PENDRIN EXPRESSION IS AFFECTED IN EPITHELIAL AND MACROPHAGES CELLS BY B. pertussis INFECTION

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

Buenos Aires

Congreso; REUNIÓN CONJUNTA DE SOCIEDADES DE BIOCIENCIAS; 2017

Sociedad Argentina de Inmunología

Pendrin is a transmembrane anion exchanger (encode by SLC26A4gene) whose expression was first described in epithelial cellsand later suggested in other cells of the immune system. In the airway,pendrin mediates the uptake of Cl- from the airway apical surfaceand the export of both HCO3- and thiocyanate into the airwaysurface liquid. The bicarbonate exported by pendrin produces anoptimal pH environment for inflammatory mediators activity and favorsthe secretion of proteins involved in antimicrobial mechanismsin the lung. A transcriptomic study recently demonstrated the up-regulationof pendrin in mouse lung during B. pertussis (Bp) infection ina pertussis toxin-dependent (PTx) manner. Immunohistochemistryof Bp infected mice revealed pendrin expression in the lungs epitheliaand possibly in macrophages. In order to gain a deeper insightinto pendrin influence in Bp host infection we here examined theexpression of pendrin in human bronchial epithelial cell (HBE) andhuman monocyte cell line (THP-1) during the Bp infection. qRT-PCRresults showed that SLC26A4 expression in HBE cells is up-regulatedsoon after Bpwt infection. Ptx was found involved in host cellresponse 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 significantup-regulation of SLC26A4 early after Bpwt infection. Again, a lowerup-regulation was observed in BpΔPtx infection. As the intracellularinfection progressed, however, SLC26A4 level was found down-regulatedin macrophages infected with either Bp strain as comparedwith uninfected cells showing that this pathogen is able to modulatethis response in a PTx independent manner. Altogether these resultssuggest that pendrin might contribute to host defense responseduring Bp infection but also show that Bp is able to manipulate itsexpression in macrophage during the development of intracellularinfections.