Pendrin expression is affected in epithelial and macrophages cells by B. pertussis infection

VALDEZ, HUGO; LAMBERTI, YANINA; GORGOJO, JUAN PABLO; RODRIGUEZ, MARIA EUGENIA

Congreso; Reunión conjunta de sociedades de biociencias. LXIV Reunión Anual de la Sociedad Argentina de Inmunología (SAI).; 2017

Pendrin is a transmembrane anion exchanger (encode by SLC26A4 gene) whose expression was first described in epithelial cells and later suggested in other cells of the immune system. In the airway, pendrin mediates the uptake of Cl- from the airway apical surface and the export of both HCO3- and thiocyanate into the airway surface liquid. The bicarbonate exported by pendrin produces an optimal pH environment for inflammatory mediators activity and favors the secretion of proteins involved in antimicrobial mechanisms in the lung. A transcriptomic study recently demonstrated the up-regulation of pendrin in mouse lung during B. pertussis (Bp) infection in a pertussis toxin-dependent (PTx) manner. Immunohistochemistry of Bp infected mice revealed pendrin expression in the lungs epithelia and possibly in macrophages. In order to gain a deeper insight into pendrin influence in Bp host infection we here examined the expression of pendrin in human bronchial epithelial cell (HBE) and human monocyte cell line (THP-1) during the Bp infection. qRT-PCR results showed that SLC26A4 expression in HBE cells is up-regulated soon after Bpwt infection. Ptx was found involved in host cell response since the infection with a PTx deficient mutant (BpΔPtx) induced significantly lower pendrin up-regulation. On the other hand, THP1 Bp intracellular infection assays also showed a significant up-regulation of SLC26A4 early after Bpwt infection. Again, a lower up-regulation was observed in BpΔPtx infection. As the intracellular infection progressed, however, SLC26A4 level was found down-regulated in macrophages infected with either Bp strain as compared with uninfected cells showing that this pathogen is able to modulate this response in a PTx independent manner. Altogether these results suggest that pendrin might contribute to host defense response during Bp infection but also show that Bp is able to manipulate its expression in macrophage during the development of intracellular infections.