Effects of female sexual chemosignals on mucosal immunity in BALB/c and C57BL/6 male mice

Effects of female sexual chemosignals on mucosal immunity in BALB/c and C57BL/6 male mice The immune response to immunogenic stimuli depends on various factors such as the cytokine context, way of entry, and immune status of the organism. In mice, the entry of the female’s chemosignals into the male organism via the respiratory system activates the mucosal immune response, which leads to the development of enhanced resistance to infections and is of adaptive value. However, the activation of mucosal immunity depends on the genetic predispositions of the immune response. BALB/c and C57BL/6 are prototypically Th2-and Th1-type mouse strains, respectively; therefore, they can serve as the perfect model organisms for studying the activation mechanism of the lungs’ mucosal immune activation in response to the female’s chemosignals. The respiratory tract’s mucosal immune response to intranasal application of LPS, urea solution, saline solution, and female urine used as a chemosignal was investigated in the BALB/c and C57BL/6 male mice. Application of both female urine and LPS increased the total white blood cell count and protein concentration in the bronchoalveolar lavage fluid (BLF) in BALB/c male mice but not in C57BL/6 male mice, suggesting an important role of the Th2 pathway in the lungs’ mucosal immune response. At the same time, urine application provoked a significantly lower plasma corticosterone elevation than LPS. Thus, the sexual signals associated with infection risks provide genotype-dependent mobilization of the innate immunity without significant activation of physiological stress mechanisms. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Russian Journal of Genetics: Applied Research Springer Journals

Effects of female sexual chemosignals on mucosal immunity in BALB/c and C57BL/6 male mice

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Publisher
Pleiades Publishing
Copyright
Copyright © 2017 by Pleiades Publishing, Ltd.
Subject
Biomedicine; Human Genetics
ISSN
2079-0597
eISSN
2079-0600
D.O.I.
10.1134/S2079059717050112
Publisher site
See Article on Publisher Site

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