute to asthma pathogenesis. However, because of its central role in innate immunity, NF-kB and modulators of NF-kB signaling are more typically associated with modulating the host immune response to agents associated with asthma exacerbation. Prior to this research, only one additional publication has explored the in vivo role of NLRP12. In this previous work, NLRP12 was found to attenuate the development of contact hypersensitivity. The underlying mechanism was found to be associated with altered dendritic cell and granulocyte migration in response to chemokine signaling. This finding was consistent with results from human association studies that reported identifying an association between specific mutations in NLRP12 and a subgroup of atopic dermatitis patients. Because contact hypersensitivity and asthma share many of the same immunopathological features, we sought to characterize the in vivo contribution of NLRP12 in common mouse models of allergic airway inflammation. Anti-inflammatory biopharmaceuticals are considered to be a key element in the clinical regulation of innate and allergic airway inflammation in several human lung diseases. Thus, proteins that function as negative regulators of inflammation are of immense clinical and scientific value. NLRP12 has been shown to be a robust inhibitor of various inflammatory pathways and influence the development of contact hypersensitivity. Subepithelial collagen deposition is a commonly observed feature of asthma and is typically associated with airway remodeling and hyper-responsiveness. The deposition of fibrin, collagen and collagen precursors is facilitated by a host of genes and many are regulated, either directly or indirectly by NF-kB. However, the airway remodeling that is typically observed in human asthma is not recapitulated in short term acute OVA mouse models. Because NLRP12 has been shown to function as a negative regulator of NF-kB, it is possible that loss of NLRP12 could result in accelerated airway remodeling. To evaluate this possibility, we PF-04217903 utilized Masson’s Trichrome staining of lung sections to assess collagen and collagen precursor deposition in the lungs. Consistent with the characteristics of this model, we did not observe an increase in Trichrome positive staining following the short term acute OVA airway challenge in any of the mice tested. Thus, the deletion of Nlrp12 did not appear to have an effect on collagen deposition in the OVA mediated allergic airway disease model. NLRP12 has been shown to influence both canonical and noncanonical NF-kB signaling and classical and nonclassical MHC class I gene expression in vitro. In vivo, Nlrp12 deficiency significantly influences the development of contact hypersensitivity. Based on these findings we hypothesized that the Nlrp122/2 mouse would provide a suitable model to study the contribution of this gene.