Limits...
Impaired sense of smell and altered olfactory system in RAG-1(-∕-) immunodeficient mice.

Rattazzi L, Cariboni A, Poojara R, Shoenfeld Y, D'Acquisto F - Front Neurosci (2015)

Bottom Line: Our results show that these mice have a reduced engagement in different types of odors and this phenotype is associated with disorganized architecture of glomerular tissue and atrophy of the main olfactory epithelium.Most intriguingly this defect manifests specifically in adult age and is not due to impairment in the patterning of the olfactory neuron staining at the embryo stage.Together these findings provide a formerly unreported biological evidence for an altered function of the olfactory system in RAG-1 (-∕-) mice.

View Article: PubMed Central - PubMed

Affiliation: William Harvey Research Institute, Barts and The London School of Medicine and Dentistry Queen Mary University of London, UK.

ABSTRACT
Immune deficiencies are often associated with a number of physical manifestations including loss of sense of smell and an increased level of anxiety. We have previously shown that T and B cell-deficient recombinase activating gene (RAG-1)(-∕-) knockout mice have an increased level of anxiety-like behavior and altered gene expression involved in olfaction. In this study, we expanded these findings by testing the structure and functional development of the olfactory system in RAG-1 (-∕-) mice. Our results show that these mice have a reduced engagement in different types of odors and this phenotype is associated with disorganized architecture of glomerular tissue and atrophy of the main olfactory epithelium. Most intriguingly this defect manifests specifically in adult age and is not due to impairment in the patterning of the olfactory neuron staining at the embryo stage. Together these findings provide a formerly unreported biological evidence for an altered function of the olfactory system in RAG-1 (-∕-) mice.

No MeSH data available.


Related in: MedlinePlus

Decreased thickness and cellularity of the main olfactory epithelium of RAG-1−∕− mice. The pictures in (A,B) show the hematoxilin and eosin staining of the MOE of 7 week-old RAG-1−∕− and control C57/BL6 mice. The pictures in (A′,B′) are higher magnification of the boxed areas in (A,B) and highlight the differences in thickness (black segments) between the two tissues (arrowheads). The different cellular layers of MOE are indicated with arrows and correspond to: cilia, chemosensory cilia; OSN, olfactory sensory neurons; connective, connective tissue and cartilage. Quantitation if OE thickness is displayed in (C). Pictures are representative of n = 3 mice of each genotypes. Scale bars: 150 μm (A,B).
© Copyright Policy
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4563081&req=5

Figure 5: Decreased thickness and cellularity of the main olfactory epithelium of RAG-1−∕− mice. The pictures in (A,B) show the hematoxilin and eosin staining of the MOE of 7 week-old RAG-1−∕− and control C57/BL6 mice. The pictures in (A′,B′) are higher magnification of the boxed areas in (A,B) and highlight the differences in thickness (black segments) between the two tissues (arrowheads). The different cellular layers of MOE are indicated with arrows and correspond to: cilia, chemosensory cilia; OSN, olfactory sensory neurons; connective, connective tissue and cartilage. Quantitation if OE thickness is displayed in (C). Pictures are representative of n = 3 mice of each genotypes. Scale bars: 150 μm (A,B).

Mentions: On the opposite site of the glomeruli, olfactory neurons innervate the olfactory epithelium (Leinwand and Chalasani, 2011; Murthy, 2011; Takeuchi and Sakano, 2014). These tissues present in the turbinates of the nose act as “platform” for the olfactory neurons and undergo continuous regeneration. Given that olfactory bulbectomy has been shown to severely affect olfactory epithelium regeneration (Suzuki et al., 1998; Makino et al., 2009), we reasoned that the absence of fully functional olfactory neurons would impact the status of OE in RAG-1−∕−. Consistent with our expectation, staining of sagittal paraffin sections with haematoxylin and eosin showed reduced cellularity and thickness of the MOE in RAG-1−∕− tissues compared to wild-type control (Figures 5A,B, respectively; Figure 5C, OE thickness: wild type 0.1900 ± 0.01581 vs. RAG-1−∕− 0.1000 ± 0.01558; p < 0.005) further supporting the idea that the absence of immune cells may cause histological changes in olfactory neurons and an impairment of olfaction mainly in adult mice.


Impaired sense of smell and altered olfactory system in RAG-1(-∕-) immunodeficient mice.

Rattazzi L, Cariboni A, Poojara R, Shoenfeld Y, D'Acquisto F - Front Neurosci (2015)

Decreased thickness and cellularity of the main olfactory epithelium of RAG-1−∕− mice. The pictures in (A,B) show the hematoxilin and eosin staining of the MOE of 7 week-old RAG-1−∕− and control C57/BL6 mice. The pictures in (A′,B′) are higher magnification of the boxed areas in (A,B) and highlight the differences in thickness (black segments) between the two tissues (arrowheads). The different cellular layers of MOE are indicated with arrows and correspond to: cilia, chemosensory cilia; OSN, olfactory sensory neurons; connective, connective tissue and cartilage. Quantitation if OE thickness is displayed in (C). Pictures are representative of n = 3 mice of each genotypes. Scale bars: 150 μm (A,B).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4563081&req=5

Figure 5: Decreased thickness and cellularity of the main olfactory epithelium of RAG-1−∕− mice. The pictures in (A,B) show the hematoxilin and eosin staining of the MOE of 7 week-old RAG-1−∕− and control C57/BL6 mice. The pictures in (A′,B′) are higher magnification of the boxed areas in (A,B) and highlight the differences in thickness (black segments) between the two tissues (arrowheads). The different cellular layers of MOE are indicated with arrows and correspond to: cilia, chemosensory cilia; OSN, olfactory sensory neurons; connective, connective tissue and cartilage. Quantitation if OE thickness is displayed in (C). Pictures are representative of n = 3 mice of each genotypes. Scale bars: 150 μm (A,B).
Mentions: On the opposite site of the glomeruli, olfactory neurons innervate the olfactory epithelium (Leinwand and Chalasani, 2011; Murthy, 2011; Takeuchi and Sakano, 2014). These tissues present in the turbinates of the nose act as “platform” for the olfactory neurons and undergo continuous regeneration. Given that olfactory bulbectomy has been shown to severely affect olfactory epithelium regeneration (Suzuki et al., 1998; Makino et al., 2009), we reasoned that the absence of fully functional olfactory neurons would impact the status of OE in RAG-1−∕−. Consistent with our expectation, staining of sagittal paraffin sections with haematoxylin and eosin showed reduced cellularity and thickness of the MOE in RAG-1−∕− tissues compared to wild-type control (Figures 5A,B, respectively; Figure 5C, OE thickness: wild type 0.1900 ± 0.01581 vs. RAG-1−∕− 0.1000 ± 0.01558; p < 0.005) further supporting the idea that the absence of immune cells may cause histological changes in olfactory neurons and an impairment of olfaction mainly in adult mice.

Bottom Line: Our results show that these mice have a reduced engagement in different types of odors and this phenotype is associated with disorganized architecture of glomerular tissue and atrophy of the main olfactory epithelium.Most intriguingly this defect manifests specifically in adult age and is not due to impairment in the patterning of the olfactory neuron staining at the embryo stage.Together these findings provide a formerly unreported biological evidence for an altered function of the olfactory system in RAG-1 (-∕-) mice.

View Article: PubMed Central - PubMed

Affiliation: William Harvey Research Institute, Barts and The London School of Medicine and Dentistry Queen Mary University of London, UK.

ABSTRACT
Immune deficiencies are often associated with a number of physical manifestations including loss of sense of smell and an increased level of anxiety. We have previously shown that T and B cell-deficient recombinase activating gene (RAG-1)(-∕-) knockout mice have an increased level of anxiety-like behavior and altered gene expression involved in olfaction. In this study, we expanded these findings by testing the structure and functional development of the olfactory system in RAG-1 (-∕-) mice. Our results show that these mice have a reduced engagement in different types of odors and this phenotype is associated with disorganized architecture of glomerular tissue and atrophy of the main olfactory epithelium. Most intriguingly this defect manifests specifically in adult age and is not due to impairment in the patterning of the olfactory neuron staining at the embryo stage. Together these findings provide a formerly unreported biological evidence for an altered function of the olfactory system in RAG-1 (-∕-) mice.

No MeSH data available.


Related in: MedlinePlus